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What is potassium cyanide and how does it affect the human body. About potassium cyanide

2014-05-21
What is cyanide?

Cyanide is a fast-acting, deadly chemical that can exist in various forms. Cyanide may be a colorless gas such as hydrogen cyanide (HCN) or cyanogen chloride (CNCL) or be in crystalline form such as sodium cyanide (NaCN) or potassium cyanide (KCN). Cyanide is sometimes described as having a "bitter almond" odor, but this is not always the case and not everyone can smell it.

Where is cyanide found and how is it used?

Cyanide can be isolated from some natural substances, some foods and some plants such as cassava, lima beans and almonds.

Cyanide is found in cigarette smoke and combustion products of synthetic materials such as plastic. In the manufacturing industry, cyanide is used to make paper, textiles and plastics. It is present in the chemicals used to develop photographs.

Hydrogen cyanide, called Zyklon-B, was used as a poison gas by the Germans in World War II.

Reports have shown that during the Iran-Iraq War in the 1980s, hydrogen cyanide may have been used along with other chemicals against residents of the Kurdish city of Halabja in northern Iraq.

How cyanide works

Inhaling cyanide gas causes the most harm, but ingesting cyanide can cause severe consequences.

Cyanide gas is considered most dangerous in enclosed spaces where the gas will be trapped.

The gas quickly dissipates in open space, making it less harmful when outdoors.

Cyanide blocks the ability of body cells to use oxygen. When this happens, the cells die.

Cyanide is more harmful to the heart and brain than to other organs, since they are the main consumers of oxygen.

Signs and symptoms of cyanide exposure.

With minor exposure, the following signs:

Dizziness
- Headache
- Nausea and vomiting
- Fast breathing
- Cardiopalmus
- Weakness

Exposure to large amounts of cyanide by any means may cause the following symptoms:

Convulsions
- Loss of consciousness
- Low blood pressure
- Lung damage
- Respiratory failure
- Slow heart rate

What to do if you are exposed to cyanide.

If cyanide is in the air, leave the room immediately and get fresh air.

If cyanide gas was released outdoors, move away from the area where it was released. If you cannot get out of the area where the cyanide gas has been released, lower yourself to the ground since cyanide is lighter than air.

If you think you have been exposed to cyanide, you should remove your clothing, quickly wash your entire body with soap and water, and get medical care as fast as possible.

If your eyes burn or your vision is blurry, rinse your eyes with clean water for 10 to 15 minutes. If you wear contact lenses, remove them and place them with contaminated clothing.

What do Grigory Rasputin, Vladimir Lenin and an unknown elephant named Yambo have in common? A lover of action-packed detective novels, in which treacherous crimes are accompanied by an almond aroma, can easily answer this question.

Potassium cyanide is a substance that became an effective replacement for the “royal poison” and took part in many political feuds, where it was necessary to remove those disliked by the regime from the road statesmen. At one time, they tried to deal with the help of this poison not only with the power-hungry old man, the leader of the Communist Party and other prominent persons, but also with the unfortunate animal from the Odessa circus. Moreover, the elephant Yambo went down in history because his poisoning, like the poisoning of Rasputin, was not successful.

This strongest inorganic poison is inaccessible to the average person today, so cyanide poisoning is very rare. However, the industry uses a sufficient amount of toxic and toxic substances to suffer, even without being the hero of an Agatha Christie novel.

Taking precautions when coming into contact with hazardous chemical compounds is often not enough and it is necessary to know how potassium cyanide affects humans in order to provide first aid in a timely manner.

What is potassium cyanide and what is it eaten with?

It is not known for certain when humanity first became acquainted with derivatives hydrocyanic acid and their properties. Cyanides boast ancient origins and rich history: These substances were first mentioned by the ancient Egyptians, who obtained them from peach pits.

The assumption of a deadly poison in such a popular delicacy seems absurd, however, more than two and a half hundred plants of the plum genus have similar properties. Why has no one been poisoned by eating the fruits of these trees yet?

The secret is quite simple: the poison is contained in fruit seeds. During metabolism, a natural glycoside called amygdalin is broken down by enzymes in gastric juice and forms toxic compounds. After hydrolysis, the amygdalin molecule loses glucose and breaks down into benzaldehyde and hydrocyanic acid.

IN medical literature There are no documented cases of death from eating the fruit, since cyanide poisoning requires eating so many seeds raw. However, a child can become poisoned by swallowing 10 or more seeds, so parents need to be extremely careful.

Jams, compotes, and tinctures made from these fruits do not actually pose a threat, even if you do not remove the seeds from the fruits. After heat treatment and canning, amygdalin loses its toxic properties, and the potassium salt of hydrocyanic acid itself is highly soluble in water and alcohol.

Cyanide itself is an unremarkable white powder, but its compounds with iron molecules differ in a variety of shades of blue color. Thanks to this property, the substance is more popularly known as “blue,” and one of the most famous dyes based on it is Prussian blue. It was from this substance that it was first chemically synthesized by a Swedish scientist.

Areas of human activity in which one may encounter cyanide today:

agriculture and entomology (used as an insecticide);
mining and processing production;
creation of galvanic coatings;
production of plastic and products made from it;
developing photographic film;
production of fabric dyes and paints for artists in all shades of blue;
military affairs (during Nazi Germany).

Industrial enterprises where potassium cyanide is actively used can pose a danger even to the non-industrial population. Poisonous wastewater pollute water bodies and cause the death of their inhabitants and mass poisoning among people.

It has been proven that the sense of smell largely depends on a person’s genetic characteristics. The characteristic almond aroma appears during the hydrolysis of hydrocyanic acid - the smell of hydrogen cyanide, which is released in the process. There is a possibility of poisoning by the vapors of this substance, so it is highly not recommended to empirically test what cyanide smells like.

How does potassium cyanide work?

There is an opinion that if a small amount of this substance enters the stomach, instant death occurs. This statement is only half true.

Indeed, potassium cyanide is a dangerous poison for humans, but in fact, the use of this substance does not lead to immediate death. The mechanism of its action on the human body is more complex than it might seem:

A special enzyme, cytochrome oxidase, is responsible for the absorption of oxygen at the cellular level. During the studies, the venous blood of the test animals was bright scarlet, like arterial blood. This indicated that when it enters the body, the poison blocks this enzyme.
Next, oxygen metabolism is disrupted and oxygen starvation of cells occurs. Oxygen molecules circulate freely in the blood, bound to hemoglobin.
Cells gradually begin to die, normal functioning is disrupted internal organs, and after that their activities cease altogether.
The result is death, which in all respects resembles suffocation.

It can be seen that death from cyanide poisoning does not occur immediately, but a person can lose consciousness very quickly due to lack of oxygen.

Damage to the body is possible not only when poison enters the stomach, but also when inhaling its vapors and when it comes into contact with the skin (especially in places of damage).

