Understanding the Toxic Actions of Organophosphates
2001; Elsevier BV; Linguagem: Inglês
10.1016/b978-012426260-7.50053-7
Autores Tópico(s)Insect and Pesticide Research
ResumoPublisher Summary The introduction of a number of organophosphate (OP) pesticides and highly toxic OP nerve agents has emphasized the importance of understanding the mechanisms of toxicity of these OP compounds in detail. The toxicity of OPs stems largely from excess acetylcholine (ACh) due to the inhibition of acetylcholinesterase (AChE) and subsequent accumulation of ACh in the target tissues, especially those cells in the vicinity of cholinergic receptors that are responsible for mediating the effects of ACh. The dramatic effects seen in OP intoxication include brain activation, epileptiformic convulsions, muscular tremors, which lead ultimately to flaccid paralysis, increased sweating and salivation, profound bronchial secretion, bronchoconstriction, increased activity of the intestine and diarrhea, miosis, hypertension, lowered body temperature, and hyperglycemia. The consequences of excess ACh are primarily mediated via cholinergic muscarinic and nicotinic receptor activation. The chapter explains the mechanisms and factors affecting the toxicity of OPs on cholinergic muscarinic and nicotinic receptors. When the effects of OP compounds are compared, marked differences are evident between them. This is most likely due to the marked differences in their ability to bind with their prime target, ACHE, and the differences in the rapidity of ACh accumulation in and close to the targets of ACh.
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