Poisons in our homes. Poisoning a person with poisons Making poisons at home

Omega is a highly toxic substance that is part of hemlock. Just 100 milligrams of it (8 leaves) will be enough to kill a person. How it works: all body systems gradually fail, except the brain. As a result, you, being in your right mind, begin to die slowly and painfully until you suffocate.

The most popular hemlock was among the Greeks. Interesting fact: this plant caused the death of Socrates in 399 BC. The Greeks executed him in this way for disrespect for the gods.

Source: wikipedia.org

No. 9 - Aconite

This poison is obtained from the fighter plant. It causes arrhythmia, which ends in suffocation. They say that even touching this plant without gloves can result in death. It is almost impossible to detect traces of poison in the body. The most famous case of use is that Emperor Claudius poisoned his wife Agrippina by adding aconite to her mushroom dish.

Source: wikipedia.org

#8 - Belladonna

In the Middle Ages, belladonna was used as a women's cosmetic (rouge for cheeks). Special drops were even obtained from the plant to dilate the pupils (at that time this was considered fashionable). You could also swallow belladonna leaves - one is just enough for a person to die. Berries are also not a miss: you only need to eat 10 of them to die. In those days, a special poisonous solution was made from the latter, which was used to lubricate arrowheads.

Source: wikipedia.org

#7 - Dimethylmercury

This is the slowest and most insidious killer. This is because even 0.1 milliliter that accidentally gets on your skin will be enough to be fatal. The most notorious case: in 1996, a chemistry teacher at Dartmouth College in New Hampshire dropped a drop of poison onto her hand. Dimethylmercury burned through a latex glove; symptoms of poisoning appeared after 4 months. And 10 months later the scientist died.

Source: wikipedia.org

#6 - Tetrodotoxin

This poison is found in blue-ringed octopuses and pufferfish. With the former, things are very bad: octopuses deliberately attack their prey with tetrodotoxin, imperceptibly pricking it with special needles. Death occurs within a few minutes, but symptoms do not appear immediately - after paralysis sets in. The venom of one blue-ringed octopus is enough to kill 26 healthy men.

It’s easier with fugu: their poison is only dangerous when you’re about to eat the fish. It all depends on the correct preparation: if the cook is not mistaken, the tetrodoxin will all evaporate. And you will eat the dish without any consequences, except for incredible adrenaline rushes...

Source: wikipedia.org

#5 - Polonium

Polonium is a radioactive poison for which there is no antidote. The substance is so dangerous that just 1 gram of it can kill 1.5 million people in a few months. The most sensational case of the use of polonium was the death of Alexander Litvinenko, an employee of the KGB-FSB. He died in 3 weeks, the reason was that 200 grams of poison were found in his body.

Source: wikipedia.org

#4 - Mercury

1. elemental mercury - found in thermometers. Instant death occurs if it is inhaled;
2. inorganic mercury - used in the manufacture of batteries. Lethal if swallowed;
3. organic mercury. Sources are tuna and swordfish. It is recommended to eat no more than 170 grams per month. Otherwise, organic mercury will begin to accumulate in the body.

The most famous case of use is the poisoning of Amadeus Mozart. He was given mercury tablets to treat syphilis.

Below I will try to provide explanations for those who came to the topic of poisons and poisonings the hard way. If I don’t touch on something, or you want to receive more detailed instructions and explanations, don’t hesitate to ask questions, we’ll sort everything out.

1. Common sense. You shouldn't grab potassium cyanide, ricin or anything like that, just because these are the most deadly and effective poisons. These poisons are very difficult to obtain, therefore accidental poisoning is extremely unlikely. It is better to choose a less effective poison that will look more natural in this situation.

A BANAL EXAMPLE: if a person suffers from insomnia, then an overdose of sleeping pills mixed with alcohol looks much more natural than cyanide poisoning. Potassium cyanide does not promote deep and sound sleep, no?

2. Don't underestimate your opponent. The investigator is not at all the stupid and grotesque character that flashes on TV screens. Having the results of the examination in hand, he will understand perfectly well that the death was not accidental at all. Using the magical principle “Who benefits from this anyway?”, he has a great chance of getting on the trail of the poisoner.

3. Single poisoning - fight! You should not poison a person one-on-one if you are not 100% sure of the effectiveness of the poison and your alibi. The best time to use poison for its intended purpose is a feast. Witnesses!!sudden!! there must be a lot of death. There should be no witnesses to your involvement in this. A person who feels unwell during a feast is unlikely to immediately admit it - he will blame it all on alcohol and too fatty food. And he will lose precious minutes that could save his life.

4. Alcohol is a friend for all times! Even the most harmless substances are not friends with Mr. Ethanol. Poisons even more so. Many substances dissolve in alcohol, and alcohol itself dulls the senses - an ideal companion!

5. Don't be too clever. If the target is ordinary drunks, methanol will do a much better job than cyanide. If you have a heart disease, it’s easier to replace the medicine with a more effective one. If you are a drug addict, choose the substance so that it looks like an overdose.

*** For those who like to smoke, you can find options for going completely psychedelic. Optionally - with cruelty, in order to ensure the target a vacation in a madhouse through a berserk rage against a neighbor and her cute dog. For speed lovers, drive a heart into a board, which is not at all that difficult.

6. Preparation. You should not indulge in such matters without considering all the consequences. It is worth carefully thinking over an alibi for yourself: for example, if your wife decided to die, then you should tell everyone a month before this event how bad everything is, how your relationship is collapsing, perhaps you should make an appointment with a psychotherapist. All your words and actions are your alibi. This should not be neglected.

7. Is all this necessary... The responsibility always lies with you. Poisons may give a false sense of freedom and impunity, but this is not the case. You can be easily found and easily detained. Remember to be safe and ask if something is not clear. And remember:

You are responsible for what you do. Killing a granny/mother/wife for the sake of an inheritance or killing a pedophile maniac are completely different things. Use your power wisely.

Nicotine

Characteristics

Nicotine is a dark brown sticky/oily liquid. The lethal dose of pure nicotine is considered to be about 0.06 grams, but for the homemade version it is about 3-4 drops. Death from poisoning occurs within 12-24 hours.

1. Remove tobacco from ten cheaper cigarettes.

2. Grind the tobacco very well, then place it in a small beaker.

3. Pour in isopropyl alcohol (bourbonal can be used in a pinch).

4. Cover the beaker with aluminum foil.

5. Place the beaker in a Bunsen burner or electric fireplace and heat it carefully and gently. Don't let the alcohol get out of hand. If the alcohol is boiling, remove the beaker with tongs and return it back when the bubbles from boiling stop appearing. If you don't do this, the alcohol vapor will ignite! If this happens (the vapors ignite), you should remove the beaker, blow off the flame and continue heating the alcohol.

6. After one hour of heating, filter the contents of the beaker using filter paper. Discard any residue remaining on the filter paper.

7. Evaporate the resulting liquid in strong sunlight or by gently heating it. The remainder after the procedures remaining in the container will be nicotine.

With ten cigarettes you can get a dose for about 3 people.

1. The liquid was applied to the shaved back of the rabbit's neck (the rabbit could not lick the liquid). The rabbit immediately showed slower movements. After 11 o'clock the rabbit went berserk and died.

2. 2 ml was given orally to the rabbit. These were the same effects as above, but the rabbit died after 12 hours.

Nicotine is a good skin abuser and touching it is strictly prohibited. The best way to give it orally is in the form of strong coffee - 3-4 drops from a dropper will be enough.

According to some sources, the lethal dose is not 0.06 grams, but 0.5-1 grams.

Potato alkaloid

Characteristics

Green-gray liquid. Lethal dose: 0.06 g. Time to death: less than 2 minutes.

Preparation and Precautions

The preparation procedure is exactly the same as for nicotine except for the fact that the spuds on GREEN potato skins are used instead of tobacco.

Test results

1. 3 ml were given orally to a healthy rabbit. The rabbit immediately began to scream. Blood started coming out of his mouth. After 100 seconds the rabbit died.

2. The same dose was given to a small rabbit. After 7 seconds the rabbit died.

Notes

Cannot be used through the skin - only orally or by injection.

Ricin

Characteristics

Ricin (castor bean poison) appears as a white powder. Lethal dose of ricin: 0.035 g. Death occurs within a couple of minutes from oral administration and several hours from injection.

Manufacturing (only with medical gloves!)

Ricin is obtained from castor beans, the fruit of the plant Ricinus communis (Russian name for castor bean).

1. Take the skins of several castor beans and weigh the white part of the nuts.

2. Grind the beans and add 4 of their weight of acetone.

3. Leave the mixture in a plastic container for three days.

4. Filter the mixture. Dry the remainder. The resulting powder is ricin.

If the mixture is left in acetone for another three days, we obtain ricin in liquid form.

Test results

1 ml of liquid ricin was given orally to the rabbit. The rabbit has problems breathing. There was mucus coming from the mouth. After four hours the rabbit died.

2 ml of liquid ricin was given orally to the rabbit. After 2 minutes the rabbit died.

Notes

The liquid version is most convenient for mixing, especially into alcohol. The powder form may be difficult to dissolve, but can be used in food since ricin powder does not have a strong taste.

Cyanide

Buy yellow blood salt (yellow, not red, these are different substances, do not be confused!). Dehydrate with low heat on a baking sheet (no higher than 150 degrees) so that it turns white, but does not burn (if it turns black, it means it is overheated). Then mix 3 parts of dehydrated blood salt with 5 parts of potash, place in a hermetically sealed iron container and heat in a muffle furnace at 600-700 degrees for several hours. (can be left overnight). Turn off the heat and wait until it cools down.

Knock the resulting stone out of the container with a hammer. Its upper part will be pure cyanide, and its lower part will be potash, they are visually different. You break this stone into large pieces in a basin with a hammer, grind it into powder in a mortar and store it only in an airtight container.

A muffle furnace is a must. It needs to be heated for a long time and the temperature should not be exceeded.