How does poisoning manifest itself?

As with most intoxications, the result of a person’s encounter with this poison can take both acute and chronic forms.

Acute poisoning occurs immediately a few minutes after ingesting the poison or inhaling cyanide powder. This effect of potassium cyanide on humans is due to the fact that the substance is quickly absorbed into the blood through the mucous membranes of the mouth and stomach.

Poisoning can be divided into four main phases, each of which is characterized by special features:

The first prodromal phase, during which symptoms just begin to appear:

discomfort and bitterness in the mouth;
sore throat, irritation of mucous membranes;
increased salivation;
slight numbness of the mucous membranes;
dizziness accompanied by nausea and vomiting;
squeezing pain in the chest.

At the second stage, there is an active development of oxygen starvation of the body:

drop in blood pressure, slowing heart rate and pulse;
increased pain and heaviness in the piles;
difficulty breathing, shortness of breath;
general weakness, severe dizziness;
redness and protrusion of the eyes as if suffocating, dilated pupils;
the appearance of a feeling of fear, panic.

The above picture is complemented by convulsive twitching, convulsions, and involuntary defecation and urination may occur. When a lethal dose is consumed, the patient loses consciousness.
At this stage, death is inevitable. Death occurs 20-40 minutes after the first signs appear as a result of respiratory paralysis and cardiac arrest.

At full strength, the poison acts in the body for about four hours. If death does not occur during this time, the patient, as a rule, remains alive. But even after complete recovery, the activity of areas of the cerebral cortex is disrupted, the functionality of which can no longer be restored.

A person’s life can be saved if you immediately call an ambulance and promptly provide first aid before the medical team arrives:

provide the patient with free breathing;
remove constrictive clothing and things that may have been exposed to poison;
flush the stomach as quickly as possible big amount water, a weak solution of potassium permanganate or soda.

If the victim is unconscious, it is necessary, if possible, to resuscitate him using artificial respiration and cardiac massage. Upon arrival of the doctor, the patient will be given a specific antidote that will neutralize the effect of the poison.

Such poisonings are very serious and dangerous, so treatment should occur in a hospital and be prescribed after examining the patient and taking his tests.

Potassium cyanide antidote

As they say last news in the field of chemistry and biology, a new fast-acting antidote against cyanide was recently invented. Scientists claim that this substance can neutralize the toxin within three minutes. However, it is not yet widely used, and the antidotes used by modern medicine act very slowly.

Help, as a rule, is provided with the help of nitrogenous substances and compounds that easily release sulfur from the group of methemoglobin-forming agents. There are several varieties of such antidotes, which differ in their methods of application, but act on the same principle: they “tear off” oxygen from hemoglobin so that it gains the ability to cleanse cells of toxin. Most often, the victim is given amyl nitrite to sniff, sodium nitrite or methyl blue is injected intravenously in the form of a solution.

One of the most unexpected antidotes and the reason for the failure of the killers of Rasputin and the elephant Yambo is glucose. They tried to treat both of them with sweets filled with cyanide. When the poison has already entered the blood, glucose is useless and can only serve as an auxiliary agent for the treatment of poisoning, but it can weaken the effect of the toxin by entering into synthesis with it. Sulfur has the same property, the presence of which in large quantities in the victim’s stomach reduces the effectiveness of the poison.

Industrial workers exposed to potassium cyanide take precautions and often use sugar as an additional means of protection. However, this cannot fully protect against the accumulation of toxic substances in the body. If chronic poisoning is suspected, it is necessary to undergo a medical examination to prescribe the correct treatment.

And now it is attracting the close attention of many specialists. Cyanide compounds were already used in ancient times, although, of course, their chemical nature was not known then. Thus, the ancient Egyptian priests knew how to make an essence from peach leaves, which they used to kill guilty people. In Paris, in the Louvre, on a roll of papyrus there is a warning saying: “Do not pronounce the name of Iao under pain of punishment with a peach,” and in the Temple of Isis an inscription was found: “Do not open - otherwise you will die from the peach.” Now we know that the active component here was hydrocyanic acid, formed during the enzymatic transformations of certain substances of plant origin. A number of prominent chemists of the past studied the structure, methods of production and use of cyanide. Thus, in 1811, Gay-Lussac first showed that hydrocyanic acid is a hydrogen compound of a radical consisting of carbon and nitrogen, and Bunsen in the middle of the 19th century. developed a method for the industrial production of potassium cyanide. Many years have passed since potassium cyanide and other cyanides were important as means of deliberate poisoning and when to these fast-acting poisons Forensic experts showed particular interest. History knows of cases of the use of cyanide for mass destruction of people. For example, the French army used hydrocyanic acid as a poisonous substance during the First World War; in Hitler’s extermination camps, the Nazis used poisonous gases, cyclones (esters of cyanacetic acid), and American troops in South Vietnam used toxic organic cyanides (CS type gases) against civilians. It is also known that in the United States the death penalty has been used for a long time by poisoning convicts with hydrocyanic acid vapor in a special chamber.

Due to their high chemical activity and ability to interact with numerous compounds of various classes, cyanides are widely used in many industries, agriculture, and scientific research, and this creates many opportunities for intoxication. Thus, hydrocyanic acid and a large number of its derivatives are used in the extraction of precious metals from ores, in galvanoplastic gilding and silvering, in the production of aromatic substances, chemical fibers, plastics, rubber, organic glass, plant growth stimulants, herbicides. Cyanides are also used as insecticides, fertilizers and defoliants. Hydrocyanic acid is released in a gaseous state during many industrial processes, and is also formed when cyanide comes into contact with other acids and moisture. There may also be cyanide poisoning due to eating large quantities of almond, peach, apricot, cherry, plum and other plants of the Rosaceae family or infusions from their fruits. It turned out that they all contain the glycoside amygdalin, which in the body, under the influence of the emulsin enzyme, decomposes to form hydrocyanic acid, benzaldehyde and 2 glucose molecules:

Largest quantity amygdalin is found in bitter almonds, the peeled grains of which contain about 3%. Slightly less amygdalin (up to 2%) in combination with emulsin is found in apricot seeds. Clinical observations showed that the death of the poisoned usually occurred after eating about 100 peeled apricot seeds, which corresponds to approximately 1 g of amygdalin. Like amygdalin, plant glycosides such as linamarin, found in flax, and laurocerazine, found in the leaves of the cherry laurel tree, split off hydrocyanic acid. There are a lot of cyanide substances in young bamboos and their shoots (up to 0.15% of wet weight). In the animal world, hydrocyanic acid is found in the secretion of the skin glands of millipedes ( Fontaria gracilis).

