Mechanism of action of antidotes. Classification of poisoning. Detoxification methods. Antidotes (question for independent study). What is the specificity of antidote therapy? What are the antidotes? Introduction of new antidotes into practice

Antidotes are medicines or special compounds, the use of which in the prevention and treatment of poisoning is due to their specific antitoxic effect.

The use of antidotes underlies preventive or therapeutic measures to neutralize the toxic effects of chemicals. Since many chemicals have multiple mechanisms of toxic action, in some cases it is necessary to simultaneously administer various antidotes and at the same time use therapeutic agents that eliminate not the causes, but only individual symptoms of poisoning. Moreover, since the underlying mechanisms of action of most chemical compounds are not well understood, treatment of poisoning is often limited to symptomatic therapy. The experience gained in clinical toxicology shows that some drugs, in particular vitamins and hormones, can be classified as universal antidotes due to the positive preventive and therapeutic effect that they have in various poisonings. This is explained by the fact that poisoning is based on common pathogenetic mechanisms. There is still no generally accepted classification of antidotes. The most rational classification system is based on the reduction of antidotes into main groups depending on the mechanism of their antitoxic action - physical, chemical, biochemical or physiological. Based on the conditions under which antidotes react with poison, a distinction is made between local antidotes, which react with the poison before it is absorbed by the tissues of the body, and resorptive antidotes, which react with the poison after it enters the tissues and physiological fluids.

It should be noted that antidotes of physical action are used exclusively for the prevention of intoxication, and antidotes of resorptive action are used both for the prevention and treatment of poisoning.

2.6.1. Physical antidotes

These antidotes have a protective effect mainly due to the adsorption of the poison. Due to their high surface activity, adsorbents bind solid molecules and prevent their absorption by the surrounding tissue. However, molecules of the adsorbed poison may later separate from the adsorbent and return to the stomach tissue. This separation phenomenon is called desorption. Therefore, when using physical antidotes, it is extremely important to combine them with measures aimed at the subsequent removal of the adsorbent from the body. This can be achieved by gastric lavage or the use of laxatives if the adsorbent has already entered the intestines. Preference here should be given to saline laxatives (for example, sodium sulfate), which are hypertonic solutions that stimulate the flow of fluid into the intestines, which practically eliminates the absorption of solid matter by tissues. Fat laxatives (such as castor oil) can promote the absorption of fat-soluble chemicals, resulting in an increased amount of poison absorbed into the body. In cases where the exact nature of the chemical is unknown, the use of saline laxatives is recommended. The most typical antidotes in this group are activated carbon and kaolin. They have a great effect in acute poisoning with alkaloids (organic substances of plant origin, for example, atropine) or salts of heavy metals.

2.6.2. Chemical antidotes

The mechanism of their action involves a direct reactionbetween poison and antidote. Chemical antidotes can be either local or resorptive.

Local action. If physical antidotes have a low-specific antidote effect, then chemical ones have a fairly high specificity, which is due to the very nature of the chemical reaction. The local action of chemical antidotes is achieved as a result of neutralization reactions, the formation of insoluble compounds, oxidation, reduction, competitive substitution and complex formation. The first three mechanisms of action are of particular importance and are better studied than others.

A good example of neutralizing poisons is the use of alkalis to counteract strong acids accidentally ingested or on the skin. Neutralizing antidotes are also used to carry out reactions that result in the formation of compounds with low biological activity. For example, if strong acids enter the body, it is recommended to rinse the stomach with warm water to which magnesium oxide (20 g/l) has been added. In case of poisoning with hydrofluoric or citric acid, the patient is given a pasty mixture of calcium chloride and magnesium oxide to swallow. In case of contact with caustic alkalis, gastric lavage should be performed with a 1% solution of citric or acetic acid. In all cases of exposure to caustic alkalis and concentrated acids, it should be borne in mind that emetics are contraindicated. Vomiting causes sudden contractions of the stomach muscles, and since these corrosive fluids can attack the stomach tissue, there is a risk of perforation.

Antidotes, which form insoluble compounds that cannot penetrate mucous membranes or skin, have a selective effect, that is, they are effective only in cases of poisoning by certain chemicals. A classic example of this type of antidotes is 2,3-dimercaptopropanol, which forms insoluble, chemically inert metal sulfides. It gives a positive effect in cases of poisoning with zinc, copper, cadmium, mercury, antimony, and arsenic.

Tannin (tannic acid) forms insoluble compounds with salts of alkaloids and heavy metals. The toxicologist must remember that tannin compounds with morphine, cocaine, atropine or nicotine have varying degrees of stability.

After taking any antidotes of this group, it is necessary to perform gastric lavage to remove the formed chemical complexes.

Of great interest are antidotes with combined action, in particular a composition that includes 50 g of tannin, 50 g of activated carbon and 25 g of magnesium oxide. This composition combines antidotes of both physical and chemical action.

In recent years, the topical use of sodium thiosulfate has attracted attention. It is used in cases of poisoning by arsenic, mercury, lead, hydrogen cyanide, bromine and iodine salts.

Sodium thiosulfate is used orally in the form of a 10% solution (2-3 tablespoons).

Local use of antidotes for the above poisonings should be combined with subcutaneous, intramuscular or intravenous injections.

In cases of ingestion of opium, morphine, aconite or phosphorus, oxidation of the solid substance is widely used. The most common antidote for these cases is potassium permanganate, which is used for gastric lavage in the form of a 0.02–0.1% solution. This drug has no effect in case of poisoning with cocaine, atropine and barbiturates.

Resorptive action. Resorptive antidotes of chemical action can be divided into two main subgroups:

antidotes that interact with certain intermediate products formed as a result of the reaction between the poison and the substrate;

b) antidotes that directly interfere with the reaction between the poison and certain biological systems or structures. In this case, the chemical mechanism is often associated with the biochemical mechanism of antidote action.