Safety precautions: work in a ventilated area, do not eat cyanide with spoons or sprinkle it on yourself, wear gloves. After the synthesis, do not allow pets into the room for a few more days, since grains of cyanide that will fly far away when breaking the stone with a hammer will remain on the floor; this will be enough for them.

An antiserum-based antidote for venomous animal bites includes a mixture of at least two antisera produced against different venoms. The antivenom administration kit includes an antivenom and an injection agent. The antidote has a higher immunogenicity. 4 s. and 7 salary files, 3 tables, 2 ill.

The invention relates to antitoxins and a method for their production. More specifically, the invention relates to snake antivenoms and a method for producing them. A number of animals, including gilamonsters snakes, spiders and bees, produce venoms that are dangerous to humans, for example, around the world every year about a million people suffer from poisonous snake bites, with 100,000 of these estimated to die and 300,000 others suffering throughout life. the rest of their lives with one or another form of disability. This is likely a large underestimation due to the lack of detailed reports from some parts of the world. Venoms secreted by snakes mainly to kill prey or for protection purposes are complex biological mixtures consisting of more than 50 components. Death of a snakebite victim occurs as a result of respiratory or circulatory failure caused by various neurotoxins, cardiotoxins (also called cytotoxins), coagulation factors and other substances acting alone or synergistically. Snake venoms also contain a number of enzymes that, when ingested by the victim, begin to break down the tissue. Thus, poisons contain substances designed to affect vital processes, such as nervous and muscular functions, heart function, blood circulation and permeability of the membranes. The main constituents of snake venoms are proteins, but low molecular weight compounds such as peptides, nucleotides and metal ions are also present. Venomous snakes can be divided into 4 main families: Colu bridae, Viperidae, Hydrophidae and Erapictac. The taxonomy of these snakes is described in Table. 1 and 2. Rattlesnakes, which are found exclusively in the Americas, are members of the subfamily of venomous snakes of the family known as Crotalinae, species Crotalus or Sistrusus (rattlesnakes) Bothrops, Aqka strodon and Trimerisurus. Both types of rattlesnakes can also be divided into species and subspecies. These snakes are also called "pit vipers" due to the presence of facial heat-sensitive pits, but their most famous feature is the ring, which, when present, distinguishes them from all other snakes. Each species or subspecies is distributed in a distinct geographic region in North or South America. The venom of each species of rattlesnake contains components that may be common to all rattlesnakes, common only to some small groups, or it may be specific to only one species or subspecies. The antivenom is serum or a partially purified antibody fraction of serum from animals that have been made immune to the toxicity of the venom by a regimen of injection of increasing doses of snake venom. Scientific research into the antidote began with the development of Henry Seawell in 1887 and has continued throughout the present century. Currently, a large number and variety of monospecific and polyspecific antivenoms are produced throughout the world. Classification of poisonous snakes. Class Reptilla (reptiles)

Order Sqamata (snakes and lizards)

Suborder Serpentes (snakes)

Subsuborder Alethinophidia (spectacled snakes)

Superfamily Colu broidea (creeping snakes)

As used herein, the term "Monospecific antivenom" refers to an antivenom produced against the venom of one species or subspecies of venomous animals. The term "polyspecific antivenom" refers to an antivenom produced against a mixture of two or more venoms from different species or subspecies of venomous animals. The terms monospecific and polyspecific antiserum are used herein to avoid confusion that may be caused by the use of the common alternative expressions "monovalent" and "polyvalent" antiserum. This terminology is used because the term "valency" is used by immunologists to express the number of bonding sites (binding sites) present in an antibody or antibody cleavage product, so, for example, an Ig G molecule is divalent while an F (ab) fragment which has only one bond site is monovalent. The use of the term "specific" in the description of the antiserum eliminates any confusion. In G. Seawell's first research work, pigeons were inoculated with sublethal doses of rattlesnake venom, followed by injections of increasing doses to levels above those that would initially cause death when administered. Thus, it was revealed that the birds have developed resistance to the poison. In 1889, Kaufmann obtained similar results using the European snake Viperk beras, and in 1892, Calmette, working in Saigon with cobra venom, reported that resistance could be imparted by gradual injections of venom. However, it was Kanthak who first instilled resistance in another animal, after mixing venom with blood from an immunized animal, he discovered resistance to lethal doses of snake venom. Calmette's main goal was to habituate the animal to frequent, repeated, gradually increasing doses of poison (usually cobra venom). He found that after 16 months, immunized horses became tolerant to 80 times the lethal dose of the poison. He also showed that antiserum obtained from blood taken from these horses had a neutralizing effect of 20,000 units when administered to rabbits, i.e. 1 ml of serum could neutralize the minimum lethal dose of poison for 20,000 g of rabbits. The main known antivenoms are refined concentrates of equine serum globulins, prepared in liquid or dry form. Antivenoms are obtained from horses that have been immunized against only one venom to produce a monospecific antivenom or a mixture of venoms to produce a polyspecific antivenom. Antidotes have been prepared to treat the major types of snake envenomation. Since then, over the last century, the methods of obtaining have changed little. Immune equine serum may be subjected to a crude purification step, usually using ammonium sulfate to isolate the globulin fraction, and in some cases this is the form of the final product. Since antidotes in this form can cause severe serum reactions, it is known to use pepsin digestion to remove the Fc portion of the immunoglobulin, which is primarily responsible for such immunogenic reactions. The effectiveness of known antidotes in neutralizing both the harmful and apparently non-harmful effects of a specific poison can vary greatly and depends on a number of factors. Most important among these factors are the specificity of the antivenom, the titer of the antibodies produced, and the degree of concentration or purification of the final product. In general, the most specific antidote with a great future is the one that will neutralize the provoking poison. Monospecific antidotes, developed against one poison, are therefore more effective against the corresponding poison. However, such antivenoms are only used to treat snake bites if the species or subspecies of the attacking snake has been identified. If the attacking snake is not identified, as is usually the case in a field situation, a polyspecific antivenom, formulated against a range of different venoms, is preferred to increase the likelihood of an antivenom that is effective against the venom of an unidentified snake. Known multispecific antivenoms, however, lack the specificity of monospecific antivenoms and are therefore less effective at neutralizing the pharmacological activity of the venom. The unexpected discovery was made that an antivenom (referred to here as a "mixed monospecific antivenom") containing a mixture of different antisera developed separately for different venoms is more effective in neutralizing the pharmacological activity of the venom than the known polyspecific antivenom obtained by producing a single antiserum for a whole range of venoms , but retains the broad specificity of polyspecific antivenoms. According to a first aspect of the invention, there is provided an antidote comprising a mixture of at least two different antisera raised against different venoms. It is believed that antivenoms containing a mixture of different antisera are more effective than known polyspecific antivenoms, since the former may contain a higher proportion of antibodies directed against low molecular weight and/or insufficiently immunogenic components of venoms. Snake venoms are complex multicomponent mixtures of protein, nucleotides and metal ions. These components differ in molecular weight, in the degree of their antigenicity and in their concentration in the venom. When a venom is injected into an animal to produce antiserum, a range of antibody populations can arise. The concentration and medium of the antibodies produced will vary according to various criteria, for example the number of epitopes on the surface of the component, the immunogenicity of each epitope, the concentration of each component. Lethal, neurotoxic venom components (including, for example, rattlesnake venoms) often include low molecular weight, weakly immunogenic components present only in low concentrations. It is unlikely that such components will cause high antibody titers. This problem is believed to be exacerbated in the production of a multispecific antivenom by the use of an immunizing mixture comprising a mixture of venoms in which low molecular weight and weakly immunogenic components are further diluted with highly immunogenic components. The production of a polyspecific antivenom results in an antivenom in which antibodies to some components do not exist or are present in such low concentrations that their effectiveness is negligible. In contrast, the mixed monospecific antivenoms of the invention contain a mixture of antisera raised against different venoms in separate groups of animals. In the production of antisera, the individual number of possible antibody populations that are available for each serum is the same, but the number of epitopes in the immunogen is much smaller. Thus, it is believed that antiserum components contain a higher proportion of protective antibodies against low molecular weight, weakly immunogenic components than multispecific antivenoms. Combining monospecific antisera to produce a mixed monospecific antiserum results in an antivenom that has all the populations of the monospecific serum and therefore provides better protection, and also has the advantages of a polyspecific antivenom in that the cross-reactivity of the antivenom is maximized. It will be appreciated that each antivenom component of the mixed monospecific antivenom according to the invention may itself be a monospecific antivenom or a polyspecific antivenom. For example, a mixed monospecific antivenom may include a mixture of a polyspecific antivenom produced against venoms A+B and a monospecific antivenom produced against venom C. Preferably, each antivenom component is a monospecific antivenom. For example, a mixed monospecific antivenom may include a mixture of monospecific antivenoms raised against poisons A, B, and C. Antisera that include a mixed monospecific antivenom can be mixed in any suitable proportion. Preferably, the mixed monospecific antivenom contains antiserum mixed in a proportion appropriate to the geographic area in which the mixed monospecific antivenom is intended for use. Factors that may be considered in the preparation of such a "custom" mixed monospecific antivenom are the population, distribution, behavior and toxicity of the particular venomous animal in a particular area. The composition of a mixed monospecific antivenom can be determined by statistical analysis of human bites in a specific geographic area by specific species or subspecies of venomous animals. Preferably, each component of the mixed monospecific antivenom antiserum is present in direct proportion to the relative frequency of bites to humans in a particular geographic area by the particular species or subspecies of the venomous animal against which the venom is produced. For example, the Diamond-back rattlesnake is classified into two geographic types known as the Eastern (C. ademauteus) and Western (C. atrox/Diamoud-back). Therefore, a mixed monospecific antivenom can be prepared that is suitable for snakes in a particular geographic area. The inclusion of an antiserum against snakes that are not found in the area, which would dilute the effectiveness of any product, is therefore unnecessary. This ability to produce custom antivenoms allows the compounded monospecific antivenoms of the invention to approach or even improve upon the effectiveness of a homologous monospecific antivenom without conducting a statistical study of snakebite patterns in a geographic area. Antisera including the antivenom can be produced in any suitable animal, for example mice, rats, sheep, goats, donkeys or horses. It is preferable to develop the antiserum in sheep. The production of antiserum in sheep is particularly advantageous over the traditional method of production of antiserum in horses, since the antiserum selected in sheep does not contain any of the particularly immunogenic Ig Gu Gg G(T) components of equine antiserum, which cause unwanted immunogenic serum reactions in humans or animals. , to which such an antidote is administered. The antiserum that includes the antivenom may be a whole antiserum. Preferably, the antiserum may be partially cleaved (digested) into F(av 1) 2 or F(av) fragments. It is advisable to remove Fc fragments to reduce the patient's immunogenic response to the antivenom. The production of antibody fragments can be accomplished using conventional techniques, for example by digestion of pepsin or papain. An antiserum, which includes an antivenom, can be produced against the venom of any venomous animal, including snakes, Gila monsters, spiders and bees. The antivenom may contain antiserum produced for the venom of only one type of animal, for example, antiserum produced for the venom of different species or subspecies of snakes. Alternatively, the antivenom may include an antiserum raised against the venom of more than one type of animal. Preferably the venom is snake venom. Even more preferably, the poison is rattlesnake venom. The venom against which each antiserum is raised may consist entirely of venom, partially purified venom, or one or more selected components of the venom. Preferably, the poison is a whole poison. According to another aspect of the invention, there is provided a method for producing an antidote according to the first aspect of the invention, comprising mixing at least two different antisera. According to a third aspect of the invention, there is provided a pharmaceutical composition comprising an effective amount of an antidote according to the first aspect of the invention in combination with a pharmaceutically acceptable carrier, diluent or excipient. Preferably, the pharmaceutical composition is suitable for parenteral administration to a patient. Even more preferably, a pharmaceutical composition suitable for internal injection. According to a fourth aspect of the invention, there is provided a method of neutralizing a poison, comprising administering to a subject suffering from the effects of a poison an antidote according to the first aspect of the invention in an effective amount. According to a fifth aspect of the invention, there is provided a kit for administering an antidote to a human or animal body, comprising: a) an antidote according to the first aspect of the invention, b) a means for injecting an antidote into the body. In fig. Figure 1 shows the activity of A2 phosphate in 1 μg of four crotalide poisons; in fig. 2 - the amount of antidote required to neutralize 50% of A2 phospholipase activity in 1 μg of crotalide poison. It is understood that the invention has been described by way of example for illustrative purposes only, and modifications and other changes may be made within the scope of the invention. Experimental studies. 1. Obtaining antidotes. The antidote was obtained by immunizing a group of Welsh sheep with poison according to the well-known immunization scheme of Sidki et al. (Table 3). The poison for immunization was proposed by Professor F. Russell of the University of Arizona. The venom was collected from a large number of snakes of the same species. Specimens of different ages and geographic locations were included, and venom was collected throughout the year. These factors are known to influence the composition of the venom and are therefore important for efficient antivenom production. Blood (300 ml) from the group was collected and drained monthly, and the serum was aspirated after achieving clot formation at 4° C. for 18 hours. The concentrate was prepared from the antiserum stock by sodium sulfate precipitation. The immunoglobulin fraction is then partially purified by precipitation of sodium sulfate from the antiserum stock. Volumes of antiserum are mixed with different volumes of 6% sodium sulfate, and the resulting mixture is stirred for 1.5 hours at room temperature to precipitate immunoglobulin. After centrifugation at 3500 rpm for 60 min, the clot is washed twice with 18% sodium sulfate, and the final clot is then reconstituted with phosphate buffer solution (PBS) to a volume equal to that of the original antiserum depot. The solution is then cialized against 20 volumes of PVA and the product is stored at 4° C. until required. The product can be analyzed by micro-Kjeldahl to determine the exact protein concentration in the sample. If required, this Gg J can be cleaved to form F(av 1) 2 and F(av) using pepsin or papain, respectively. These products can also be analyzed by S S/PAGE, micro-Kjeldahl and ELIZA to ensure retention of potency. 2. Comparison of the antidote "in vitro". Introduction