Cyanide toxicity to various types animals are different. Thus, high resistance to hydrocyanic acid has been observed in cold-blooded animals, while many warm-blooded animals are very sensitive to it. As for man, he is apparently more resistant to the action of hydrocyanic acid than some higher animals. This is confirmed, for example, by an experiment carried out at great risk to himself by the famous English physiologist Barcroft, who in a special chamber together with a dog was exposed to hydrocyanic acid at a concentration of 1:6000. The experiment continued until the dog became comatose and began to have convulsions. The experimenter did not notice any signs of poisoning at this time. Only 10–15 minutes after removing the dying dog from the chamber did he experience impaired attention and nausea.

There is a lot of data indicating the formation of cyanide in the human body under physiological conditions. Cyanides of endogenous origin are found in biological fluids, exhaled air, and urine. It is believed that their normal level in blood plasma can reach 140 mcg/l. In this regard, vitamin B 12 (cyanocobalamin) should also be mentioned, which, as is known, is a growth factor necessary for the body for normal hematopoiesis and the functioning of the nervous system, liver and other organs. According to the chemical structure, vitamin B 12 is a complex polycyclic compound with a cobalt atom in the center of the molecule to which a CN group is attached.

Mechanism of biological action of cyanide

Cyanides can penetrate into the internal environment of the body with poisoned food and water, as well as through damaged skin. Inhalation exposure to volatile cyanides, primarily hydrocyanic acid and cyanogen chloride, is very dangerous. Back in the 60s of the 19th century, attention was paid to the fact that venous blood flowing from the tissues and organs of animals poisoned with cyanide takes on a scarlet, arterial color. It was later shown that it contains approximately the same amount of oxygen as arterial blood. Consequently, under the influence of cyanide, the body loses the ability to absorb oxygen. Why is this happening?

Rice. 15. Scheme of the cellular oxidation process. NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate) are coenzymes of dehydrogenases; FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide) are coenzymes of flavin enzymes; tsV, tsS, tsS 1 tsA - cytochromes; tsA 3 - cytochrome oxidase

The answer to this question was obtained in Germany at the end of the 20s in the works of Otto Warburg, who established that, penetrating into the bloodstream, cyanide very soon ends up in cellular structures, primarily in mitochondria, where enzymatic processes of tissue oxidation (consumption) take place oxygen cells). As can be seen from Fig. 15, the first link of these processes includes the abstraction of hydrogen from the oxidizing substrate. In this case, each hydrogen atom is divided into a proton and an electron. This part Oxidative reactions in cells are catalyzed by enzymes from the group of dehydrases, as well as the so-called flavin (yellow) Warburg enzyme. The second link of cellular oxidation consists of the transfer of electrons to oxygen, which makes it possible to interact with activated hydrogen atoms (protons) and leads to the formation of one of the most important final products oxidation - water molecules. This link of oxidative reactions functions thanks to a special group of enzymes - cytochromes and cytochrome oxidase, containing iron atoms of variable valence. It is this chemical property that is the source of electrons that attach to oxygen. As follows from the above diagram, electrons sequentially pass from one cytochrome to another, from them to cytochrome oxidase, and then to oxygen. In a figurative expression, “a chain of cytochromes is like a chain of basketball players passing the ball (electron) from one player to another, inexorably bringing him closer to the basket (oxygen).” This final stage of cellular oxidation can be schematically represented as the following two reactions:

1) 2protein - R -Fe 2+ + 1/2O 2 2protein - R - Fe 3+ + 1/2O 2 2-,

reduced oxidized

cytochrome oxidase cytochrome oxidase

2) 1/2O 2 2- + 2H + > H 2 O.

It turned out that hydrocyanic acid, or more precisely CN-ion, due to its special chemical affinity for ferric iron, selectively (albeit reversibly) interacts with oxidized cytochrome oxidase molecules. This inhibits the normal process of tissue respiration. Thus, by blocking one of the iron-containing respiratory enzymes, cyanides cause a paradoxical phenomenon: there is excess oxygen in cells and tissues, but they cannot absorb it, since it is chemically inactive. As a result, a pathological condition known as tissue, or histotoxic, hypoxia quickly forms in the body, which is manifested by suffocation, severe cardiac dysfunction, convulsions, and paralysis. When non-lethal doses of poison enter the body, the matter is limited to a metallic taste in the mouth, redness of the skin and mucous membranes, dilated pupils, vomiting, shortness of breath and headache. On the other hand, if an animal organism is adapted to a low level of oxygen metabolism, then its sensitivity to cyanide is sharply reduced. The outstanding Russian pharmacologist N.P. Kravkov c. At the beginning of this century, a curious fact was established: during hibernation, hedgehogs tolerate doses of potassium cyanide that are many times greater than lethal ones. N.P. Kravkov explained the resistance of hedgehogs to cyanide by the fact that during hibernation at low body temperatures, oxygen consumption is significantly reduced and animals better tolerate inhibition of its uptake by cells. However, not all poison that enters the body interacts with respiratory enzymes. A certain amount of it is excreted unchanged in the exhaled air and undergoes detoxification with the formation of harmless products in the blood due to reactions with sugars, sulfur-containing compounds, and oxygen. Probably, it is precisely this circumstance that determines the absence of pronounced cumulative properties in hydrocyanic acid and other cyanides. In other words, when these poisons act in subtoxic doses, the body copes with them on its own, without outside intervention. Thus, if the concentration of hydrocyanic acid in the inhaled air does not exceed 0.01–0.02 mg/l, then it turns out to be practically safe for several hours. An increase in the concentration of poison only to 0.08–0.1 mg/l is already life-threatening due to the depletion of the protective mechanisms for neutralizing cyanide.

The ability of CN ions to reversibly inhibit tissue respiration and thereby reduce the level of metabolic processes unexpectedly turned out to be very valuable for the prevention and treatment of radiation injuries. This is due to the fact that in the mechanism of the damaging effect of ionizing radiation on cellular structures, the leading role is played by the products of water radiolysis (H 2 O 2, HO 2, O, OH, etc.), which oxidize many macromolecules, including tissue respiration enzymes. Cyanides, reversibly blocking these enzymes, protect them from the action of these biological active substances, formed under the influence of radiation. In other words, the cyanide-enzyme complex becomes relatively resistant to irradiation. After radiation exposure, it dissociates due to a decrease in the concentration of CN ions in the biophase due to their neutralization in the blood and release from the body. Amygdalin is the most widely used cyanide radioprotective agent. It is curious that more than 40 years ago, in experiments on several species of animals, the anti-radiation (both therapeutic and prophylactic) effect of carbon monoxide was established. Experimental data indicate that the blockade of hemoglobin by carbon monoxide is of radioprotective importance, and not its inhibition of tissue respiration enzymes. Apparently, this is accompanied by a general decrease in the level of oxygen metabolism, which in turn reduces the formation of these oxygen-containing radicals. However, in practice this property of carbon monoxide is not used, since it manifests itself at a high concentration of carboxyhemoglobin.