Antidotes of the first subgroup are used in case of cyanide poisoning. To date, there is no antidote that would inhibit the interaction between cyanide and the enzyme system affected by it. After absorption into the blood, cyanide is transported by the bloodstream to the tissues, where it interacts with the ferric iron of oxidized cytochrome oxidase, one of the enzymes necessary for tissue respiration. As a result, oxygen entering the body stops reacting with the enzyme system, which causes acute oxygen starvation. However, the complex formed by cyanide with iron of cytochrome oxidase is unstable and easily dissociates.

Consequently, treatment with antidotes proceeds in three main directions:

1) neutralization of poison in the bloodstream immediately after it enters the body;

2) fixation of poison in the bloodstream in order to limit the amount of poison entering the tissues;

3) neutralization of the poison entering the blood after the dissociation of cyanomethemoglobin and the complex of cyanide and substrate.

Direct neutralization of cyanide can be achieved by introducing glucose, which reacts with hydrocyanic acid, resulting in the formation of slightly toxic cyanohydride. A more active antidote is ß-hydroxyethylmethylenediamine. Both antidotes should be administered intravenously within a few minutes or seconds after the poison enters the body.

The more common method is one in which the task is to fix the poison circulating in the bloodstream. Cyanides do not interact with hemoglobin, but actively combine with methemoglobin, forming cyanomethemoglobin. Although it is not highly stable, it can persist for some time. Therefore, in this case, it is necessary to introduce antidotes that promote the formation of methemoglobin. This is done by inhaling amyl nitrite vapor or intravenous injection of sodium nitrite solution. As a result, free cyanide present in the blood plasma binds to a complex with methemoglobin, losing much of its toxicity.

It must be borne in mind that antidotes that form methemoglobin can affect blood pressure: if amyl nitrite causes a pronounced, short-term drop in pressure, then sodium nitrite has a prolonged hypotonic effect. When administering substances that form methemoglobin, it should be taken into account that it not only takes part in the transfer of oxygen, but can itself cause oxygen starvation. Therefore, the use of methemoglobin-forming antidotes must follow certain rules.

The third method of antidote treatment is to neutralize cyanide released from complexes with methemoglobin and cytochrome oxidase. For this purpose, sodium thiosulfate is injected intravenously, which converts cyanides into non-toxic thiocyanates.

The specificity of chemical antidotes is limited because they do not interfere with the direct interaction between the venom and the substrate. However, the effect that such antidotes have on certain parts of the mechanism of toxic action has an undoubted therapeutic significance, although the use of these antidotes requires high medical qualifications and extreme caution.

Chemical antidotes that directly interact with a toxic substance are highly specific, allowing them to bind toxic compounds and remove them from the body.

Complexing antidotes form stable compounds with di- and trivalent metals, which are then easily excreted in the urine.

In cases of poisoning with lead, cobalt, copper, vanadium, disodium calcium salt of ethylenediaminetetraacetic acid (EDTA) has a great effect. The calcium contained in the antidote molecule reacts only with metals that form a more stable complex. This salt does not react with ions of barium, strontium and some other metals with a lower stability constant. There are several metals with which this antidote forms toxic complexes, so it should be used with great caution; in case of poisoning with cadmium, mercury and selenium, the use of this antidote is contraindicated.

For acute and chronic poisoning with plutonium and radioactive iodine, cesium, zinc, uranium and lead, pentamil is used. This drug is also used in cases of cadmium and iron poisoning. Its use is contraindicated for persons suffering from nephritis and cardiovascular diseases. Complexing compounds in general also include antidotes whose molecules contain free mercapto groups - SH. Of great interest in this regard are dimercaptoprome (BAL) and 2,3-dimercaptopropane sulfate (unithiol). The molecular structure of these antidotes is comparatively simple:

H 2 C – SH H 2 C – SH | |

HC – SH HC – SH

H 2 C – OH H 2 C – SO 3 Na

BAL Unithiol

Both of these antidotes have two SH groups that are close to each other. The significance of this structure is revealed in the example below, where antidotes containing SH groups react with metals and non-metals. The reaction of dimercapto compounds with metals can be described as follows:

Enzyme + Me → Me enzyme

HSCH 2 S – CH 2

HSCH + enzyme Me → enzyme + Me– S – CH

HOCH 2 OH–CH 2

The following phases can be distinguished here:

A) reaction of enzymatic SH groups and the formation of an unstable complex;

B) reaction of the antidote with the complex;

C) release of the active enzyme due to the formation of a metal-antidote complex, excreted in the urine. Unithiol is less toxic than BAL. Both drugs are used in the treatment of acute and chronic poisoning with arsenic, chromium, bismuth, mercury and some other metals, but not lead. Not recommended for selenium poisoning.

There are no effective antidotes for the treatment of poisoning by nickel, molybdenum and some other metals.

2.6.3. Biochemical antidotes

These drugs have a highly specific antidote effect. Typical for this class are antidotes used in the treatment of poisoning with organophosphorus compounds, which are the main components of insecticides. Even very small doses of organophosphates inhibit the function of cholinesterase as a result of its phosphorylation, which leads to the accumulation of acetylcholine in tissues. Since acetylcholine is of great importance for the transmission of impulses in both the central and peripheral nervous systems, its excessive amount leads to disruption of nerve functions and, consequently, to serious pathological changes.

Antidotes that restore the function of cholinesterase belong to hydroxamic acid derivatives and contain the oxime group R – CH = NOH. The oxime antidotes 2-PAM (pralidoxime), dipyroxime (TMB-4) and isonitrosine are of practical importance. Under favorable conditions, these substances can restore the function of the cholinesterase enzyme, weakening or eliminating the clinical signs of poisoning, preventing long-term consequences and promoting successful recovery.