Snake venom is a multicomponent mixture of proteins, metal ions and nucleotides. Although the exact nature of each individual venom is specific to the snake's genotype, there are some common proteins. One such common protein is the enzyme phospholipase A 2 (PLA 2). This enzyme is primarily responsible for the breakdown of body fats, but may also have a number of other activities, such as cell rupture due to lipid hydrolysis products and neurotoxicity due to the pharmacologically active site of the enzyme. PLA2 activity in crotalid or rattlesnake venoms can be determined by a simple colorometric assay. PLA2 hydrolyzes fats, producing fatty acid and glycerol, resulting in a drop in the pH of the system. PLA2+fat ___ fatty acid+glycerol

This drop in pH can be controlled by introducing a colored pH indicator into the system. Assessment of PLA2 activity. The following assay can be used to regulate phospholipase A2 (PL K2. EC 3.1.1.4.) activity of specific venoms. The activity of poisons is assessed by measuring the release of free fatty acid from a phospholipid substrate (phosphatidylcholine) from Sigma Chemical, product number P-9671 (using the pH indicator Cresol Red, Sigma Chemical, product number C-9877). Buffer sample:

1. 100 mm NaCl

2. 100 mm KCl (All grades of GPR reagent)

3. 10 mm CaCl 2

For routine analysis, take 500 ml of this solution and adjust the pH to 6.8 using dilute sodium hydroxide solution. Preparation of the indicator: 10 mg of red creosol (sodium salt, Sigma, N C-9877) is dissolved in a buffer sample (10 ml) and the vessel is wrapped in thin foil. Substrate preparation: phosphatidylcholine (1.2 g from egg yolk, type XY-E, 60% L-alpha form, Sigma, N 9671) is dissolved in methanol (1 ml) and the solution is adjusted to 10 ml with buffer (final concentration 120 mg/ ml). This should be done again for each series of experiments. Method: Crude freeze-dried monovalent venom is dissolved in distilled water to a final concentration of 10 mg/ml. Typically, 10 ml of poison solution is taken for each series of experiments. The substrate solution is then prepared as follows. To 1 ml of freshly prepared lipid suspension add 25 ml of assay buffer and 0.3 ml of Triton-X-100 (VDN N 30632). Stir the solution thoroughly until it becomes clear. Adjust pH to 8.6 using dilute sodium hydroxide. Add 1 ml of the resulting indicator solution and adjust the final volume of the substrate solution to 30 ml with buffer. The substrate solution should be red in color, otherwise the pH of the buffer should be checked. This solution should also be wrapped in silver foil. 100 μg of buffer is added to 2.8 ml of substrate solution in a plastic 3-ml cuvette and CD 573 nm is measured. Add 100 mm of poison solution and start the stopwatch. To a second cuvette containing 2.8 ml of substrate solution and 100 µl of buffer, another 100 µl of buffer is added to adjust for any occasional drop in pH. This is carried out in parallel with the analysis cuvette. Readings were made every minute for 30 minutes. Then plot OD as a function of time, taking into account the prerequisites for the drop in pH of the control sample, and subtract this value from the value obtained by adding the poison. After this, all readings are expressed as a percentage of the systematic control reading. Neutralization studies. Neutralization experiments were carried out using Ig G sections of the appropriate antiserum. These preparations are prepared by salt precipitation from the entire antiserum (18% sodium sulfate, 25°C for 1.5 hours). The assay and substrate buffers used for these studies were identical to those used in the experiments described above. 1 liter of antivenom in a 10-fold dilution in buffer (stock solution) is diluted two more times and 100 µl of the amount is added to 100 µl of a solution of a particular venom (10 µg). Prepare two additional sets of samples to control the pH drop (200 µl assay buffer) and general hydrolysis (100 µl buffer and 100 µl venom solution). Then the samples are kept for 30 minutes at room temperature. During this period, prepare the substrate solution and check the pH. After this, the zero OD time of 2.8 ml quantities of the substrate solution is measured. This is done immediately before adding 200 µl of venom/antivenom solution (after a 30-minute incubation period). An additional 15 min incubation is carried out at room temperature, and then the OD is read. The results are then processed as described above and expressed as the percentage of poison neutralized by hydrolysis. Results. The above tests were carried out using the venoms of four rattlesnakes, which were Apiscivorous, C. adamanteus, C. atrox and C. scutulatus. In fig. Figure 1 shows that each of these venoms contains potent PLA2 enzymes and shows the order of activity: A. piscivorous > C. adamanteus = C. scutulatus > C. atrox. The PLA2 neutralizing ability of the antidotes described above is then determined. A neutralization study was carried out using a mixed monospecific antivenom prepared by mixing equal volumes of equal concentrations of monospecific Ig G obtained by immunizing four groups of sheep against the venom of A pisivorous, C. adamanteus, C. atrox and C. scutulatus. Concentrations were determined using the Kjeldahl nitrogen analysis method and equalized by adding appropriate amounts of PVA. Control neutralization studies were also conducted using multispecific antidotes prepared for each of the venoms and using multispecific antidotes prepared for a 1:1:1:1 mixture of these venoms. The control experiments used exactly the same protocols, including venom sources, immunization, purification, and testing, as the mixed monospecific antivenom experiment. The results are shown in Figure 2, which shows that the mixed monospecific antivenom has greater or equal potency than the corresponding multispecific antisera in neutralizing PLA2 venom activity. Indeed, three of the four venoms tested required significantly less antivenom to achieve 50% neutralization. In addition, mixed monospecific antivenoms also have similar or greater potency than homologous monospecific antivenom, indicating that mixed monospecific antivenom has a higher degree of cross-reactivity. These results led to the conclusion that in the case of PLA2 neutralization, the mixed monospecific antiserum is much more effective than its polyspecific counterpart.