From the structure of heparin it follows that its molecule, including glucuronic and sulfurous acids, as well as glucosamine, by splitting off any of these components, will contribute to the detoxification of cyanide, and possibly the reactivation of cytochrome oxidase.

Neutralization of cyanide in the body can also be achieved using β-hydroxyethylmethylenamine:

HO-CH 2 -CH 2 -N=CH 2 +HCN > HO-CH 2 -CH 2 -N

CH 3

This was shown by the experiments of V.N. Rosenberg. Apparently, under conditions of tissue hypoxia, hydroquinone relieves respiratory enzymes from excess electrons and, in addition, activates the dehydrase link of cellular oxidation, which is resistant to cyanide.

Methylene blue, as a drug that has the ability to accept hydrogen, also interferes with cellular oxidation processes. Since in the mechanism of the toxic effect of cyanide, the accumulation of protons (hydrogen nuclei) plays the role of a factor inhibiting the course of biological oxidation reactions, the binding of excess protons will stimulate these reactions. Therefore, in a certain sense, methylene blue should also be considered as a drug equivalent to one of the respiratory enzymes. However, it is almost impossible to clearly separate this effect from the methemoglobin-forming effect during cyanide intoxication.

Rice. 16. Comparative antidote effectiveness of the most significant anticyanides

The comparative antidote effectiveness of the most significant anticyanides, studied in experiments on dogs, is presented in Fig. 16, where the numbers in circles indicate the number of lethal doses from which a given antidote or combination protects. Long-term practice of experimental treatment of severe cyanide poisoning in our laboratory confirms these data. In particular, the combination of sodium nitrite and sodium thiosulfate was particularly effective. Emergency intravenous sequential administration of these antidotes saved animals from death even in the convulsive-paralytic stage of intoxication.

Experience shows that, along with the comprehensive use of antidotes, to successfully combat cyanide intoxication, it is necessary to use such resuscitation measures as artificial respiration, cardiac stimulation, oxygen inhalation, etc. In this regard, the instructions on first aid in case of poisoning with hydrocyanic acid and its salts, developed about 30 years ago in Frankfurt am Main by one of the companies for the extraction of gold and silver from ores. Here are its main provisions:

"Keep calm! Act quickly!

Remove the victim from the contaminated area; immediately remove any parts of clothing that are restricting the body, do not allow the patient to cool down (coverings, heating pads) and call a doctor.

a) If the victim is still conscious, then... break the ampoules with amyl nitrite and let the patient inhale for 10-15 seconds, but in general no more than 8 times. If cyanide is ingested by swallowing, prepare a mixture of 2 g of ferrous sulfate and 10 g of magnesium oxide in 100 cm 3 of water and give this mixture to the victim to induce vomiting (in no case should it be given in case of loss of consciousness).

b) If the victim is unconscious, then immediately perform vigorous artificial respiration..., give amyl nitrite (as described in point “a”). Do not stop artificial respiration, especially when delivered to the hospital, and perform it until the patient regains consciousness. As soon as the doctor arrives, it is recommended that he inject ... sodium nitrite solution and finally, with the same injection needle, ... sodium thiosulfate solution.

c) If cyanide gets into a wound or abrasion on the skin and splashes of hydrocyanic acid get on the skin, then these places should be thoroughly washed with water and then with a 5% solution of sodium bicarbonate... If splashes get into the eyes, carry out a particularly thorough and prolonged rinse and take the victim to the eye doctor."

Notes:

Sanotsky I.V. Prevention of harmful chemical effects on humans is a complex task of medicine, ecology, chemistry and technology. - ZhVKhO, 1974, No. 2, p. 125–142.

Gadaskina I. D. Theoretical and practical significance studying. transformation of poisons in the body. - In the book: Mater. scientific session, Rev. 40th anniversary of the Research Institute of Occupational Hygiene and prof. diseases. L., 1964, p. 43–45.

Koposov E. S. Acute poisoning. - In the book: Reanimatology. M.: Medicine, 1976, p. 222–229.

It is alleged that Scheele himself became a victim of this poison during one of the experiments.

Singur N. A. Clinical picture, issues of therapy and prevention of poisoning with apricot kernels. - In the book: Issues of forensic medical examination / Ed. M. I. Avdeeva. M.: Modgiz, 1954, p. 133–148.

Warburg O. Uber die katalytischen Wirkungen der lebendigen Substanz. Berlin, 1928.

Rose S, Chemistry of Life. M.: Mir, 1969, p. 139.

It is interesting to note that cyanide poisoning was an experimental model in which the molecular mechanisms of oxygen uptake by cells were studied.

Quote by: Arbuzov S. Ya. Awakening and anti-drug effects of nervous system stimulants. L.: Medgiz, 1960.

Rogozkin V.D., Belousov B.P., Evseeva N.K. Radioprotective effect of cyanide compounds. M.: Medgiz, 1963.

Quote by: Pravdin N. S. Guide to industrial toxicology. M.; L.: Biomedgiz, 1934, issue. I.

Prominent Soviet scientist academician USSR Academy of Medical Sciences N.N. Savitsky (1946) provided a number of theoretical and clinical-experimental evidence of the protective, neutralizing effect of physiological methemoglobin in relation to endogenous cyanides. The author even showed that the amount of methemoglobin found in the blood of healthy people can bind up to one-third of a lethal dose of cyanide.

Quote by: Melnikova V.F. Hydrocyanic acid and cyanide compounds. - In the book: Guide to the toxicology of toxic substances / Ed. A. I. Cherkes, N. I. Lugansky, P. V. Rodionov. Kyiv: Health, 1964.

For example, NaNO2 in case of acute severe poisoning is initially administered slowly in an amount of 10–20 ml of a 1–2% solution.

Kolesov O. E., Cherepanova V. N. On the issue of the antidote effect of cobalt mercaptides during cyanide intoxication. - Pharmacol. and Toksikol., 1964, issue. 1, p. 167–173.

Nazarov G.F., Oksengendler G.I., Leikin Yu.I. On the issue of the antihypoxic effect of heparin. - In the book: Theoretical immunology - practical healthcare. Tallinn, 1978, p. 274–275.

Rosenberg V.N. On the antidote properties of β-oxyethylmethyleneamine in cyanide poisoning. - Pharmacol. i toksikol., 1967, No. 1, p. 99–100.

Vinogradov V. M., Pastushenkov L. V., Frolov S. F. The use of electron acceptors for the prevention and treatment of oxygen starvation. - In the book: Research and pharmacological study of substances that increase the body’s resistance to extreme influences. L., 1908, p. 111–116

Quote by: Los K. Synthetic poisons / Trans. with him. M.: Foreign publishing house. lit., 1963, pp. 168–169.