Practice, however, has shown that the best results are achieved in cases where biochemical antidotes are used in combination with physiological antidotes.

2.6.4. Physiological antidotes

The example of poisoning with organophosphorus compounds shows that suppression of cholinesterase function leads, first of all, to the accumulation of acetylcholine in synapses. There are two possibilities to neutralize the toxic effect of the poison:

A) restoration of cholinesterase function;

B) protection of physiological systems sensitive to acetylcholine from the excessive action of this mediator of nerve impulses, which leads to

Diets initially to acute agitation and then to functional paralysis.

An example of a drug that suppresses sensitivity to acetylcholine is atropine. The class of physiological antidotes includes many drugs. In case of acute central nervous system excitation, which is observed in many poisonings, it is recommended to administer narcotics or anticonvulsants. At the same time, in case of acute suppression of the respiratory center, central nervous system stimulants are used as antidotes. To a first approximation, it can be argued that physiological (or functional) antidotes include all drugs that cause physiological reactions that counteract poison.

Therefore, it is difficult to make a clear distinction between antidotes and drugs used in symptomatic therapy.

Control questions

How are toxic substances classified according to purpose of use?
What types of poisoning do you know?
List the experimental parameters of toxicometry.
Name the derived parameters of toxicometry.
What is the essence of the toxicity receptor theory?
In what ways do harmful substances enter the body?
What is the biotransformation of toxic substances?
Ways to remove foreign substances from the body.
What are the features of acute and chronic poisoning?
List the main and additional factors that determine the development of poisoning.
Name the types of combined effects of poisons.
What are antidotes?

^ PART 3. COMPETITION AND PROFESSIONAL

Antidotes are substances that can neutralize or stop the action of poison in the human body. The effectiveness of antidotes depends on how accurately the poison/toxin entering the body was determined and how quickly medical care was provided to the victim.

Types of antidotes

There are several types of substances in question - they are all used for different types of poisoning, but there are also those that belong to the category of universal ones.

Universal antidotes:

Most often, the following antidotes are used for acute poisoning:

Unithiol . It belongs to the universal type of antidotes (antidotes) and does not have high toxicity. Used for poisoning with salts of heavy metals (lead, etc.), in case of overdose of cardiac glycosides, and poisoning with chlorinated hydrocarbons.
Unithiol is administered intramuscularly every 6-8 hours on the first day after poisoning or overdose, on the second day the antidote is administered every 12 hours, in subsequent days - 1 (maximum two) times a day.
EDTA (thetacin calcium) . Used only for poisoning with salts of heavy metals (lead and others). The antidote is capable of forming complexes with metals, which are characterized by easy solubility and low molecularity. It is this ability that allows for the rapid and most complete removal of heavy metal salt compounds from the body through the urinary system.
EDTA is administered simultaneously with glucose intravenously. The average daily dose for an adult is 50 mg/kg.
Oximes (dipyroxime and/or alloxime) . These antidotes are classified as cholinesterase reactivators. The substance is used for poisoning with anticholinesterase poisons, most effectively when used in the first 24 hours.
Nalorphine . Used for poisoning with drugs from the morphine group. When using nalorphine, drug withdrawal syndrome is subsequently observed - the patient is worried about,.
The antidote in question is administered intramuscularly or intravenously every 30 minutes. The total dose of the administered drug should not exceed 0.05 g.
Lipoic acid . It is most often used as an antidote for poisoning with toadstool toxins. The effect of using lipoic acid for mushroom poisoning is only possible if the antidote is administered in the first few hours after poisoning.
This antidote is administered only for symptoms of severe liver damage at a dose of 0.3 grams per day for a maximum of 14 days.
. The drug is an antidote for poisoning with cardiac glycosides, nicotine, dichloroethane, potassium and ergot.
It is administered during the first day after poisoning in an amount of 0.7 grams.
Methylene blue . Used for poisoning with hydrogen sulfide, cyanides, sulfonamides, nitrates, naphthalene.
It is administered intravenously in combination with glucose. If a 1% antidote solution is used, the dosage will be 50-100 ml, in the case of a 25% solution - 50 ml.
Calcium gluconate . This substance is well known to everyone and is often perceived as the simplest and most harmless drug. But in fact, it is calcium gluconate that is most often used as an antidote for stinging insects. If this antidote is inadvertently injected past a vein, necrosis of the subcutaneous fat layer may develop.
Calcium gluconate is administered in an amount of 5-10 ml intravenously, if we are talking about a 10% solution of the drug. It is recommended to repeat the procedure after the first injection after 8-12 hours.
Ethanol . Antidote for poisoning with methyl alcohol and ethylene glycol. As a side effect when used, there is a deterioration in myocardial activity (its contractility decreases).
Apply 100 ml of 30% ethyl alcohol solution orally every 2-4 hours. If methanol is diagnosed in the blood, then an ethyl alcohol solution is administered intravenously in combination with glucose or sodium chloride.
Potassium chloride . Most effective as an antidote for poisoning with cardiac glycosides. As a side effect, irritation of the gastric mucosa and hyperkalemia are noted.
This antidote is administered intravenously in combination with glucose; 50 ml of a 10% potassium chloride solution can be taken orally.
Sodium thiosulfate . An antidote that is used for poisoning with lead, arsenic, hydrocyanic acid, mercury, etc. Side effects when using sodium thiosulfate include nausea, skin rashes of various types and thrombocytopenia.
A 30% solution of the presented antidote, 30-50 ml, is administered intravenously, and 20 minutes after the initial administration, the procedure is repeated, but at half the indicated dose.

Antidotes in folk medicine

Traditional medicine involves the use of medicinal plants for food or chemical poisoning. The following agents are actively used as antidotes:

In addition, traditional medicine actively uses baking soda and table salt for poisoning.