CLAIM

1. An antidote for the bite of a poisonous animal based on an antiserum, characterized in that it includes a mixture of at least two antisera produced against different poisons. 2. Antidote according to claim 1, characterized in that each component of the antiserum is monospecific. 3. Antidote according to claims 1 and 2, characterized in that each antiserum includes F(ab 1) 2 or F(ab) fragments obtained by partial digestion of the IgG of the entire serum. 4. Antidote according to claims 1 - 3, characterized in that each antiserum is a sheep antiserum. 5. Antidote according to claims 1 - 4, characterized in that each antiserum is present in an amount determined by the toxicity and frequency of bites of people in a specific geographical area by a specific poisonous animal, against the venom of which each antiserum was developed. 6. The antidote according to claim 5, characterized in that each component of the antiserum is present in direct proportion to the frequency of bites of people in a specific geographic area by specific species or subspecies of a poisonous animal, against the venom of which each antiserum was developed. 7. Antidote according to claims 1 - 6, characterized in that each antiserum is developed against snake venom. 8. Antidote according to claim 7, characterized in that each antiserum is developed against rattlesnake venom. 9. A method of obtaining an antidote for the bite of a poisonous animal, including mixing antisera, characterized in that at least two antisera are taken. 10. A method of antidote to poison, including administering the antidote to a subject suffering from the action of the poison, characterized in that the antidote is administered according to claims. 1-8 in effective amount. 11. A kit for introducing an antidote into the human or animal body, including an antidote and a means for injecting the antidote, characterized in that as an antidote it contains the antidote according to claims 1-8.

Today, the topic of poisons is of interest to most of the people inhabiting our planet. And this is not surprising, because we live in difficult times, during terrorist attacks and armed clashes, when morality is gradually forgotten. Many people are now interested in how poisons are made at home. First of all, it is worth remembering that this kind of activity can not only deprive a person of freedom for a long time, but also be very dangerous for the manufacturer himself, since one can easily be poisoned by inhaled toxic fumes or even dust.

What is poison?

So, first of all, let's find out what poison is. Poisons are substances that cause poisoning of the body or its death. Moreover, their effect and nature depend on the dose and composition used. In this case, it is customary to divide toxic substances into twelve groups. Among them are those that affect the circulatory (hematic), nervous (neurotoxins), muscular (mitotoxins) systems, as well as those that affect cells (protoplasmic poisons).

What is it made of?

The production of poisons at home most often occurs from some components of plants and other improvised means. There is even a so-called list of the most toxic poisons that you can create at home. Let's look at it in more detail.

Ergot

So, in last place is a fungus that forms on rye and is called “ergot.” This substance causes hallucinations, which are accompanied by inappropriate behavior; it also provokes convulsions and often gangrene of the limbs.

Foxglove (buttercup)

The plant contains poisons such as digitalis and digitoxin, which in large doses can stop the heart. In this case, the person first begins to feel dizzy, the pulse drops, shortness of breath appears, and then cyanosis, and death occurs.

Lily of the valley

Making poisons at home can also be done from lily of the valley, because the convallomarin it contains causes the most severe poisoning.

Castor bean

Castor beans contain one of the most dangerous toxic substances - ricin, which is fatal after five days of suffering. In this case, colic, vomiting, internal bleeding, destruction of tissue proteins, and decomposition of the lungs are observed. It should be noted that there is currently no antidote for this toxic substance.

Curare

The production of poisons at home was practiced by the Indians of South America. They used the curare plant. An arrow dipped in its juice can kill a large animal within ten minutes.

Toadstool

The toadstool is also capable of killing a person, since it contains a potent poison - amanitotoxin, which cannot be destroyed even with prolonged heat treatment.

Wrinkled sapling

The production of poisons at home can also be made from wrinkled saplings, the stems of which contain the toxic substance tremetol. By the way, it is often confused with nettle leaves, which is what caused the poisoning of several hundred people in the last century.

How are poisons used?

Thus, it is not enough to prepare poisons at home; they also need to be applied correctly. So, some of them are effective only when they enter the circulatory system, but in the stomach they simply decompose without causing harm to the body.

One of the symbols of Thailand is a mythical plot depicting the victory of the bird Garuda over the snake Nag. And this is no coincidence: for many centuries, the inhabitants of Siam - as Thailand was called until 1949 - literally thousands died every year from poisonous snake bites. And there are a lot of them in this country: out of more than 175 species of all living ones, 85 are poisonous.

Problems of medical research in the field of toxicology have been dealt with in Siam for a very long time. The local Red Cross Society was founded in this country back in 1893 and was under the patronage of the royal family. Currently, 10 species of snakes from the region are bred and studied at the Queen Saovabha Memorial Institute. Moreover, the poison of each species is used to produce a specific antidote (antidote). For example, an antidote made from the venom of the Siamese cobra is effective only against the bites of this type of snake and is completely useless against the bite of a viper or king cobra.

Horses are used to produce antidotes in Thailand. They serve as a kind of living biological factory for the production of antidotes. The process of obtaining antidotes looks like this: healthy horses are given small injections of snake venom, immunity is developed in their blood over several months, and only then the horse’s blood is taken, which serves as the starting material for making antidotes. The ampoules are sent from here throughout the country to special centers. And there are hundreds of them in Thailand. Every adult knows exactly where to go in case of danger.

According to WHO, in the middle of the 20th century, the number of people affected by snake bites was 500,000. Before the use of modern antidotes, 20 40%, and in some countries up to 70% of people bitten, died. Thanks to the use of serum, the number of deaths was reduced to 2 3%, occurring mainly in India, the countries of Southeast Asia and South America. In Europe, deaths from snake bites are rare.

Now in Thailand, on average, no more than 20 people die per year, while at the beginning of the 20th century this figure was 10 thousand. Moreover, only those who did not manage to seek medical help in time die. For comparison: in India, the number of deaths for the same reason is 20 thousand people per year. These figures eloquently demonstrate how necessary the work of such institutions is.

Snake breeding is a later addition to the institute's activities. In 1993, since some species of snakes became difficult to catch in the wild, it was decided to start breeding them. Nowadays, several species of cobras and vipers are bred to obtain poison. The snakes are fed in the nursery once a week. Their diet is 1 2 mice. Some species feed only on live water snakes. Although, as a result of training, even these fastidious reptiles learned to eat mice and even fish sausages.

The most difficult species to breed in captivity is the ribbon krait. And Malayan vipers and Siamese cobras feel most comfortable in these conditions. These snakes lay up to 30 small eggs, resulting in 200 to 500 snake farms of these two species each year. All female snakes arriving at the farm are checked for pregnancy. If there is one, the females are placed in the most favorable conditions for incubating eggs.

The breeding of venomous snakes has also led to research into the diseases they suffer from, since only healthy reptiles are needed to produce venom. Therefore, veterinarians carefully monitor their condition and treat them if necessary.

Although it must be said that snakes are not aggressive creatures at all, they attack a person only if they are provoked to do so, voluntarily or involuntarily. So the first rule when accidentally meeting a snake is to never make sudden movements and, if possible, move away slowly.

By the beginning of the 20th century, it became obvious that most of the imported antivenoms available at that time were unable to provide the necessary treatment. Therefore, there was an urgent need to create a local production facility for the production of drugs capable of creating effective antidotes based on the venom of snakes from this region.

The then ruler of Siam, King Vajiravudha, no less than his subjects, was concerned about the problem of high mortality from snake bites. In 1920, after the death of his mother, Queen Saovabha, in memory of this sad event, the king donated significant funds to the local Red Cross organization for the construction of new buildings needed to expand research work in the field of toxicology. And in December 1922, with the direct participation and assistance of specialists from the Pasteur Institute in Paris, a research center for the study of vaccines and serums, called the Queen Saowabha Memorial Institute, was opened in the capital of the state, Bangkok.

The main directions of biomedical and clinical research of the institute were: study of the life cycle and physiology of snakes, classification of poisons and their effects on humans, creation and improvement of vaccines against poisons, rabies and other infectious diseases
diseases.

In order to obtain poison, the snake must be placed on a smooth table surface where it has no support and, therefore, cannot rush at a person. Then, with a stick with a hook at the end, the snake is picked up and placed on the table, and then rotated several times, causing it to become “dizzy.” After this, the snake’s head is pressed to the table and picked up. To ensure safety, the operator clamps the snake's cheek bones, then brings it to the venom receptacle and allows it to bite.

If the snake does not want to voluntarily give up venom, it is stimulated by massaging the venom glands. The operation to take the poison is stopped when it stops flowing from the glands. Venom is taken from snakes every two weeks.

snake poison

Snake venom is produced by the temporal salivary glands and has the appearance of a yellowish transparent liquid. When dried, it retains its poisonous properties for decades.

Snake venom is a complex mixture of proteins that have the properties of enzymes and enzymatic poisons. They contain proteolytic enzymes that destroy proteins, protease and estarase enzymes that clot blood, and a number of others.

According to the nature of poisoning, the venom of Thai snakes can be classified into two groups: neurotoxic and hematovasotoxic. The first group includes cobras, kraits and sea snakes, the second group includes vipers. Neurotoxic poisons, having a curare-like effect, stop neuromuscular transmission, resulting in death from paralysis. Hemovasotoxic poisons cause vascular spasm, followed by vascular permeability, and then swelling of tissues and internal organs. Death is caused by hemorrhage and swelling of parenchymal organs - the liver and kidneys, and in the affected part of the body the internal loss of blood and plasma can amount to several liters.

After being bitten by some types of snakes, a person who does not receive medical care in time can live no more than 30 minutes.

Horsepower

The Thai Red Cross horse farm is located in Hua Hin (near Bangkok). The average lifespan of a horse is 25 years.
and it is used as a donor only from 4 years of age to 10 years of age. Blood from horses for the production of antidotes is taken no more than once a month, and its quantity is

5 6 liters. Despite such an impressive blood draw, the horse’s body is able to quickly restore the number of red blood cells.

The blood plasma is then transported to Bangkok, where it is highly purified and tested for safety and effectiveness in accordance with World Health Organization requirements.