INTRODUCTION 2

Cyanides are salts of hydrocyanic acid. In the IUPAC nomenclature, cyanides also include C-derivatives of hydrocyanic acid - nitriles. Cyanides include a large group of chemical compounds derived from hydrocyanic (cyanide) acid. All of them contain a cyano group - CN. There are inorganic cyanides (hydrocyanic acid, sodium and potassium cyanides, cyanide, cyanogen chloride, cyanogen bromide, calcium cyanide) and organic cyanides (esters of cyanoformic and cyanoacetic acids, nitriles, thiocyanates, glycoside amygdalin, etc.). 3

OBTAINING CYANIDES 3

APPLICATION OF CYANIDES 4

Organic cyanides are used to control agricultural pests, in organic syntheses, the pharmaceutical industry, etc. 4

EFFECT OF CYANIDES ON THE BODY 6

MEASURES FOR CYANIDE POISONING 7

TREATMENT OF POISONING 8

Hydrocyanic acid (HCN) 9

HUMAN POISONING WITH PRYANIC ACID 10

Action on nervous system 11

Effect on the respiratory system 11

Effect on the cardiovascular system 12

Changes in the blood system 12

SYMPTOMS OF PYROCANIC ACID POISONING 13

TOXICITY OF CYANIDES TO DIFFERENT SPECIES OF ANIMALS 14

INTERESTING FACTS 16

REFERENCES 17

Introduction

Currently, it is impossible to imagine a single type of human activity that is not directly or indirectly related to the influence of chemical substances on the body, the number of which amounts to tens of thousands and continues to grow continuously. These include pesticides (insecticides, pesticides, herbicides), household preparations (paints, varnishes, solvents, synthetic detergents), medicinal substances, chemical additives to food products, and cosmetics. Of no small importance in this regard are biologically active compounds of plant origin: alkaloids, glycosides, organic acids, many of which are not destroyed by drying, long-term storage, or heat treatment of the plants themselves or the meat of animals poisoned by them.

Another group of poisons is formed as a result of the vital activity of microorganisms. Microbial poisons (for example, botulinum toxin) are sometimes hundreds of times more powerful than highly toxic synthetic substances in biological action. We must also keep in mind that in nature there are many poisonous creatures: arthropods, mollusks, fish, snakes that can become dangerous to humans.

Leading toxicologists note with justified concern and alarm that the rapid development of the chemical industry, the introduction of chemical technology in many sectors of the national economy and in everyday life create chemical pollution of the environment and a serious threat to public health, leading to significant economic losses (diseases and death of animals, environmental associated with humans, for example, fish, deterioration of the nutritional properties of agricultural plants and much more).

WHAT ARE CYANIDES Cyanides are very poisonous. In the 20th century, cyanide was used as a poisonous substance against people and rodents in agriculture. At the beginning of the 20th century, hydrocyanic acid was used by the French as a chemical warfare agent (CWA), such as cyanogen chloride.

OBTAINING CYANIDES

The main method for producing alkali metal cyanides is the interaction of the corresponding hydroxide with hydrocyanic acid, in particular, this is the main industrial method for producing the largest-tonnage cyanide - sodium cyanide. Another industrial method for producing sodium cyanide is by fusing calcium cyanamide with coal and sodium chloride or soda:

CaCN 2 + C + 2 NaCl 2 NaCN + CaCl 2

The melt formed in the process (“cyan alloy”, “black cyanide”) contains 40 - 47% cyanide in terms of NaCN and is used for cyanidation of steel, and was also used as a raw material for the production of sodium and potassium cyanide, as well as yellow blood salt.

Other cyanides are obtained mainly by exchange reactions of alkali metal cyanides with the corresponding salts.

Alkali metal cyanides can also be prepared by reacting the metal with cyanide:

N≡C-C≡N + 2Na 2NaCN

or from thiocyanates, heating them in the presence of iron powder.

“I took out a box of potassium cyanide from the supply and put it on the table next to the cakes. Doctor Lazavert put on latex gloves, took several crystals of poison from it and ground it into powder. Then he removed the top of the cakes and sprinkled the filling with enough powder, he said, to kill an elephant. There was silence in the room. We watched his actions excitedly. All that remains is to put the poison in the glasses. We decided to put it in at the last moment so that the poison would not evaporate...”

This is not an excerpt from a detective novel, and the words do not belong to a fictional character. Here are the memories of Prince Felix Yusupov about the preparation of one of the most famous Russian history crimes - the murder of Grigory Rasputin. It happened in 1916. If until the middle of the 19th century arsenic was the main assistant of poisoners, then after the introduction of the Marsh method into forensic practice (see the article “Mouse, Arsenic and Kale the Detective”, “Chemistry and Life”, No. 2, 2011) arsenic was used less and less. But potassium cyanide, or potassium cyanide (potassium cyanide, as it was called before), began to be used more and more often.

What it is...

Potassium cyanide is a salt of hydrocyanic acid, or hydrocyanic acid, Н–СN; its composition is reflected by the formula KCN. Hydrocyanic acid in the form aqueous solution was first obtained by the Swedish chemist Carl Wilhelm Scheele in 1782 from the yellow blood salt K4. The reader already knows that Scheele developed the first method for the qualitative determination of arsenic (see “Mouse, Arsenic and Kale the Detective”). He opened chemical elements chlorine, manganese, oxygen, molybdenum and tungsten, received arsenic acid and arsine, barium oxide and other inorganic substances. Over half of those known in the 18th century organic compounds also isolated and described by Karl Scheele.

Anhydrous hydrocyanic acid was obtained in 1811 by Joseph Louis Gay-Lussac. He also established its composition. Hydrogen cyanide is a colorless volatile liquid that boils at 26°C. The root “cyan” in its name (from the Greek - azure) and the root of the Russian name “cyanic acid” are similar in meaning. This is no coincidence. CN – ions form blue compounds with iron ions, including the composition KFe. This substance is used as a pigment in gouache, watercolor and other paints under the names “Prussian blue”, “milori”, “Prussian blue”. You may be familiar with these paints from gouache or watercolor sets.

Detective authors unanimously claim that hydrocyanic acid and its salts have “the smell of bitter almonds.” Of course, they did not sniff hydrocyanic acid (neither did the author of this article). Information about the “smell of bitter almonds” was gleaned from reference books and encyclopedias. There are other opinions. The author of “Chemistry and Life” A. Kleshchenko, who graduated from the Faculty of Chemistry of Moscow State University and is familiar with hydrocyanic acid first-hand, in the article “How to poison a hero” (“Chemistry and Life”, 1999, No. 2) writes that the smell of hydrocyanic acid is not similar to almond.

Crime writers have fallen victim to a long-standing misconception. But on the other hand, the directory “Harmful Chemicals” was also compiled by specialists. One could, after all, get prussic acid and smell it. But something is scary!

