Mechanism of Organophosphorus Pesticide Poisoning

Organophosphorus pesticides can enter the human body through the digestive tract, respiratory tract and intact skin and mucous membranes. Occupational pesticide poisoning is mainly caused by skin pollution. The absorbed organophosphorus pesticides are distributed in various organs in the body, with the largest content in the liver, and the content in the brain depends on the ability of the pesticide to penetrate the blood-brain barrier.

Organophosphorus in the body is first biotransformed by oxidation and hydrolysis; oxidation enhances toxicity, such as parathion, which is oxidized to more toxic paraoxon under the action of mixed-function oxidase in the smooth endoplasmic reticulum of the liver; hydrolysis It can reduce the toxicity, and parathion is hydrolyzed by phosphatase and loses its effect when it is oxidized. Secondly, the metabolites after oxidation and hydrolysis are partially excreted with the urine through the combined reaction of glucuronic acid and sulfuric acid; part of the hydrolyzed products, such as p-nitrophenol or p-nitrocresol, are directly excreted in the urine without the need for binding. reaction.

The main mechanism of organophosphorus pesticide poisoning is to inhibit the activity of cholinesterase. Organophosphorus combines with cholinesterase to form phosphorylated cholinesterase, which makes cholinesterase lose its catalytic acetylcholine hydrolysis effect. The accumulated acetylcholine has three effects on cholinergic nerves:

1. Muscarinic effects

2. Nicotine-like effects

3. Central nervous system effects

There are two forms of phosphorylated cholinesterase formed by the combination of organophosphorus and cholinesterase. One is unstable in combination, such as parathion, systemic phosphorus, phorate, etc., which can be partially hydrolyzed to recover energy; Lathion, etc., can no longer restore the inhibited cholinesterase, which can be described as cholinesterase aging.

Cholinesterase cannot be reactivated and can cause delayed effects, such as axonal degeneration of the peripheral nerves and long tracts of the spinal cord, resulting in delayed peripheral neuropathy