Note:In no case should you trust remedies from the category of traditional medicine, because even the most effective medicinal plants in most cases cannot have the desired effect. Only after consultation with a doctor is it permissible to use some folk remedies.

Any use of antidotes must be agreed with doctors - independent use can lead to a deterioration in the health of the victim. In addition, an incorrectly administered dose of antidote or an incorrect course of treatment can aggravate the situation, leading to death. We should not forget that some antidotes can provoke the development of side effects - they also have a negative effect on the patient’s health.

Tsygankova Yana Aleksandrovna, medical observer, therapist of the highest qualification category

Study questions:

1. The concept of antidotes. Classification.

2. Requirements for therapeutic and prophylactic antidotes. Requirements for first aid antidotes.

3. Features of the prevention and treatment of acute poisoning.

4. Radioprotectors and early treatment of ARS.

5. Radioprotectors (radioprotective agents).

6. Standard radioprotectors and early treatment agents.

7. Promising radioprotectors being developed.

9. Means of preventing and stopping primary radiation.

When using antidotes, it is necessary, on the one hand, to prevent the action of poisons on the body with the help of special chemicals, and on the other hand, to normalize or at least slow down the unfavorable functional changes that develop in various organs and systems.

There is still no single, generally accepted definition of “antidote”. The most acceptable is the following: antidotes (antidotes) are medical agents that can neutralize poison in the body through physical or chemical interaction with it or provide artagonism with poison in action on enzymes and receptors.

To assess the effect of antidote agents, a large number of criteria are used: single and daily dose, duration of action, pharmacological properties, teratogenic, mutagenic, etc. effects. Like any medications, antidotes are characterized by these characteristics. However, taking into account the specifics of their use, other characteristics are usually used, in particular, therapeutic (preventive) effectiveness, duration of action of the antidote, time of its protective action, and protection coefficient.

There are several classifications of antidote agents. The classification of antidotes proposed by S.N. Golikov in 1972 is the one that most satisfies modern requirements.

3. 1. Classification of antidotes:

- local antidotes, neutralizing poison during resorption by body tissues through physical or chemical processes of interaction with it;

- antidotes with general resorptive action, the use of which is based on reactions of chemical antagonism between antidotes and a toxic substance or its metabolites circulating in the blood, lymph, located (deposited) in the tissues of the body;

- competitive antidotes, displacing and binding poison into harmless compounds, as a result of a more pronounced chemical affinity of the antidote with the enzyme, receptors, and structural elements of cells;

- antidotes, physiological antagonists of OM, the effect of which is opposite to the effect of poison on one or another physiological system of the body, make it possible to eliminate the disorders caused by poison and normalize the functional state;

- immunological antidotes, providing for the use of specific vaccines and serums for poisoning.

Basic criteria for assessing the effect of antidotes.

1. Therapeutic (preventive) effectiveness is determined by the number of lethal doses of poison, the signs of poisoning of which can be prevented (for prophylactic antidotes) or eliminated (medical care antidote) under optimal conditions for using the drug (formulation) or in accordance with the adopted regulations.

2. Duration of action of the antidote (applies only to antidotes intended for medical use).

3. The time during which the therapeutic effect of the drug manifests itself in poisoned people (depending on the severity of intoxication).

3. Time of protective action of the antidote. It is determined by the time from the moment of application of the antidote to poisoning, during which clinical signs of intoxication are prevented.

Classification of poisonings by types of toxic agents

Depending on what toxic agent caused the poisoning, there are:

Ø carbon monoxide and lighting monoxide poisoning;

Ø food poisoning;

Ø poisoning with pesticides;

Ø poisoning with acids and alkalis;

Ø poisoning with drugs and alcohol.

The main groups of substances that cause acute poisoning are

Ø medicines;

Ø alcohol and surrogates;

Ø cauterizing liquids;

Ø carbon monoxide.

When characterizing poisonings, existing classifications of poisons are used according to the principle of their action (irritating, cauterizing, hemolytic, etc.).

Depending on the route of entry of poisons into the body, inhalation (through the respiratory tract), oral (through the mouth), percutaneous (through the skin), injection (parenterally administered) and other poisonings are distinguished.

Clinical classification is based on assessing the severity of the patient’s condition (mild, moderate, severe, extremely severe poisoning), which takes into account the conditions of occurrence (domestic, industrial) and the cause of this poisoning. (accidental, suicidal, etc.) is of great importance in forensic medicine.

Classification of poisonings according to the nature of the toxic substance’s effect on the body

Based on the nature of the effect of a toxic substance on the body, the following types of intoxication are distinguished:

Ø Acute intoxication - an athological condition of the body that is the result of a single or short-term exposure; accompanied by pronounced clinical signs

Ø Subacute intoxication - a pathological condition of the body that is the result of several repeated exposures; clinical signs are less pronounced compared to acute intoxication

Ø Hyperacute intoxication - acute intoxication, characterized by damage to the central nervous system, the signs of which are convulsions, loss of coordination; death occurs within a few hours

Ø Chronic intoxication is a pathological condition of the body that is the result of long-term (chronic) exposure; not always accompanied by pronounced clinical signs.

Detoxification is the destruction and neutralization of various toxic substances by chemical, physical or biological methods.

Detoxification is the natural and artificial removal of toxins from the body.

Natural detoxification methods are divided into

Ø Natural: liver cytochrome oxidase system - oxidation, immune system - phagocytosis, binding to blood proteins, excretory - excretion through the liver, kidneys, intestines, skin and lungs.

Ø Stimulated: the use of medication and physiotherapeutic methods that stimulate natural detoxification methods.

Artificial detoxification methods are divided into

Ø Physical-mechanical removal of toxic substances from the body by cleansing the skin, mucous membranes and blood using modern methods:

Ø sorption - hemosorption, enterosorption, lymphosorption, plasma sorption,

Ø filtration techniques - hemodialysis, ultrafiltration, hemofiltration, hemodiafiltration,

Ø apheresis methods - plasmapheresis, cytapheresis, selective elimination (cryosedimentation, heparincryosedimentation).

