Mechanism of action of poisons: Difference between revisions
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'''[[ | A '''[[Poison]]''' is a substance that, when administered in small quantities, causes disease-like changes or [[death]] based on its chemical properties. Poisons act in the body through various mechanisms: | ||
* '''Etching''' | * '''Etching''' | ||
::This term refers to | ::This term refers to local denaturation of tissue components by caustics, i.e. strong acids with pK < 2, e.g. H<sub>2</sub>SO<sub>4</sub>, HCl or HNO<sub>3</sub> sub>, or strong bases (lyes) with pK > 11.5, e.g. NaOH, KOH, NH<sub>4</sub>OH. | ||
::{{ | ::{{Details|Ingestion of Acids and Alkalies}} | ||
* '''Covalent non-specific interactions with biomolecules (proteins, nucleic acids and polysaccharides)'''. | * '''Covalent non-specific interactions with biomolecules (proteins, nucleic acids and polysaccharides)'''. | ||
:: | ::Example of these poisons are very reactive aldehydes. Aldehyde group -CHO reacts willingly with amino group -NH<sub>2</sub> or sulfhydryl group -SH, occurring abundantly in proteins. An example is methanal ([[formaldehyde]]) HCHO, its aqueous saturated solution is known as [[formalin]]. | ||
* '''Violation of acid-base balance'''. | * '''Violation of acid-base balance'''. | ||
:: | ::Some poisons [[Acid-base balance disorders|disrupt the acid-base balance]] of the organism<ref>[https://dl1.cuni.cz/course/view.php?id=110 E-course on acid-base balance at university MOODLE]< /ref>. [[Ethylene glycol]] is oxidized by [[alcohol dehydrogenase|alcohol dehydrogenase]] to glycolic, glyoxalic, and oxalic (oxalic) acids, which cause [[metabolic acidosis|metabolic acidosis]]. [[Salicylates]] stimulate the respiratory center. The resulting hyperventilation leads to [[respiratory alkalosis|respiratory alkalosis]]. After these substances enter the cells, they turn off oxidative phosphorylation in the mitochondria, decrease ATP production, block [[Citrate cycle|citrate cycle]] enzymes and stimulate [[Glycolysis|anaerobic glycolysis]]. The result is overproduction and accumulation of acidic metabolites, mainly lactate, pyruvate and acetoacetate, and thus [[metabolic acidosis]] develops. | ||
::{{ | ::{{Details|Alcohol intoxication#Ethylene glycol}} | ||
* ''' | * '''Effect on Membranes''' | ||
:: | ::Ethanol, [[detergent]]s and hydrocarbons change the fluidity of the membranes, which is reflected in the function of the membrane components. Changes in membrane microviscosity will change the conformation of membrane channels, receptors and enzymes, thereby disrupting their functions (membrane transport, information transfer, membrane potential). [[Fluidity]] of membranes is a control mechanism for heavy metal absorption. | ||
::{{ | ::{{Details|Alcohol intoxication}} | ||
* ''' | * '''Interaction with the transfer of oxygen in the organism''' | ||
:# | :# Binding of poison to hemoglobin {{Details|Carbon monoxide poisoning}} | ||
:# | :# Oxidation of hemoglobin to [[methemoglobin]] {{Details|Intoxication by methemoglobinizing substances}} | ||
:# | :# Inhibition of [[cytochrome oxidase|cytochrome oxidase]] {{Details|Hydrogen cyanide and cyanide intoxication}} | ||
* ''' | * '''Inhibition of enzymes''' | ||
:# | :# Non-specific interactions, binding to sulfhydryl group -SH. | ||
:# | :# Binding of the poison to the active site of the enzyme. | ||
* ''' | * '''Interaction with specific receptors and disruption of cell signaling or membrane channel function'''. | ||
:: | ::Sodium channel, nicotinic and muscarinic receptors, [[psychopharmaceuticals]], [[addictive substances]]. | ||
== | == Links == | ||
=== | === Literature === | ||
=== | === References === | ||
<references/> | <references/> | ||
[[ | [[Category:Pathobiochemistry]] | ||
[[ | [[Category:Biochemistry]] | ||
[[ | [[Category:Forensic medicine]] | ||
Revision as of 17:13, 25 November 2022
A Poison is a substance that, when administered in small quantities, causes disease-like changes or death based on its chemical properties. Poisons act in the body through various mechanisms:
- Etching
- This term refers to local denaturation of tissue components by caustics, i.e. strong acids with pK < 2, e.g. H2SO4, HCl or HNO3 sub>, or strong bases (lyes) with pK > 11.5, e.g. NaOH, KOH, NH4OH.
For more information see Ingestion of Acids and Alkalies.
- Covalent non-specific interactions with biomolecules (proteins, nucleic acids and polysaccharides).
- Example of these poisons are very reactive aldehydes. Aldehyde group -CHO reacts willingly with amino group -NH2 or sulfhydryl group -SH, occurring abundantly in proteins. An example is methanal (formaldehyde) HCHO, its aqueous saturated solution is known as formalin.
- Violation of acid-base balance.
- Some poisons disrupt the acid-base balance of the organism<ref>E-course on acid-base balance at university MOODLE< /ref>. Ethylene glycol is oxidized by alcohol dehydrogenase to glycolic, glyoxalic, and oxalic (oxalic) acids, which cause metabolic acidosis. Salicylates stimulate the respiratory center. The resulting hyperventilation leads to respiratory alkalosis. After these substances enter the cells, they turn off oxidative phosphorylation in the mitochondria, decrease ATP production, block citrate cycle enzymes and stimulate anaerobic glycolysis. The result is overproduction and accumulation of acidic metabolites, mainly lactate, pyruvate and acetoacetate, and thus metabolic acidosis develops.
- For more information see Alcohol intoxication#Ethylene glycol.
- Effect on Membranes
- Ethanol, detergents and hydrocarbons change the fluidity of the membranes, which is reflected in the function of the membrane components. Changes in membrane microviscosity will change the conformation of membrane channels, receptors and enzymes, thereby disrupting their functions (membrane transport, information transfer, membrane potential). Fluidity of membranes is a control mechanism for heavy metal absorption.
- For more information see Alcohol intoxication.
- Interaction with the transfer of oxygen in the organism
- Binding of poison to hemoglobin For more information see Carbon monoxide poisoning.
- Oxidation of hemoglobin to methemoglobin For more information see Intoxication by methemoglobinizing substances.
- Inhibition of cytochrome oxidase For more information see Hydrogen cyanide and cyanide intoxication.
- Binding of poison to hemoglobin
- Inhibition of enzymes
- Non-specific interactions, binding to sulfhydryl group -SH.
- Binding of the poison to the active site of the enzyme.
- Interaction with specific receptors and disruption of cell signaling or membrane channel function.
- Sodium channel, nicotinic and muscarinic receptors, psychopharmaceuticals, addictive substances.