It remains to be assumed that the perception of odors is an individual matter. And what reminds one of the smell of almonds has nothing in common with almonds for another. This idea is confirmed by Peter MacInnis in the book “Silent Killers. World History of Poisons and Poisoning”: “Detective novels always mention the aroma of bitter almonds, which is associated with sodium cyanide, potassium cyanide and hydrogen cyanide (hydrogen cyanide), but only 40–60 percent ordinary people are able to at least smell this specific smell.” Moreover, the resident middle zone Russia, as a rule, is not familiar with bitter almonds: its seeds, unlike sweet almonds, are not eaten or sold.

...and why do they eat it?

We'll get back to almonds and their smell later. And now - oh potassium cyanide. In 1845, the German chemist Robert Bunsen, one of the authors of the spectral analysis method, obtained potassium cyanide and developed a method for its industrial production. If today this substance is in chemical laboratories and in production under strict control, then at the turn of the 19th and 20th centuries, potassium cyanide was available to anyone (including attackers). Thus, in Agatha Christie’s story “The Hornet’s Nest,” potassium cyanide was bought at a pharmacy supposedly to kill wasps. The crime was foiled only thanks to the intervention of Hercule Poirot.

Entomologists used (and still use) small amounts of potassium cyanide in insect stains. Several poison crystals are placed at the bottom of the stain and filled with plaster. Cyanide reacts slowly with carbon dioxide and water vapor, releasing hydrogen cyanide. The insects inhale the poison and die. The stain filled in this way lasts for more than a year. Nobel laureate Linus Pauling told how he was supplied with potassium cyanide for making stains by the caretaker of a dental college. He also taught the boy how to handle this dangerous substance. This was in 1912. As we can see, in those years the storage of the “king of poisons” was treated quite frivolously.

Why does potassium cyanide become so popular among real and fictional criminals? The reasons are not difficult to understand: the substance is highly soluble in water, does not have a pronounced taste, the lethal (fatal) dose is small - on average 0.12 g is enough, although individual susceptibility to the poison, of course, varies. A high dose of potassium cyanide causes almost instantaneous loss of consciousness, followed by respiratory paralysis. Add to this the availability of the substance at the beginning of the 19th century, and the choice of Rasputin’s murderous conspirators becomes clear.

Hydrocyanic acid is just as poisonous as cyanides, but is inconvenient to use: it has a specific odor (it is very weak in cyanides) and cannot be used unnoticed by the victim; moreover, due to its high volatility, it is dangerous for everyone around, not just for the one for whom it is intended. But it also found use as a poisonous substance. During the First World War, hydrocyanic acid was used by the French army. In some US states it was used to execute criminals in “gas rooms”. It is also used to treat carriages, barns, and ships infested with insects - the principle is the same as that of young Pauling’s stain.

How does it work?

It’s time to figure out how such a simple substance acts on the body. Back in the 60s of the 19th century, it was established that the venous blood of animals poisoned with cyanide has a scarlet color. This is characteristic, if you remember, of arterial blood rich in oxygen. This means that an organism poisoned by cyanide is unable to absorb oxygen. Hydrocyanic acid and cyanide somehow inhibit the process of tissue oxidation. Oxyhemoglobin (a combination of hemoglobin with oxygen) circulates throughout the body in vain, without giving oxygen to the tissues.

The reason for this phenomenon was discovered by the German biochemist Otto Warburg in the late 20s of the twentieth century. During tissue respiration, oxygen must accept electrons from the substance undergoing oxidation. Enzymes are involved in the process of electron transfer. common name"cytochromes". These are protein molecules containing a non-protein hemin fragment associated with an iron ion. The cytochrome containing the Fe 3+ ion accepts an electron from the substance being oxidized and turns into the Fe 2+ ion. This, in turn, transfers an electron to the next cytochrome molecule, oxidizing to Fe 3+. Thus, the electron is transferred along the chain of cytochromes, like a ball that “a chain of basketball players passes from one player to another, inexorably bringing him closer to the basket (oxygen).” This is how English biochemist Stephen Rose described the work of tissue oxidation enzymes. The last player in the chain, the one who throws the ball into the oxygen basket, is called cytochrome oxidase. In oxidized form it contains the Fe 3+ ion. This form of cytochrome oxidase serves as a target for cyanide ions, which can form covalent bonds with metal cations and prefer Fe 3+.

By binding cytochrome oxidase, cyanide ions remove the molecules of this enzyme from the oxidative chain, and the transfer of electrons to oxygen is disrupted, that is, oxygen is not absorbed by the cell. Was discovered interesting fact: hedgehogs located in hibernation, are able to tolerate doses of cyanide many times greater than lethal. And the reason is that at low temperatures the absorption of oxygen by the body slows down, like everything else. chemical processes. Therefore, a decrease in the amount of enzyme is easier to tolerate.

Readers of detective stories sometimes get the idea that potassium cyanide is the most poisonous substance on Earth. Not at all! Nicotine and strychnine (substances of plant origin) are tens of times more toxic. The degree of toxicity can be judged by the mass of toxin per 1 kg of laboratory animal weight, which is required to cause death in 50% of cases (LD 50). For potassium cyanide it is 10 mg/kg, and for nicotine - 0.3. Next come: dioxin, a poison of artificial origin - 0.022 mg/kg; tetrodotoxin secreted by puffer fish - 0.01 mg/kg; batrachotoxin secreted by the Colombian tree frog - 0.002 mg/kg; ricin contained in castor bean seeds - 0.0001 mg/kg (a clandestine terrorist laboratory for the production of ricin was uncovered by British intelligence services in 2003); β-bungarotoxin, venom of the South Asian bungaros snake, - 0.000019 mg/kg; tetanus toxin - 0.000001 mg/kg.

The most toxic is botulinum toxin (0.0000003 mg/kg), which is produced by bacteria certain type, developing in anaerobic conditions(without air access) in canned food or sausage. Of course, they have to get there first. And from time to time they get there, especially in home-made canned goods. Homemade sausage is now rare, but at one time it was often the source of botulism. Even the name of the disease and its causative agent comes from the Latin botulus- "sausage". During its life, the botulinum bacillus releases not only toxin, but also gaseous substances. Therefore, swollen cans should not be opened.

Botulinum toxin is a neurotoxin. It disrupts the functioning of nerve cells that transmit impulses to the muscles. The muscles stop contracting and paralysis occurs. But if you take a toxin in low concentration and target certain muscles, the body as a whole will not be harmed, but the muscle will be relaxed. The drug is called “Botox” (botulinum toxin), it is both a medicine for muscle spasms and a cosmetic product for smoothing wrinkles.

As we see, the most poisonous substances in the world were created by nature. Extracting them is much more difficult than obtaining the simple compound KCN. It is clear that potassium cyanide is both cheaper and more accessible.

However, the use of potassium cyanide for criminal purposes does not always give a guaranteed result. Let's see what Felix Yusupov writes about the events that took place in the basement on the Moika on a cold December night in 1916:

“...I offered him eclairs with potassium cyanide. He refused at first.

“I don’t want it,” he said, “it’s too sweet.”