It must be said that the Thais have great respect for this noble animal. After the horse can no longer be a donor, it is “retired” to special farms, where it lives out its life on full government support.

Dmitry Vozdvizhensky | Photo by Andrey Semashko

Many doctors know how to poison a person at home and how to avoid suspicious signs, however, such an act is criminally punishable. Nevertheless, today some people resort to this method in order to eliminate a rival, often this happens in criminal communities.

Natural products are dangerous if you know what can poison a person. Death is influenced not only by pathogens, but also by compounds. A well-known poison is botulinum toxin, which is produced by special microbes that can multiply intensively in a protein environment. It is the cause of intoxication after eating spoiled canned food, mushrooms and other foods. In the digestive tract, this toxin is not destroyed by enzymes and is absorbed into the mucous membranes of the stomach and intestines.

Persons who choose what to poison a person to death rarely choose botulinum toxin, since death in this case is rare.

However, signs of illness can always be attributed to the last meal, during which canned goods, sausage and other unsafe foods were consumed. Symptoms of poisoning are nausea, vomiting and dry skin, followed by paralysis of the striated muscles.

Most people are familiar with castor oil, but few are aware of ricin, a toxin found in castor bean seeds. Criminals looking for something to quietly poison a person often settle on this poison. It is odorless white crystals that dissolve in liquid, however, when the aqueous solution is boiled, the dangerous properties of ricin disappear.

The toxic substance does not penetrate the skin; it acts only when it enters the body. In case of ricin poisoning, the latent period of intoxication varies from 15 to 24 hours, sometimes symptoms appear earlier. Thus, intestinal colic, bloody diarrhea, nausea and vomiting are detected, and hemorrhages occur on the retina.

If a significant portion of castor bean seeds enters the body, death occurs after 6 days due to damage to internal organs, as well as extensive bleeding.

This poison is sometimes chosen by attackers who think about how they can quickly poison a person. However, death is rare.

The poison of the toadstool was known to medieval politicians and healers, who knew how to poison a person to death. Today, scientists have found that the mushroom contains toxins such as phalloidins and alpha-amanitins, which act quickly and irreversibly; these substances are not destroyed by heat treatment.

The latent period without alarming signs lasts up to 40 hours before the poison enters the blood in large quantities and causes depressing signs of poisoning. It is characterized by diarrhea, vomiting and dehydration, as well as pale skin and increased heart rate. After a few days, extensive damage to the internal organs - the liver and kidneys - occurs, toxic hepatitis develops, after which death is declared.

How can you poison a person, if you do not take into account the above-mentioned means? The following components are used for this purpose:

• atropine;
• solanine;
• aflatoxin.

Atropine is a substance from the group of alkaloids, found in plants - belladonna, datura, henbane and others. Intoxication occurs 1 hour after taking the poison; the degree of poisoning may vary.

Atropine is known to affect the structure of the brain, causing loss of coordination and damage to the heart and lungs. Death occurs infrequently due to an insufficient dose of toxin.

How to briefly poison a person? In this case, the solanine found in root vegetables is a suitable option. It can be found not only in potatoes, but also in tomatoes and eggplants.

Intoxication manifests itself in the form of nausea, vomiting, cramping pain in the abdomen and a feeling of bitterness in the mouth. However, it is unlikely that it would be possible to consume a large dose of solanine, which is why victims are not at risk of death.

In addition, aflatoxins are a common method of poisoning - a group of toxic substances secreted by a microscopic fungus. If stored improperly, it affects various food products, for example, dried fruits, milk, rice, tea and much more.

The poison in large quantities causes the death of liver cells, however, the poisoning passes without serious consequences and is limited to a temporary deterioration in health

In the old days, people knew the best way to poison a person. This can be easily done with the help of ordinary mercury; the dangerous metal causes fatigue, headaches, and memory loss. In addition, there is an increase in body temperature and a decrease in blood pressure. The digestive system also suffers, and diarrhea and a metallic taste in the mouth are often observed. When a significant amount of mercury vapor is inhaled, death is inevitable, which is why this drug has been a weapon for centuries for criminals who understood how to poison a person without any trace of a crime.

There are many toxic substances. Some of them affect the human body for a long time, others kill instantly. There are many fast-acting poisons, they can be natural and chemical.

Such compounds deprive their victim of the opportunity to survive almost immediately. What is the fastest-acting poison for humans, the most famous and dangerous?

Top strong poisons in everyday life

In everyday life, people constantly encounter poisons. Many of them have a quick effect on the body, so it is recommended to know their effect and how to provide first aid to an injured person.

Acids

anthrax

Serious disease is caused by specific bacteria. There are several forms of the disease, the simplest is skin lesions. The most dangerous form of the disease is considered to be pulmonary; even with timely assistance, only five percent of victims survive.

Sarin

A poisonous substance in the form of a gas. It was created to kill insects, but found its application in the military sphere. The compound kills quickly, but death is painful. Production is prohibited throughout the world, and its reserves are often used for military purposes or by terrorists.

Amatoxins

Such poisons have a protein structure and are found in dangerous mushrooms of the Amanitaceae family. The danger lies in the fact that the first signs appear ten hours after the toxin enters the body, during which time the possibility of saving a person approaches zero. Even with a successful rescue attempt, the victim remains disabled for life and suffers from problems with internal organs.

Strychnine

Obtained from the nuts of a tropical plant. It is used in minimal quantities as a medicine. Strychnine is one of the fastest-acting poisons, superior to potassium cyanide. But death does not occur immediately, but half an hour after poisoning.

Ricin

Ricin is a poison of plant origin. Six times stronger than potassium cyanide. It is especially dangerous if it gets into the blood; in such a case, death occurs very quickly. Inhalation through the lungs is less dangerous, but also leads to serious poisoning.

VX

The compound is a combat poison and has a nerve-paralytic effect. Changes in the body occur a minute after inhalation, and death occurs within fifteen minutes. Dangerous poison is prohibited for use in the world.

Botulinum toxin

Botulism is poisoning caused by botulinum toxins. This is the most powerful poison in nature and was previously used as a biological weapon. Bacteria are used in cosmetology, but in minimal dosages. As the amount of toxin increases, death occurs from respiratory failure.

Top strong poisons in the pharmacy

Medicines are dangerous to humans if used incorrectly. They are also poisons and in overdose lead to poisoning

A fatal outcome cannot be ruled out if the permissible amount of the drug is exceeded many times. Many medications are freely available in pharmacies.

Dangerous:

• Medicines aimed at treating the cardiovascular system.
• Neuroleptics and tranquilizers.
• Painkillers.
• Antibiotics and antibacterial agents.

Weight loss drugs, drugs aimed at treating impotence, even eye drops can be dangerous to human health. You need to remember that in a minimal amount the medicine will help, but in a higher dosage it will lead to poisoning and death.

Dangerous poisons for animals

Animals suffer from poisoning no less often than people. What poisons are dangerous for dogs and cats?

Danger:

1. Human medicines. Even small amounts of some drugs can cause serious poisoning or death. Example - a medicine for the treatment of tuberculosis - used by dog ​​hunters.
2. Products for getting rid of fleas and ticks. Animals die from an overdose of such drugs.
3. Food. You should not give your pets food from the table, simple grapes lead to kidney failure, xylitol provokes a sharp drop in sugar levels and disruption of the liver.
4. Rat poison. Rat poison often causes death in domestic animals. Rodent bait has a pleasant smell, so it attracts other animals. Without help, the pet dies very quickly.
5. Medicines for animals. Medicines intended for treatment, if taken in the wrong dosage, can cause death.
6. House plants. Cats and dogs love to bite some plants; many of them contain poisonous sap that is hazardous to health.
7. Chemicals, household chemicals. Such products located in accessible places often attract the attention of animals. Poisoning develops quickly, as does death.
8. Fertilizers and pesticides. Such compounds are suitable for plants, but dangerous for animals.

Thus, there are no less dangers and poisons for animals than for humans. It is recommended to carefully monitor the animal’s behavior in order to provide first aid in a timely manner.

Irritation, a feeling of sand in the eyes, redness are just minor inconveniences with impaired vision. Scientists have proven that decreased vision in 92% of cases ends in blindness.

Crystal Eyes is the best remedy for restoring vision at any age.

Precautionary measures

It is possible to avoid serious intoxication by following safety precautions. When working with poisons, you must wear special protective clothing and gloves. It is recommended to use safety glasses and respirators.

Under no circumstances should you eat or touch your face or exposed skin with your hands while working. After completing all manipulations, wash your hands thoroughly, take a shower if necessary, and put your clothes in the wash.

Before using unknown compounds, you must read the instructions and follow them carefully. Eating unknown foods is not recommended.

What to do if you are poisoned

If poisoning occurs, you must call a doctor immediately. Before his arrival, the victim is provided with possible first aid.

Actions:

• rinse the stomach, if allowed;
• give to a person;
• use laxatives or cleansing enemas;
• administer antidotes whenever possible;
• provide fresh air, peace;
• quickly transported to a medical facility.

Fast-acting poisons are present near a person, but if safety precautions are followed, poisoning can be avoided. If signs of intoxication appear, first aid is quickly provided and doctors are called.

Video: quick poisons for humans

If you want to be healthy, douse yourself, don’t touch this rubbish, or better yet, avoid it altogether...
The deadliest things on our planet.

Death cap- Destroying Angel. The first physical signs of poisoning are usually nausea, vomiting, and bloody diarrhea. After feeling a slight discomfort, there is a sharp pain in the abdomen, severe vomiting, intense thirst, and cyanosis of the extremities, as well as yellowness of the eyes and skin as liver damage. The patient remains conscious almost until the end, with brief intervals of loss of consciousness, then coma and death.

Dog fish(Pufferfish). The poison tetraodontoxin is found in the ovaries of this fish and is not destroyed by heat treatment. In case of poisoning, speech is difficult, and paralysis of the respiratory system quickly develops, accompanied by paralysis of the central nervous system. The cause of death is most often convulsions or respiratory arrest, which occur within one to two hours after the poison enters the body.