Ø Chemical - binding, deactivation, neutralization and oxidation (antidotes, sorbents, antioxidants, indirect electrochemical oxidation, quantum hemotherapy).

Ø Biological - administration of vaccines and blood serum.

The use of an antidote allows you to prevent the effects of poison on the body, normalize the basic functions of the body, or slow down the functional or structural disorders that develop during poisoning.

Antidotes are of direct and indirect action.

Direct action antidote.

Direct action - there is a direct chemical or physical-chemical interaction between the poison and the antidote.

The main options are sorbent preparations and chemical reagents.

Sorbent preparations– the protective effect is carried out due to nonspecific fixation (sorption) of molecules on the sorbent. The result is a decrease in the concentration of poison interacting with biological structures, which leads to a weakening of the toxic effect.

Sorption occurs due to nonspecific intermolecular interactions - hydrogen and van der Waals bonds (not covalent!).

Sorption can be carried out from the skin, mucous membranes, from the digestive tract (enterosorption), from the blood (hemosorption, plasma sorption). If the poison has already penetrated the tissue, then the use of sorbents is not effective.

Examples of sorbents: activated carbon, kaolin (white clay), Zn oxide, ion exchange resins.

1 gram of active carbon binds several hundred mg of strychnine.

Chemical antidotes– as a result of the reaction between the poison and the antidote, a non-toxic or low-toxic compound is formed (due to strong covalent ionic or donor-acceptor bonds). They can act anywhere - before the poison penetrates the blood, during the circulation of the poison in the blood and after fixation in the tissues.

Examples of chemical antidotes:

Ø To neutralize acids that have entered the body, salts and oxides are used that give an alkaline reaction in aqueous solutions - K2CO3, NaHCO3, MgO.

Ø in case of poisoning with soluble silver salts (for example AgNO3), NaCl is used, which forms insoluble AgCl with silver salts.

Ø in case of poisoning with poisons containing arsenic, MgO and ferrous sulfate are used, which chemically bind it

Ø in case of poisoning with potassium permanganate KMnO4, which is a strong oxidizing agent, a reducing agent is used - hydrogen peroxide H2O2

Ø in case of alkali poisoning, use weak organic acids (citric, acetic)

Ø poisoning with hydrofluoric acid salts (fluorides) use calcium sulfate CaSO4, the reaction produces slightly soluble CaF2

Ø in case of poisoning with cyanides (salts of hydrocyanic acid HCN), glucose and sodium thiosulfate are used, which bind HCN. Below is the reaction with glucose.

Intoxication with thiol poisons (compounds of mercury, arsenic, cadmium, antimony and other heavy metals) is very dangerous. Such poisons are called thiol based on their mechanism of action - binding to thiol (-SH) groups of proteins:

The resulting poison-antidote complex is removed from the body without causing harm to it.

Another class of direct-acting antidotes is antidotes—complexones (complexing agents). They form strong complex compounds with toxic cations Hg, Co, Cd, Pb. Such complex compounds are excreted from the body without causing harm to it. Among complexones, the most common salts are ethylenediaminetetraacetic acid (EDTA), primarily sodium ethylenediaminetetraacetate.

Indirect antidote.

Indirect antidotes are substances that do not themselves react with poisons, but eliminate or prevent disorders in the body that occur during intoxication (poisoning).

1) Protection of receptors from toxic effects.

Poisoning with muscarine (fly agaric poison) and organophosphorus compounds occurs through the mechanism of blocking the enzyme cholinesterase. This enzyme is responsible for the destruction of acetylcholine, a substance involved in the transmission of nerve impulses from the nerve to the muscle fibers. If the enzyme is blocked, an excess of acetylcholine is created.

Acetylcholine binds to receptors, which signals muscle contraction. When there is an excess of acetylcholine, random muscle contractions occur - cramps, which often lead to death.

The antidote is atropine. Atropine is used in medicine to relax muscles. Anthropine binds to the receptor, i.e. protects it from the action of acetylcholine. In the presence of acetylcholine, the muscles do not contract and cramps do not occur.

2) Restoration or replacement of a biological structure damaged by poison.

In case of fluoride and HF poisoning, and in case of poisoning with oxalic acid H2C2O4, Ca2+ ions bind in the body. The antidote is CaCl2.

3) Antioxidants.

Poisoning with carbon tetrachloride CCl4 leads to the formation of free radicals in the body. Excess free radicals are very dangerous, they cause damage to lipids and disruption of the structure of cell membranes. Antidotes are substances that bind free radicals (antioxidants), such as vitamin E.

4) Competition with poison for binding to the enzyme.

Methanol poisoning:

When poisoning with methanol, very toxic compounds are formed in the body - formaldehyde and formic acid. They are more toxic than methanol itself. This is an example of lethal fusion.

Lethal synthesis is the transformation in the body during metabolism of less toxic compounds into more toxic ones.

Ethyl alcohol C2H5OH binds better to the enzyme alcohol dehydrogenase. This inhibits the conversion of methanol to formaldehyde and formic acid. CH3OH is excreted unchanged. Therefore, taking ethyl alcohol immediately after methanol poisoning significantly reduces the severity of poisoning.

Send your good work in the knowledge base is simple. Use the form below

Students, graduate students, young scientists who use the knowledge base in their studies and work will be very grateful to you.

Antidotes are of direct and indirect action.

Direct antidote

Direct action - there is a direct chemical or physical-chemical interaction between the poison and the antidote.

The main options are sorbent preparations and chemical reagents.