However, he took one, then another. I looked in horror. The poison should have taken effect immediately, but, to my amazement, Rasputin continued to talk as if nothing had happened. Then I offered him our homemade Crimean wines...

I stood next to him and watched his every move, expecting that he was about to collapse...

But he drank, smacked, savored the wine like real experts. Nothing changed in his face. At times he raised his hand to his throat, as if he had a spasm in his throat. Suddenly he stood up and took a few steps. When I asked what was wrong with him, he replied:

Nothing. Tickling in the throat.

The poison, however, had no effect. The “old man” calmly walked around the room. I took another glass of poison, poured it and gave it to him.

He drank it. No impression. The last, third glass remained on the tray.

In desperation, I poured it for myself, so as not to let Rasputin go away from the wine...”

All in vain. Felix Yusupov went up to his office. “...Dmitry, Sukhotin and Purishkevich, as soon as I entered, rushed towards me with questions:

Well? Ready? Is it over?

The poison didn’t work,” I said. Everyone fell silent in shock.

Can't be! - Dmitry cried.

Elephant dose! Did he swallow everything? - asked the others.

That’s it, I said.”

But still, potassium cyanide had some effect on the old man’s body: “He hung his head, breathed intermittently...

Are you feeling unwell? - I asked.

Yes, my head is heavy and my stomach burns. Come on, pour a little. Maybe he’ll feel better.”

Indeed, if the dose of cyanide is not so large as to cause instant death, at the initial stage of poisoning, scratching in the throat, bitter taste in the mouth, numbness of the mouth and pharynx, redness of the eyes, muscle weakness, dizziness, staggering, headache, palpitations, nausea, vomiting. Breathing is somewhat rapid, then becomes deeper. Yusupov noticed some of these symptoms in Rasputin. If at this stage of poisoning the flow of poison into the body stops, the symptoms disappear. Obviously, the poison was not enough for Rasputin. It is worth understanding the reasons, because the organizers of the crime calculated the “elephant” dose. By the way, about elephants. Valentin Kataev in his book “Broken Life, or Oberon’s Magic Horn” describes the case of an elephant and potassium cyanide.

In pre-revolutionary times, in the Odessa circus-tent of Lorberbaum, the elephant Yambo fell into a rage. The behavior of the enraged elephant became dangerous, and they decided to poison it. What do you think? “They decided to poison him with potassium cyanide, put in cakes, which Yambo was a big fan of,” writes Kataev. And further: “I didn’t see this, but I vividly imagined how a cab driver drives up to Lorberbaum’s booth and how attendants bring cakes into the booth, and there is a special medical commission there... with the greatest precautions, wearing black gutta-percha gloves, they stuff the cakes with tweezers crystals of potassium cyanide..." Isn't it very reminiscent of the manipulations of Dr. Lazovert? It should only be added that a high school boy paints an imaginary picture for himself. It is no coincidence that this boy later became a famous writer!

But let's return to Yambo:

“Oh, how vividly my imagination painted this picture... I moaned half asleep... Nausea rose to my heart. I felt poisoned by potassium cyanide... I felt like I was dying... I got out of bed and the first thing I did was grab the Odessa Leaflet, confident that I would read about the death of an elephant. Nothing like this!

The elephant that ate cakes filled with potassium cyanide turns out to be still very much alive and, apparently, is not going to die. The poison had no effect on him. The elephant only became even more violent.”

You can read about further events that happened with the elephant and with Rasputin in books. And we are interested in the reasons for the “inexplicable nonsense,” as Odessa Leaflet wrote about the case of the elephant. There are two such reasons.

First, HCN is a very weak acid. Such an acid can be displaced from its salt by a stronger acid and evaporate. Even carbonic acid is stronger than hydrocyanic acid. Carbonic acid is formed when carbon dioxide is dissolved in water. That is, under the influence of moist air containing both water and carbon dioxide, potassium cyanide gradually turns into carbonate:

KCN + H 2 O + CO 2 = HCN + KHCO 3

If the potassium cyanide used in the cases described was kept in contact with moist air for a long time, it might not work.

Secondly, the salt of weak hydrocyanic acid is subject to hydrolysis:

KCN + H 2 O = HCN + KOH.

The released hydrogen cyanide is able to attach to a molecule of glucose and other sugars containing a carbonyl group:

CH 2 OH-CHON-CHON-CHON-CHON-CH=O + HC≡N →
CH 2 OH-CHON-CHON-CHON-CHON-CHON-C≡N

Substances formed as a result of the addition of hydrogen cyanide to the carbonyl group are called cyanohydrins. Glucose is a product of the hydrolysis of sucrose. People who work with cyanide know that to prevent poisoning they should hold a piece of sugar against their cheek. Glucose binds cyanide in the blood. That part of the poison that has already penetrated into the cell nucleus, where tissue oxidation occurs in the mitochondria, is inaccessible to sugars. If an animal has high blood glucose levels, it is more resistant to cyanide poisoning, such as birds. The same is observed in patients with diabetes. When small portions of cyanide enter the body, the body can neutralize it on its own with the help of glucose contained in the blood. And in case of poisoning, 5% or 40% glucose solutions administered intravenously are used as an antidote. But this remedy works slowly.

For both Rasputin and the elephant Yambo, cakes containing sugar were stuffed with potassium cyanide. They were not eaten immediately, but in the meantime, potassium cyanide released hydrocyanic acid, and it joined the glucose. Some of the cyanide had definitely managed to be neutralized. Let us add that cyanide poisoning occurs more slowly on a full stomach.

There are other antidotes to cyanide. Firstly, these are compounds that easily split off sulfur. The body contains such substances as the amino acids cysteine and glutathione. They, like glucose, help the body cope with small doses of cyanide. If the dose is large, a 30% solution of sodium thiosulfate Na 2 S 2 O 3 (or Na 2 SO 3 S) can be specially injected into the blood or muscle. It reacts in the presence of oxygen and the enzyme rhodanase with hydrocyanic acid and cyanides according to the following scheme:

2HCN + 2Na2S2O3 + O2 = 2НNCS + 2Na2SO4

In this case, thiocyanates (rhodanides) are formed, which are much less harmful to the body than cyanides. If cyanides and hydrocyanic acid belong to the first class of danger, then thiocyanates are substances of the second class. They negatively affect the liver, kidneys, cause gastritis, and also depress thyroid gland. People who are systematically exposed to small doses of cyanide develop thyroid diseases caused by continuous education thiocyanates from cyanides. Thiosulfate reacts with cyanides more actively than glucose, but also acts slowly. It is usually used in combination with other anticyanides.