Castor bean-Castor Beans. Signs of poisoning are bitterness in the mouth, nausea, vomiting, convulsions, drowsiness, cyanosis, stupor, impaired microcirculation, blood in the urine, ultimately coma, and death; the toxic agent, even in low concentrations, causes the dissolution of red blood cells; in serious cases, hemorrhages develop throughout the body. Castor beans can also lead to premature birth in pregnant women. Autopsies of patients who have died from castor bean poisoning show that the vomit and stool contain blood.

Belladonna. All parts of the plant are deadly poisonous, especially its roots, leaves, and berries. The poison paralyzes the parasympathetic nervous system by blocking nerve endings.

Viper Venom. Snake venom affects the blood and nervous system, it is less poisonous when it enters the mouth than into the blood... The victim of a viper bite bleeds from the wound, has a fever and chills. Poisoning is accompanied by swelling or hemorrhages above the elbows or knees. These signs usually appear within two hours after the bite. Then fainting, bleeding from the nose and mouth, loss of vision, followed by loss of consciousness. Death caused by cardiorespiratory disorders is inevitable if an antidote is not administered in time.

Barbados nut or Physical nut. The threat lies in the deceptively pleasant taste of the seeds. However, make no mistake - each seed contains at least 55 percent of the active substance "Hell oil", which blocks protein synthesis in the intestinal wall and can lead to death.

Hemlock. Signs of poisoning are a gradual loss of coordination, accompanied by a fast and weakened pulse, pain in the muscles as they atrophy and eventually die. Although the mind remains clear, vision often deteriorates until the victim succumbs to pulmonary paralysis. It is believed that Socrates was poisoned with the juice of this plant, and not hemlock, as previously thought.

Cobra Venom has mainly neurotoxic effects. Its strength is enough to cause the death of a person after the first full bite. In such cases, the mortality rate may exceed 75 percent. However, taking into account all the behavioral characteristics of the king cobra, in general, only 10 percent of bites are fatal to humans.

Datura. All parts of the plant contain poisonous alkaloids. If it enters the gastrointestinal tract, it affects the nervous system, causing cardiac dysfunction and paralysis.

Lily of the valley. Contains a cardiac glycoside in a fairly high concentration, in small doses it stimulates the work of a weakened heart muscle, but in case of an overdose it leads to arrhythmias and blockade of the electrical conductivity of the heart, necessary for its normal contractions. All parts of the plant are poisonous. Poisoning manifests itself as nausea, vomiting, diarrhea, severe headache pain and pain in the epigastric region. In severe cases, the rhythm and frequency of heart contractions are disturbed, and the pulse, as a rule, becomes rare. Sometimes the nervous system is also affected. This is evidenced by agitation, visual disturbances, convulsions, and loss of consciousness.

Aconite has neurotoxic and cardiotoxic effects. Symptoms of poisoning are nausea, vomiting, numbness of the tongue, lips, cheeks, tips of fingers and toes, a crawling sensation, sensations of heat and cold in the extremities. Intoxication with aconite is characterized by a transient visual disturbance - the patient sees objects in green. There is also drooling, followed by dry mouth, thirst, headache, anxiety, convulsive twitching of the muscles of the face and limbs, and loss of consciousness. Breathing is rapid, shallow, and may suddenly stop.

Rhododendron. Contains glucoside substances - andromedotoxin, ericoline. Andromedotoxin has a local irritant and general narcotic effect, first stimulating and then depressing the central nervous system; greatly upsets the activity of the heart, in a peculiar way, like veratrine, it affects the muscle. Poisoning develops very quickly. Often, within a few hours of eating rhododendron leaves and branches, death occurs.

Tubocurarine chloride. White crystalline powder, in traumatology d-tubocurarine is sometimes used to relax muscles during reposition of fragments, reduction of complex dislocations... Side effects from the use of tubocurarine are observed only with its overdose; in this case, the patient may develop respiratory failure due to paralysis of the respiratory muscles and, as a consequence, death.

Rhubarb. Rhubarb can only be eaten in early spring, until the air temperature rises above 15-17° C. In early spring, malic acid predominates in rhubarb, then its content increases, and with increasing temperature in hot weather, oxalic acid accumulates in the petioles, which is harmful to the body: it forms poorly excreted salts and removes calcium contained in the blood. Consumption of oxalic acid in an amount of 3-4 g at once is dangerous not only for children, but also for adults. In case of poisoning, vomiting, convulsions, and kidney failure may occur. In the first two days, death can occur from asphyxia, shock, or cardiovascular failure. In the next 2 weeks after poisoning, severe complications such as acute renal failure, repeated collapses, profuse bleeding, hemorrhagic pneumonia, and gastric perforation may occur, which can lead to death.

Gila monster- a large reptile, with a very beautiful black and orange pattern throughout the body. The Latin name for this beautiful lizard is Heloderma suspectum or poison tooth. There are grooves on the upper and lower jaws, into which the channels of highly developed poisonous glands approach. When biting, the teeth go deep into the victim's body. Venom tooth bites are very painful and act almost the same as snake bites. The venom is neurotoxic, meaning that when it bites, it paralyzes its victim. For small animals, the lizard's venom is fatal; in humans it usually causes very severe swelling, but can sometimes lead to death.

Croton oil- liquid obtained from the seeds of the Croton tiglium plant. It has a strong laxative effect and irritates the skin and mucous membranes. Even in small quantities (over 20 drops) it is life-threatening. Crotonal is toxic and mutagenic. When a person inhales its vapors, irritation of the mucous membrane, pharyngitis, cough, chest pain, nausea, vomiting, and the onset of shock or unconsciousness occurs. Contact directly with the liquid results in severe skin redness, irritation, pain and burns. When poison gets inside, the whole body is poisoned, the central nervous system is damaged, and tumors form. In case of tactile contact, skin scarring occurs.

Digitalis. Nowadays, digitalis purpurea is used to produce medicines that stimulate the cardiovascular system. Active biological substances from digitalis tend to accumulate in the body and can be harmful or even fatal to a person with a healthy heart. The grass and rhizomes of foxglove are saturated with the toxin digitalin. Poisoning is accompanied by irritation of the gastrointestinal tract, the pulse becomes rapid and arrhythmic, and general weakness and shortness of breath are observed. Convulsions may develop before death.

Codeine is an almost clear, odorless substance with a rather bitter taste, which is available in either powder or liquid form. When used in high doses, like other opiates, it can cause euphoria. Serious poisoning is often possible when taking a large number of tablets of some codeine-containing medications. Due to the fact that with regular use of codeine, an addictive phenomenon is observed (similar to addiction to heroin and other drugs of the opiate group), it is released with the same restrictions as other narcotic analgesics. In case of severe codeine poisoning, breathing disorders are possible, up to paralysis with preserved consciousness, as well as a significant drop in blood pressure.

Poisonous octopus(blue ringed octopus). Its venom, which belongs to the group of neurotoxins, is so powerful that it can kill an adult, especially if the octopus bites in the neck or in the area close to the spine. There is simply no vaccine for its poison

Dimethyl sulfate. Used in the manufacture of paints, drugs, perfumes and pesticides, most poisonings from dimethyl sulfate occur due to leakage of liquid or vapor. Signs of poisoning will be more pronounced if alcohol is present. Nausea, vomiting, weakness, dizziness, and headache occur. Possible increase in temperature, excitability, pain in the limbs, visual and hearing impairment, mental disorders. In severe cases, tremor, ataxia, loss of consciousness, paroxysmal clonic-tonic convulsions resembling epileptic seizures, and coma develop. A pathological examination reveals pronounced vascular disorders and degenerative changes in the parenchymal organs, brain and adrenal glands.

Nicotine. It is estimated that the lethal dose of nicotine for humans is 1 mg per 1 kg of body weight, i.e. about 50 - 70 mg for a teenager. Consequently, death can occur if a teenager smokes half a pack of cigarettes at the same time, because a whole pack contains exactly one lethal dose of nicotine.

Wart. A fish with a row of spines on its back that release a poisonous toxin. This is the most dangerous venomous fish known and its venom causes extreme pain with possible shock, paralysis and tissue death depending on the depth of penetration. At the slightest irritation, the wart raises the spines of the dorsal fin; sharp and durable, they easily pierce the shoes of a person who accidentally steps on a fish, and penetrate deep into the foot. If the injection penetrates deeply, it can be fatal to a person if he does not receive medical attention within a few hours. If the thorn gets into a large blood vessel, death can occur within 2-3 hours. Survivors sometimes remain ill for months. The venom consists of a mixture of proteins, including hemolytic stonustoxin, neurotoxin and cardioactive cardioleptin. Typically, surviving victims suffer localized nerve damage, sometimes leading to atrophy of the attached muscle tissue. The pain can be so severe that injection victims want to cut off the injured limb.

Hydrogen sulfide- a colorless, poisonous gas heavier than air with an unpleasant odor of rotten eggs. It can be released during the process of decay and accumulates in lowlands. Very toxic. At high concentrations, a single inhalation can cause instant death. At small concentrations, adaptation to the unpleasant smell of “rotten eggs” occurs quite quickly, and it ceases to be felt. A sweetish metallic taste appears in the mouth. The first symptom of acute poisoning is loss of smell. Subsequently, headache, dizziness and nausea appear. Sometimes, after a while, sudden fainting occurs.

Oleander- a large evergreen shrub. All parts of the plant are poisonous, moreover, the smoke from the burning plant and the water in which the flowers stood are poisonous. The plant contains a number of cardiac glycosides (oleandrin, cornerin, etc.). Oleander juice, taken internally, causes severe colic in humans and animals, vomiting and diarrhea... It also affects the nervous system (even to the point of coma). Cardiac glycosides cause cardiac arrest.