Sorbent preparations - the protective effect is carried out due to nonspecific fixation (sorption) of molecules on the sorbent. The result is a decrease in the concentration of poison interacting with biological structures, which leads to a weakening of the toxic effect.

Sorption occurs due to nonspecific intermolecular interactions - hydrogen and van der Waals bonds (not covalent!).

Examples of sorbents: activated carbon, kaolin (white clay), Zn oxide, ion exchange resins.

1 gram of active carbon binds several hundred mg of strychnine.

Chemical antidotes - as a result of the reaction between the poison and the antidote, a non-toxic or low-toxic compound is formed (due to strong covalent ionic or donor-acceptor bonds). They can act anywhere - before the poison penetrates the blood, during the circulation of the poison in the blood and after fixation in the tissues.

Examples of chemical antidotes:

To neutralize acids that have entered the body, salts and oxides are used that give an alkaline reaction in aqueous solutions - K2CO3, NaHCO3, MgO.

in case of poisoning with soluble silver salts (for example AgNO3), NaCl is used, which forms insoluble AgCl with silver salts.

in case of poisoning with poisons containing arsenic, MgO and ferrous sulfate are used, which chemically bind it

in case of poisoning with potassium permanganate KMnO4, which is a strong oxidizing agent, a reducing agent is used - hydrogen peroxide H2O2

in case of alkali poisoning, use weak organic acids (citric, acetic)

poisoning with hydrofluoric acid salts (fluorides), calcium sulfate CaSO4 is used, the reaction produces slightly soluble CaF2

in case of poisoning with cyanides (salts of hydrocyanic acid HCN), glucose and sodium thiosulfate are used, which bind HCN. Below is the reaction with glucose.

The binding of the metal to the thiol groups of proteins leads to the destruction of the protein structure, which causes the cessation of its functions. The result is a disruption of the functioning of all enzyme systems of the body.

To neutralize thiol poisons, dithiol antidotes (SH-group donors) are used. The mechanism of their action is presented in the diagram.

The resulting poison-antidote complex is removed from the body without causing harm to it.

Another class of direct-acting antidotes is antidotes - complexons (complexing agents).

They form strong complex compounds with toxic cations Hg, Co, Cd, Pb. Such complex compounds are excreted from the body without causing harm to it. Among complexones, the most common salts are ethylenediaminetetraacetic acid (EDTA), primarily sodium ethylenediaminetetraacetate.

Indirect antidote

Indirect antidotes are substances that do not themselves react with poisons, but eliminate or prevent disorders in the body that occur during intoxication (poisoning).

1) Protection of receptors from toxic effects.

Acetylcholine binds to receptors, which signals muscle contraction. With an excess of acetylcholine, random muscle contractions occur - spasms, which often lead to death.

2) Restoration or replacement of a biological structure damaged by poison.

In case of fluoride and HF poisoning, and in case of poisoning with oxalic acid H2C2O4, Ca2+ ions bind in the body. The antidote is CaCl2.

3) Antioxidants.

4) Competition with poison for binding to the enzyme.

Methanol poisoning:

When poisoning with methanol, very toxic compounds are formed in the body - formaldehyde and formic acid. They are more toxic than methanol itself. This is an example of lethal fusion.

Lethal synthesis is the transformation in the body during metabolism of less toxic compounds into more toxic ones.

1. Carbon monoxide (II) - carbon monoxide (CO)

1.1 Anthropogenic sources of input

Household sources (incomplete combustion of gas in stoves and fuel in stoves);

Fires (danger of CO poisoning; 50% of deaths in fires are CO poisoning);

Chemical industry (production of ammonia, soda, methanol synthesis, production

synthetic fibers, coke);

Metallurgical industry (steel production);

- motor transport(more than half of anthropogenic CO).

a. Mechanism of toxic action.

CO combines with hemoglobin, forming carboxyhemoglobin, the ability of the blood to transport oxygen (O2) is disrupted, and there is a lack of oxygen in the body.

b. Acute poisoning.

When inhaling a concentration of up to 1000 mg/m 3 - heaviness and a feeling of squeezing of the head, severe pain in the forehead and temples, dizziness, tinnitus, redness and burning of the facial skin, trembling, a feeling of weakness and fear, thirst, increased heart rate, a feeling of lack of air , nausea, vomiting. Subsequently, while consciousness is maintained, there is numbness, weakness and indifference, a feeling of pleasant languor, then drowsiness and numbness, vagueness of consciousness increase, and the person loses consciousness. Next - shortness of breath and death from respiratory arrest.

At a concentration of 5,000 mg/m 3 - in 20-30 minutes - weak pulse, slowing and stopping of breathing, death.

At a concentration of 14,000 mg/m 3 - in 1-3 minutes - loss of consciousness, vomiting, death.

c. Chronic poisoning.

Headaches, dizziness, weakness, nausea, emaciation, lack of appetite; with prolonged contact - cardiovascular system disorders, shortness of breath, pain in the heart area.

d. Standards.

MPC (mg/m 3):

MPCr.z. (during the working day) 20.0

60 minutes 50.0

15 minutes 200.0

MPCm.r. 5.0

4th hazard class.

2. Hydrogen cyanide -HCN- hydrocyanic acid

2.1 Anthropogenic sources of input

Chemical and metallurgical industry; combustion of polymers.

Hydrocyanic acid and its salts are present in wastewater from ore processing plants, mines, mines, electroplating shops, and metallurgical plants.

2.2 Toxicity of hydrocyanic acid salts

The toxicity of HCN salts is due to the formation of HCN during their hydrolysis. Hydrogen cyanide causes rapid deterioration due to blocking respiratory enzymes in cells (blocking cytochrome oxidase in mitochondria). Cells cannot consume oxygen and therefore die.

2.3 Acute poisoning

1 mg/m3 - odor.

At high concentrations (more than 10,000 mg/m3) - almost instantaneous loss of consciousness, respiratory and cardiac paralysis.