The second type of antidotes against cyanide are the so-called methemoglobin formers. The name suggests that these substances form methemoglobin from hemoglobin (see “Chemistry and Life”, 2010, No. 10). The hemoglobin molecule contains four Fe 2+ ions, and in methemoglobin they are oxidized to Fe 3+. Therefore, it is not able to reversibly bind Fe 3+ oxygen and does not transport it throughout the body. This can occur under the influence of oxidizing substances (including nitrogen oxides, nitrates and nitrites, nitroglycerin and many others). It is clear that these are poisons that “disable” hemoglobin and cause hypoxia (oxygen deficiency). Hemoglobin “spoiled” by these poisons does not carry oxygen, but is capable of binding cyanide ions, which experience an irresistible attraction to the Fe 3+ ion. Cyanide that enters the blood is bound by methemoglobin and does not have time to enter the mitochondria of cell nuclei, where it will inevitably “spoil” all cytochrome oxidase. And this is much worse than “spoiled” hemoglobin.

American writer, biochemist and popularizer of science Isaac Asimov explains it this way: “The fact is that the body has very a large number of hemoglobin... Hemin enzymes are present in very small quantities. Just a few drops of cyanide are enough to destroy most of these enzymes. If this happens, the conveyor belt that oxidizes the body's flammable substances stops. Within a few minutes, the cells of the body die from lack of oxygen as inevitably as if someone grabbed a person by the throat and simply strangled him.”

In this case, we observe an instructive picture: some poisons that cause hemic (blood) hypoxia inhibit the action of other poisons that also cause hypoxia, but of a different type. A direct illustration of the Russian idiomatic expression: “knock out a wedge with a wedge.” The main thing is not to overdo it with the methemoglobin-forming agent, so as not to exchange the awl for soap. The content of methemoglobin in the blood should not exceed 25–30% of the total hemoglobin mass. Unlike glucose or thiosulfate, methemoglobin not only binds cyanide ions circulating in the blood, but also helps the respiratory enzyme “spoiled” by cyanide to free itself from cyanide ions. This occurs due to the fact that the process of combining cyanide ions with cytochrome oxidase is reversible. Under the influence of methemoglobin, the concentration of these ions in the blood plasma decreases - and as a result, new cyanide ions are split off from the complex compound with cytochrome oxidase.

The reaction of cyanmethemoglobin formation is also reversible, so over time, cyanide ions return to the blood. To bind them, a thiosulfate solution is injected into the blood simultaneously with an antidote (usually nitrite). The most effective is a mixture of sodium nitrite and sodium thiosulfate. She can help even late stages cyanide poisoning - convulsive and paralytic.

Where can I meet him?

Does an ordinary person, not the hero of a detective novel, have a chance to be poisoned by potassium cyanide or hydrocyanic acid? Like any substances of the first class of danger, cyanides are stored with special precautions and are inaccessible to the average attacker, unless he is an employee of a specialized laboratory or workshop. Yes, and there such substances are strictly registered. However, cyanide poisoning can occur without the involvement of a villain.

First, cyanide occurs naturally. Cyanide ions are part of vitamin B 12 (cyanocobolamine). Even in the blood plasma of a healthy person there are 140 mcg of cyanide ions per 1 liter. In blood smoking people the cyanide content is more than twice as high. But the body tolerates such concentrations painlessly. It’s another matter if cyanide contained in some plants comes in with food. Serious poisoning is possible here. Among the sources of hydrocyanic acid available to everyone are the seeds of apricots, peaches, cherries, and bitter almonds. They contain the glycoside amygdalin.

Amygdalin belongs to the group of cyanogenic glycosides that form hydrocyanic acid upon hydrolysis. This glycoside was isolated from the seeds of bitter almonds, which is why it got its name (Greek μ - “almond”). The amygdalin molecule, as befits a glycoside, consists of a sugary part, or glycone (in this case, it is a gencibiose disaccharide residue), and a non-sugary part, or aglycone. In the gencibiose residue, in turn, two β-glucose residues are linked by a glycosidic bond. The role of the aglycone is the cyanohydrin of benzaldehyde - mandelonitrile, or rather its residue connected to the glycone by a glycosidic bond.

During hydrolysis, the amygdalin molecule breaks down into two glucose molecules, a benzaldehyde molecule and a hydrocyanic acid molecule. This occurs in an acidic environment or under the action of the emulsin enzyme contained in the stone. Due to the formation of hydrocyanic acid, one gram of amygdalin - lethal dose. This corresponds to 100 g of apricot kernels. There are known cases of poisoning of children who ate 10–12 apricot kernels.

The content of amygdalin in bitter almonds is three to five times higher, but you hardly want to eat its seeds. As a last resort, they should be heated. This will destroy the emulsin enzyme, without which hydrolysis will not proceed. It is thanks to amygdalin that bitter almond seeds have their bitter taste and almond smell. More precisely, it is not amygdalin itself that has an almond smell, but the products of its hydrolysis - benzaldehyde and hydrocyanic acid (we have already discussed the smell of hydrocyanic acid, but the smell of benzaldehyde is, without a doubt, almond).

Secondly, cyanide poisoning can occur in industries where cyanide is used to create plating or to extract precious metals from ores. Gold and platinum ions form strong complex compounds with cyanide ions. Noble metals are not able to be oxidized by oxygen because their oxides are fragile. But if oxygen acts on these metals in a solution of sodium or potassium cyanide, then the metal ions formed during oxidation are bound by cyanide ions into a strong complex ion and the metal is completely oxidized. Sodium cyanide itself does not oxidize noble metals, but helps the oxidizer to fulfill its mission:

4Au + 8NaCN + 2H 2 O = 4Na + 4NaOH.

Workers engaged in such industries experience chronic exposure to cyanide. Cyanides are poisonous both if they enter the stomach, and if they inhale dust and splashes when servicing galvanic baths, and even if they come into contact with the skin, especially if there are wounds on it. No wonder Doctor Lazovert wore rubber gloves. There was a case of fatal poisoning from a hot mixture containing 80% which got on the worker’s skin.

Even people not employed in mining or plating production can be harmed by cyanide. There are known cases where wastewater from such industries ended up in rivers. In 2000, 2001 and 2004, Europe was alarmed by the release of cyanide into the Danube in Romania and Hungary. This led to dire consequences for river inhabitants and residents of coastal villages. There have been cases of poisoning from fish caught in the Danube. Therefore, it is useful to know the precautions when handling cyanide. And it will be more interesting to read about potassium cyanide in detective stories.

Bibliography:
Azimov A. Chemical agents of life. M.: Foreign Literature Publishing House, 1958.
Harmful chemicals. Directory. L.: Chemistry, 1988.
Kataev V. Broken Life, or Oberon's Magic Horn. M.: Soviet writer, 1983.
Oxengendler G.I. Poisons and antidotes. L.: Nauka, 1982.
Rose S. Chemistry of life. M.: Mir, 1969.
Encyclopedia for children "Avanta+". T.17. Chemistry. M.: Avanta+, 2001.
Yusupov F. Memoirs. M.: Zakharov, 2004.

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