Phencyclidine(phencyclidine, PCP) - widely used in veterinary medicine for short-term immobilization of large animals. It has been noted to cause dissociated anesthesia. Phencyclidine is easy to synthesize. People who use phencyclidine are primarily young people and polydrug addicts. The true prevalence of phencyclidine drug addiction is unknown, but national data indicate that cases have recently increased in the United States. PCP is either taken orally, smoked, or administered intravenously. It is also used as an additive to illegally sold delta-tetrahydrocannabinol, LSD and cocaine. The most common homemade drug of PCP is called "angel dust." Low doses of phencyclidine (5 mg) cause restlessness, agitation, incoordination, dysarthria, and anesthesia. Horizontal and vertical nystagmus, hot flashes, profuse sweat, and hyperacusis are also possible. Mental disorders include body schema disturbance, incoherent thinking, derealization, and depersonalization. Higher doses (5-10 mg) cause increased salivation, vomiting, myoclonus, hyperthermia, stupor and coma. In doses of 10 mg or more, phencyclidine causes epileptic seizures, opisthotonus and decerebrate rigidity, which can be followed by prolonged coma. Acute psychosis caused by phencyclidine should be considered a psychiatric emergency with a high risk of suicide or violent crime.

Parathion(Parathion) - organophosphorus compound - pesticide; when it is inhaled, enters the gastrointestinal tract, or is absorbed through the skin, poisoning occurs. Like some other organophosphate compounds, parathion interferes with the enzyme cholinesterase, resulting in excessive stimulation of the parasympathetic nervous system. Symptoms of poisoning include headaches, profuse sweating and salivation, lacrimation, vomiting, diarrhea and muscle spasms.

TEPP cholinesterase inhibitor-used mainly as insecticides and can cause poisoning. Symptoms include headache, loss of depth perception, convulsions, sweating, chest pain, shortness of breath, vomiting, general paralysis, involuntary urination and defecation, drop in blood pressure, death.

Yew tree. All parts of the plant are poisonous, except the red fruits. The wood, bark and leaves of yew contain the alkaloid taxin and are therefore poisonous to humans and many other animals, although, for example, hares and deer eat yew willingly and without harm to themselves. The older the yew needles, the more poisonous they are.

Carbon Tetrachloride(Carbon Tetrachloride) is a caustic volatile liquid used as a dry cleaner. When its vapors are inhaled or swallowed, it causes severe damage to the heart, liver and kidneys (for example, the patient may develop cirrhosis of the liver or kidney nephrosis), affects the optic nerve and some other nerves in the human body.

Strychnine- an alkaloid contained in the seeds of tropical plants of the genus strychnos. It has a stimulating effect on the central nervous system, and in toxic doses causes characteristic tetanic convulsions...

Clostridium botulinum(Clostridium botulinum) is a gram-positive bacterium of the genus Clostridium, the causative agent of botulism, a severe food intoxication caused by botulinum toxin and characterized by damage to the nervous system. Botulinum toxin accumulates in food products infected with C. botulunum spores during their germination if anaerobic conditions are created (for example, during canning). For humans, botulinum toxin is the most potent bacterial poison, having a detrimental effect at a dose of 10-8 mg/kg. C. botulinum spores can withstand boiling for 6 hours, high pressure sterilization destroys them after 20 minutes, 10% hydrochloric acid after 1 hour, 50% formaldehyde after 24 hours. Botulinum toxin type A(B) is completely destroyed when boiled for 25 minutes. The incubation period for botulism ranges from several hours to 2-5 days (rarely up to 10 days). On the first day, nausea, vomiting, and diarrhea are noted. Next, neurosymptoms associated with damage to nerve centers predominate: impaired accommodation, double vision, difficulty swallowing, aphonia. In severe forms of botulism, death occurs from respiratory paralysis, sometimes from sudden cardiac arrest.

Potassium cyanide- potassium salt of hydrocyanic acid, chemical formula KCN. Strong inorganic poison. When ingested through the digestive tract, the lethal dose for humans is 1.7 mg/kg. Sometimes large doses are tolerated; the effect may slow down when the stomach is filled with food. Potassium cyanide is a powerful inhibitor. When it enters the body, it blocks the cellular enzyme cytochrome c oxidase, as a result of which cells lose the ability to absorb oxygen from the blood and the body dies from interstitial hypoxia.

Castor bean is an annual bushy plant. The height of the stems reaches two and even three meters, their color is varied - green, red, brownish. The leaves are large, pinnate, green, located alternately on the stem on long petioles. Castor bean blooms with beautiful small flowers collected in racemose inflorescences.
The fruits look like a red spherical box with thorns. The box contains seeds; in appearance they resemble ticks, which is where the plant got its name. Castor bean looks beautiful, grows quickly and is often used as an ornamental plant in landscape design. In addition, it is grown as an agricultural crop to obtain castor oil. It is produced by cold pressing, as a result of which all hazardous substances remain in the cake.

In addition to castor oil and proteins, castor bean seeds contain ricin. This is a high molecular weight protein compound classified as a natural toxin. Its seeds may contain up to 3%, as well as from 0.1 to 1% of an alkaloid with a similar effect - ricinin. Next, let’s combine them under the general name “ricin.” The plant contains these poisons in small quantities in its leaves and shoots, but for clinical cases of poisoning only the seeds are important.

Effect of ricin

Ricin poisoning develops after ingestion of very small doses. Thus, the lethal dose for humans is 0.003 mg of pure substance per kg of weight, which corresponds to eating 6 castor bean seeds for children and 20 for adults. When administered intramuscularly under experimental conditions, the lethal dose for mice is 0.0075 mg/kg, for cats 0.0002 mg/kg, for dogs 0.0006 mg/kg.

Properties of ricin in its pure form:

The poison does not penetrate the skin; it acts only when ingested or through injection. Cases of castor bean poisoning occur quite often, so the toxic properties of the poison have been well studied. In laboratories, ricin is used to provoke cancer in experimental animals.

The effect of ricin occurs at the cellular level. Penetrating into cellular structures - ribosomes, the toxin disrupts protein synthesis and, accordingly, the functioning of the cell as a whole. A curious property of ricin has been proven - by splitting into subunits, it can form bonds with molecules of other toxins or polypeptides, resulting in a new toxic compound not found in nature.

Symptoms of Ricin Poisoning

In cases of ricin poisoning, symptoms develop within 15 to 24 hours. If poisoning occurred by inhaling a toxin, then signs may appear earlier - after 4–8 hours. In an allergic reaction, symptoms develop immediately after contact with the poison.

Primary symptoms:

A characteristic sign of ricin poisoning is hemorrhages (bleeding) on ​​the retina of the eye.

In severe cases, the following symptoms develop:

• convulsions;
• cyanosis;
• collapse (sharp drop in blood pressure);
• prostration.

Death occurs after 6–8 days due to severe damage to the liver and spleen, extensive hemorrhages in the stomach and intestines, and toxic kidney dystrophy. The pancreas is severely affected. Red blood cells, hemoglobin, protein and cylindrical cells appear in the urine. Characteristic changes are found in the lymph nodes of the abdominal cavity.

When it comes into contact with the skin, ricin does not have any negative effects. After contact of ricin powder with mucous membranes, burning, redness, watering or stinging in the eyes is possible. You should consider the possibility of poison getting ingested, for example, if it was left on your hands and then you ate or smoked.

Poisoning by inhalation does not occur under practical conditions. The situation was recreated in laboratory conditions, and the size of the aerosol particles must be of a certain size - too large droplets settle in the upper respiratory tract, small ones come out back with exhaled air.

First aid and treatment

There is no antidote for ricin. In case of poisoning with this toxin, general measures should be taken to prevent further absorption of the poison and the victim should be immediately taken to the hospital.

First aid is provided as follows.

1. Give 2-4 glasses of water with a suspension of activated carbon to drink.
2. Take a mucous solution inside - rice or flaxseed broth, starch, jelly.
3. Give 5-15 grams of sodium bicarbonate (baking soda) to support the kidneys.

In the hospital, the victim’s stomach is washed with a solution containing a suspension of activated carbon.

In addition to the fact that there is no antidote for ricin, this substance has a large molecule size and, therefore, is poorly excreted by the kidneys. Standard methods of cleansing the body - forced diuresis and hemodialysis - are ineffective in case of poisoning with castor bean seeds. Measures are taken to remove poison from the intestines, symptomatic and supportive treatment:

• restore blood pressure;
• alkalinization of urine is carried out to prevent precipitation of hemoglobin in the kidneys;
• Enveloping drugs are given orally to take;
• laxatives (magnesia) and deep enemas to cleanse the intestines;
• blood transfusion;
• for severe pain, morphine is administered together with atropine.

What is ricin?

In the courtyards of private homes, you can sometimes see a tall plant with large leaves, somewhat similar to maple leaves, and red balls containing seeds. Castor beans are often used for decorative purposes; they grow well and quickly. The plant received its name due to the similarity in appearance of the seeds with mites.

In agriculture, castor oil (ricin oleum) is obtained from castor bean seeds, so it is grown in large quantities. By the way, on sale you can sometimes find “Zinc ricin” ointment with castor oil, which is used for dry dermatoses.

However, few people know that in addition to its benefits, this plant can cause quite serious harm to the human body. Its seeds contain poison - ricin. This substance is present in all parts of the plant, but the seeds are the most dangerous.

The chemical production of ricin comes from castor bean cake. The result is a powdery substance that is white in color. There is no smell. In modern science, it is possible to produce poison in the form of crystals. The compound has good solubility in aqueous solutions. Becomes non-toxic at high temperatures (above 90 degrees).

Where is it located and for what purposes is it used?

Where does castor grow? Its main habitats are China, India, and Bangladesh. However, in Russia you can also often find this plant, because castor oil is a fairly popular medicinal product.

Where is this poison used? Where can I find this substance?

Ricin has not found its use for medical purposes. Although many scientists have tried to use it to produce drugs for oncology.

In most cases, the toxic properties of ricin are used specifically for criminal purposes. Powder or aerosol with such a substance is fatal to humans.

On the Internet you can sometimes come across a question about how to obtain this poison at home. This is possible, but it is always worth remembering that such actions may be considered a criminal offense. Many terrorists have developed their own recipe for making such poison.