At lower concentrations, several stages of poisoning occur:

1) Initial stage: scratching in the throat, burning-bitter taste in the mouth, salivation, numbness of the mouth, muscle weakness, dizziness, acute headache, nausea, vomiting.

2) Second stage: general weakness, pain and a feeling of tightness in the heart area, slowing of the pulse, severe shortness of breath, nausea, vomiting (shortness of breath stage) gradually increases.

3) Stage of convulsions: feeling of melancholy, increasing shortness of breath, loss of consciousness, severe convulsions.

4) Stage of paralysis: complete loss of sensitivity and reflexes, involuntary urination and defecation, respiratory arrest, death.

2.4 Chronic poisoning

Headache, weakness, fatigue, increased general malaise, poor coordination of movements, sweating, increased irritability, nausea, pain in the epigastric region, pain in the heart.

2.5 MPC for HCN and its salts (in terms of hydrogen cyanide)

MPCr.z. 0.3 mg/m3

MPCs.s. 0.01 mg/m3

MPCv. (in water sources) 0.1 mg/l

1st class of danger.

3. Nitrogen oxides (NOAndNO2)

3.1 Anthropogenic sources of input

Combustion of fossil fuels;

Transport;

Production of nitric and sulfuric acids;

Bacterial decomposition of silage.

3.2 Toxic effects

NO is a blood poison that prevents the transfer of oxygen by hemoglobin.

NO2 - pronounced irritating and cauterizing effect on the respiratory tract, leading to the development of pulmonary edema; thiol poison, blocks SH groups of proteins.

3.3 Acute poisoning

NO - general weakness, dizziness, numbness of the legs. With more severe poisoning - nausea, vomiting, increased weakness and dizziness, decreased blood pressure. In case of severe poisoning - bluish lips, weak pulse, slight chills. After a few hours - improvement, after 1-3 days - severe weakness, severe headache, numbness of the arms and legs, drowsiness, dizziness.

At 8 mg/m3 - odor and slight irritation.

At 14 mg/m3 - irritation of eyes and nose.

Inhalation for 5 minutes 510-760 mg/m 3 - pneumonia.

950 mg/m3 - pulmonary edema for 5 minutes.

Acute poisoning is characterized by two phases:

First - swelling, then - bronchitis and its consequences.

3.4 Chronic poisoning

NO: dysfunction of the respiratory and circulatory organs;

NO2: inflammation of the mucous membrane of the gums, chronic bronchitis.

3.5 Standards

MPCm.r. 0.4 mg/m 3 MPCmr. 0.085 mg/m3

MPCs.s. 0.06 mg/m3 MPC.s. 0.04 mg/m3

3rd hazard class2nd hazard class

4. Sulfur oxide (IV) - sulphur dioxideSO2

4.1 Anthropogenic sources of input

Combustion of coal and petroleum products:

80% - in industry and everyday life;

19% - metallurgy;

1% - transport.

Min S - natural gas, max S - coal, oil (depending on the grade).

In metallurgy - in the smelting of copper, zinc, lead, nickel; from sulfide ores (pyrites)

4.2 Mechanism of action

It has a multilateral general toxic effect. Disturbs carbohydrate and protein metabolism, inhibits enzymes. Has an irritating effect. Disturbs the function of the liver, gastrointestinal tract, cardiovascular system, kidneys.

4.3 Acute poisoning

In mild cases (concentration ~ 0.001% by volume) - irritation of the upper respiratory tract and eyes. Watery eyes, sneezing, sore throat, cough, hoarseness. For moderate damage: general weakness, dry cough, pain in the nose and throat, nausea, pain in the epigastric region, nosebleeds. In severe cases - acute suffocation, painful cough, pulmonary edema, death.

4.4 Chronic poisoning

Violation of the respiratory, cardiovascular systems and gastrointestinal tract. One of the forms of damage is bronchitis: cough, chest pain, shortness of breath, weakness, fatigue, sweating. Liver damage - toxic hepatitis - heaviness and pain in the right hypochondrium, nausea, bitterness in the mouth. Stomach damage - pain on an empty stomach or after eating, heartburn, nausea, loss of appetite, stomach and duodenal ulcers.

4.5 Standards

MPCr.z. 10 mg/m3

MPCm.r. 0.5 mg/m3

MPCs.s. 0.05 mg/m3

Hazard class 2.

5 . Arsenic (As)

5.1.Anthropogenic sources of pollution

Metallurgy (arsenic is an impurity in many ores): production of Pb, Zn, Ni, Cu, Sn, Mo, W;

Production of sulfuric acid and superphosphate;

Combustion of coal, oil, peat;

Production of arsenic and As-containing pesticides;

Tanneries.

Emissions into the air with smoke and wastewater.

5.2 Toxic effects

Thiol poison has a wide spectrum of action:

Metabolic disease;

Increased permeability of vessel walls, destruction of red blood cells (hemolysis);

Destruction of tissues at the point of direct contact with arsenic;

Carcinogenic effect;

Embryotoxic and teratogenic effect.

5.3 Acute poisoning

In mild cases - general malaise, headache, nausea; then - pain in the right hypochondrium and lower back, nausea, vomiting.

Severe poisoning:

When administered through the mouth - a metallic taste, burning and dry mouth, pain when swallowing several hours after poisoning.

When entering through the respiratory system - irritation of the upper respiratory tract and eyes - tears, sneezing, coughing, hemoptysis, chest pain, swelling of the face and eyelids.

Then - severe weakness, dizziness, headache, nausea, vomiting, abdominal pain, numbness of fingers and toes. Then - uncontrollable vomiting of blood, convulsions, nosebleeds, hemorrhages in various parts of the body.

After 8-15 days - sharp pain in the limbs, severe weakness, drowsiness, severe headaches, convulsions, paralysis, death from respiratory paralysis.

5.4 Chronic poisoning

Increased fatigue, weight loss, nausea, dizziness, pain in the limbs, stomach, intestines, chest, throat, cough, swelling of the face and eyelids. Hair and nail loss, hemorrhage, darkening of the skin. Irritability, vomiting, unstable stool, lack of appetite.

5.5 Standards

Arsenic and its inorganic compounds (in terms of arsenic):

MPCs.s. 0.003 mg/m3

MPCv. (water) 0.05 mg/l

Hazard class 2.

6 . Mercury (Hg)

6.1 Anthropogenic sources of input

Obtaining mercury and mercury-containing substances;

Combustion of fossil fuels;

Non-ferrous metallurgy;

Coking of coal;

Production of chlorine and soda;

Burning garbage.

Intake: in the form of vapors, water solubility of salts and organic compounds.

6.2. Toxic effect

Thiol poison has a wide spectrum of action.

The manifestation of the toxic effect depends on the form in which mercury enters the body.

The peculiarity of mercury vapor is its neutrotoxicity, its effect on higher nervous activity.

6.3. Acute poisoning

Mercury vapor:

Symptoms appear 8-24 hours after poisoning.

General weakness, headache, pain when swallowing, fever, bleeding, inflammation in the mouth, abdominal pain, stomach damage (nausea, vomiting, loose stools), kidney damage.

6.4 Chronic poisoning

Mainly - the effect on the central nervous system.

Decreased performance, fatigue, increased excitability. Weakened memory, anxiety, self-doubt, irritability, headaches.

Further - weakness, drowsiness, apathy, emotional instability, trembling of the hands, tongue, eyelids (in severe cases of the whole body). Increased mental excitability, fearfulness, general depression, stubbornness and irritability, weakened memory, neuralgia.

6.5. Standards

Metallic mercury (vapor):

MPCr.z. 0.01 mg/m3

MPCs.s. 0.0003 mg/m3

1st class of danger.

7 . Lead (Pb)

7.1 Anthropogenic sources of input

Lead and lead-zinc plants (non-ferrous metallurgy);

Car exhaust gases (tetraethyl lead is added to increase the octane number);

Wastewater from the following industries: metalworking, engineering,

petrochemical, match, photographic materials;

Burning coal and household waste.

7.2 Toxic effects

Thiol poison, but less toxic than mercury and arsenic.

Affects the central nervous system, peripheral nervous system, bone marrow, blood, blood vessels, genetic apparatus, cells.

7.3 Acute poisoning

Acute (lead salt poisoning): cramping abdominal pain, constipation, general weakness, dizziness, pain in the limbs and lower back.

7.4 Chronic poisoning

Externally: lead (black) border along the edge of the gums, earthy-gray skin color.

Changes in the nervous system: headache, dizziness, fatigue, irritability, sleep disturbance, memory impairment, epileptic seizures.

Movement disorders: paralysis of individual muscles, tremors of the hands, eyelids and tongue; pain in the limbs, changes in the blood system - lead anemia, metabolic and endocrine disorders, disorders of the gastrointestinal tract, cardiovascular system.

7.5 Standards

Pb metal. MPCr.z. 0.01 mg/m 3, Pb salts MPC.s. 0.0003 mg/m3,

MPCs.s. 0.003 mg/m3.

Hazard class 2.

8 . Chrome (Cr)

8.1 Anthropogenic sources of input

Emissions from enterprises where chromium is mined, received, processed and used (including electroplating and tanning industries).

8.2 Toxic effects

Toxicity depends on valency:

Cr(VI) > Cr(III) > Cr(II)

Affects the kidneys, liver, pancreas, has a carcinogenic effect. Irritating effect, Cr (VI) is an allergen.

8.3 Acute poisoning

Aerosol compounds of Cr (VI), chromates, bichromates - runny nose, sneezing, nosebleeds, irritation of the upper respiratory tract; in severe cases - acute renal failure.

8.4 Chronic poisoning

Damage to the upper respiratory tract and the development of bronchitis and bronchial asthma; liver damage (functional dysfunction, development of cirrhosis), allergic skin diseases - dermatitis, ulcers, “chromic eczema”.

Chromates are the main cause of industrial contact dermatitis on the hands, forearms, face, and eyelids.

With prolonged contact with chromium compounds, the likelihood of cancer increases.

8.5 Standards

Cr+6 in terms of CrO3 (chromates, bichromates):

MPCm.r. 0.0015 mg/m3

MPCs.s. 0.0015 mg/m3

1st class of danger.

9 . Copper (Cu)

9.1 Anthropogenic sources of input

Non-ferrous metallurgy enterprises;

Galvanic production;

Burning coal and oil.

9.2 Toxic effects

Thiol poison

9.3 Acute poisoning

If ingested - nausea, vomiting blood, abdominal pain, diarrhea, impaired coordination of movements, death from renal failure.

When inhaling the aerosol - coughing attacks, abdominal pain, nosebleeds. Temperature increase.

9.4 Chronic poisoning

Disorders of the nervous system, kidney liver, destruction of the nasal septum.

9.5 Standards

CuSO4 MPC.z. 0.5 mg/m3

MPCm.r. 0.003 mg/m3

MPCs.s. 0.001 mg/m3

Hazard class 2.

Mechanism of action of antidotes. Classification of poisoning. Detoxification methods. Antidotes (question for independent study). What is the specificity of antidote therapy? What are the antidotes? Introduction of new antidotes into practice

2.6.1. Physical antidotes

2.6.2. Chemical antidotes

2.6.3. Biochemical antidotes

2.6.4. Physiological antidotes

Types of antidotes

Antidotes in folk medicine

3. 1. Classification of antidotes:

Send your good work in the knowledge base is simple. Use the form below

Similar documents