Effect of ricin on humans

What happens to the body during ricin poisoning?

It is worth noting that accidental intoxications are quite rare. Most poisonings are planned. There are several options for this.

Options:

• Ingestion with food or drinks,
• Inhalation of airborne powder
• Use of solution for injection.

Ricin does not have a negative effect on the skin. It is not absorbed through them in its pure form. Poisoning in this way is possible when mixing the poison with any solvents.

When ingested, ricin disrupts protein synthesis. It has a destructive effect on red blood cells, which either die or stick together as a result. As a result, cell destruction occurs and the functioning of organs and systems is disrupted.

The result can be death after quite a long period of suffering. The lethal dosage for an adult is twenty seeds; six is ​​enough for children.

Symptoms and signs of poisoning

What should you pay attention to in order to detect ricin poisoning in time?

Symptoms do not begin to appear immediately, but after a certain time (about 15 hours) when the toxin enters the mouth.

If poisoning occurs through the respiratory tract, the first signs can be noticed within four hours.

List of signs:

• nausea, vomiting,
• burning sensation on the mucous membranes,
• diarrhea, sometimes mixed with blood,
• pain in the stomach and intestines,
• bleeding in the eyes,
• convulsive state
• decrease in pressure,
• the skin becomes bluish,
• coughing,
• respiratory dysfunction,
• enlarged lymph nodes in the abdominal cavity,
• muscle paralysis.

In the absence of help, death occurs in about a couple of days. The man dies in severe pain. Unfortunately, there is no antidote for ricin.

First aid and treatment of intoxication

In case of ricin poisoning, it is very important to provide first aid to the person in a timely manner. The further outcome and life of the victim depends on this.

Therapy:

• Doctors must be called
• The victim should rinse the stomach with plenty of water with the addition of activated carbon,
• Then the poisoned person should be given a decoction of rice or jelly to drink,
• A person needs to be given a small amount of soda to alleviate the “suffering” of the kidneys.

Therapy is carried out in a hospital. There is no antidote for ricin. The medical institution takes all necessary measures to provide the necessary assistance.

Measures:

• If necessary, additional gastric lavage is performed,
• Various means are used to restore the functioning of systems and organs,
• Laxatives are used
• Blood transfusion is performed
• Various painkillers are prescribed.

Particular attention is paid to the kidneys due to the fact that ricin is excreted rather poorly by them, and they are subject to heavy load.

In the future, vitamin therapy is used, treatment is carried out until the entire body is completely restored.

What could be the consequences?

Ricin poisoning can cause quite serious consequences. With such intoxication, all body systems suffer.

What could be:

• The functioning of the digestive system is disrupted, the intestines suffer.
• The liver and pancreas also suffer quite severely. In the future, it is possible to develop toxic hepatitis and disrupt insulin production.
• The functioning of the urinary system may also be disrupted, and chronic diseases may worsen.

Ricin poisoning poses a great danger to humans. You should not plant this plant if there are small children in the house. After all, babies are very curious and put everything in their mouth. As a result, severe ricin toxicity may occur.

If signs of poisoning are detected, first aid must be provided to the person as quickly as possible, his life depends on it. And then transfer the victim to doctors for further treatment.

Ricin in the hands of terrorists and doctors

Food for thought

In early January 2003, British police arrested a group of terrorists, some of whom were trained in Chechnya. They didn't make bombs or hijack planes, but had their criminal activities been successful, the consequences could have been no less catastrophic.
In an underground laboratory, the criminals set up the production of ricin, a powerful poison, and meanwhile one of the detainees worked at a military base and had access to preparing food for soldiers. Adding a dose of poison into the cauldron that could kill hundreds of people at the same time would not be too difficult - the lethal dose of ricin is 80 times less than that of potassium cyanide, and is about 1 mg for a person. In 1978, Bulgarian dissident Georgi Markov was killed in London using this poison. He died from an injection with an umbrella, in the needle-tip of which a capsule with ricin was hidden.

Origin and effect of the poison

Where did this deadly substance come from and who invented it? It turns out that nature itself. The poison is contained in the seeds of a widespread plant that has been used in traditional medicine for centuries - castor bean (Ricinus communis).

Fig 1. Castor bean (Ricinus communis)

“But how can that be? - the knowledgeable reader will be surprised. - After all, castor oil is obtained from castor beans. More recently, it was used not only for the production of motor oils and strengthening hair, but also taken orally as a good laxative!” Indeed, ricinoleic acid triglyceride, known as castor oil, can be bought at the pharmacy without any prescription - this substance is completely harmless. Even if you swallow castor bean seeds whole without chewing, there will be no harm: they will pass through the entire digestive tract without being destroyed by enzymes.
But if the surface of castor bean seeds is damaged, the one who swallowed them - be it a person or a pet - will die. The fact is that after extracting the oil from castor bean seeds, all the poison remains in the cake. It is this that serves as the raw material for the production of ricin. Each fruit contains three spotted seeds from 5 to 15 mm long (Fig. 2).

Fig 2. Castor bean seeds - a source of ricin

Ricin poisoning can occur not only through food. If you inhale a powder or aerosol containing poison, the consequences can be equally dire. Meanwhile, the first signs of poisoning are sometimes mistaken for symptoms of an infectious disease. They do not appear immediately, but only a few hours after the poison enters the body. If it ends up in food, a person experiences weakness, abdominal pain, accompanied by vomiting and diarrhea with blood. Then the body becomes dehydrated and blood pressure drops. When ricin enters the lungs, the symptoms of poisoning resemble severe bronchitis or pneumonia. And the saddest thing is that there is no antidote for ricin yet. If a person is poisoned, he dies within 1-5 days, since the poison irreversibly damages the lungs, liver and kidneys.
Both in America and in Western European countries, frightened by terrorist attacks, doctors are specially introduced to the symptoms of ricin poisoning and tell the population about them, since in the hands of criminals this substance can be extremely dangerous. Ricin poisoning almost never happens in everyday life. The poison, fortunately, is very unstable and quickly decomposes under the influence of ultraviolet radiation, that is, simply put, under the rays of the sun.

Mechanism of action

But what kind of poison is this? How does it work and why is it so dangerous?
Ricin is a glycoprotein, that is, a protein whose amino acid chains form complexes with carbohydrate structures. This protein is a dimer, that is, it includes two protein chains - A and B. Chain A consists of 267 amino acid residues, with some of its fragments folded into spherical structures, and others into spirally twisted ribbons; one of the tapes contains
adenine ring (Fig. 3.). Proteins that closely resemble the A chain are not that rare. Wheat, barley and some other grains have them, which are not at all poisonous.

Figure 3. Three-dimensional representation of ricin chains modeled from X-ray diffraction data. In the upper part of the figure, the dotted line indicates circuit A, and in the lower solid line, circuit B.

In castor beans, such a protein turns into poison because it is cross-linked by a disulfide bridge with another protein chain - the B chain. This chain, consisting of 262 amino acid residues, is formed like a dumbbell. Monomer B is a lectin, a protein that can bind carbohydrates. At both ends of the dumbbell, it contains areas cross-linked with the sugar galactose, which, in turn, can form hydrogen bonds with other sugars galactose and N-acetylgalactosamine located on the surface of the cell membrane.
Due to this feature, lectins have a high affinity for receptors located on cell membranes and are able to deliver substances to which they are connected; Ricin enters the cell through normal endocytosis. In this case, monomer B facilitates the penetration of protein A into the cell. Once inside, it becomes very dangerous - it attaches to the ribosome (a kind of molecular machine for protein synthesis) and disrupts its functioning. A single ricin molecule in the cytoplasm can inactivate more than 1500 ribosomes per minute due to depurination of RNA in the protein-synthesizing apparatus. As a result, protein synthesis in the cell stops and it dies.

Ricin - for peaceful purposes

The mechanism of action of the poison has been studied quite well, and this opens up opportunities for using the substance for peaceful purposes. Medical science has more than once succeeded in taming and even taming poisons - there are many examples of this.
So they are trying to use ricin for medical purposes, making it kill not all cells, but only cancer cells or, say, some cells of the immune system when they interfere with transplantation.
To create an immunotoxin, the ricin monomer (chain A) is attached to antibodies - now they will perform the function of the lectin part. This product is highly specific and destroys only cells to which antibodies have affinity. When bone marrow is transplanted into a patient, ricin-based immunotoxins successfully destroy T-lymphocytes present in the donor's bone marrow. This reduces the possibility of rejection of the tissue transplanted to the recipient. Bone marrow transplant operations thus become more successful.
A similar approach is used in the treatment of leukemia and lymphoma. To do this, the patient's bone marrow is taken and treated with a ricin-based immunotoxin to destroy cancer cells. This bone marrow is then implanted back into the patient. Targeted delivery of small amounts of toxins to cancer cells gives better results than chemotherapy, in which large doses of poisons lead to the death of not only diseased but also healthy cells.
But that's not all. The scope of ricin is constantly expanding. Thus, scientists used its ability to interact with cell membranes in order to better understand the peculiarities of the nervous system. It turned out that by injecting ricin into the membrane of the nerve bundle, neurons can be selectively destroyed. At the same time, the peripheral nerves responsible for sensory and motor functions turned out to be especially sensitive to the poison. Neurons of the central nervous system are more resistant to it, which can be explained by the absence of sugars on the surface of their membranes, to which the ricin molecule has an affinity. Well, since there is no receptor, it means that the poison cannot penetrate the cell and paralyze the work of ribosomes. Thanks to the research, it became possible to model various types of neuronal damage and find ways to eliminate them, as well as draw up an anatomical map of neurons, noting on it the characteristics of the receptors of many of them.
In general, the conclusion from all that has been said is obvious: the substance itself, be it gunpowder, medicine or poison, is not good or bad, it all depends on whose hands it falls into.

E.V. Moskalev, Candidate of Technical Sciences
Based on materials from the magazine “Chemistry and Life XXI Century” No. 3, 2003
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