Abstract

Publisher Summary Highly toxic acetylcholinesterase (AChE)-inhibiting organophosphates (OPs) and carbamates (CMs) are used as pesticides throughout the world. Most OPs are currently used as pesticides, paraciticides in veterinary medicine, warfare agents, or flame retardants. However, carbamates are used as pesticides in human and veterinary medicine and in prophylaxis of OP nerve agent poisoning. Thiocarbamates are used as fungicides or herbicides and have very low human toxicity. In vertebrates, two main cholinesterases involved areacetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). The inhibition of AChE and BuChE by OPs and CMs is a reaction similar to that of the hydrolysis of acetylcholine (ACh). Electrophysiological studies help to resolve the functional mechanism of OP and CM toxicity. The chapter describes the electromyography in patients with OP and CM intoxication. The acute cholinergic syndrome is the result of excess ACh accumulation at all cholinergic transmission sites. Organophosphate induced delayed polyneuropathy (OPIDP) is characterized by distal degeneration of motor and sensory axons in both the peripheral nerves and the spinal cord. The irreversible inhibition of AChE activity at cholinergic synapses explains the acute OP cholinergic toxicity. Not all toxic effects of OP compounds can be attributed to AChE inhibition. Interaction of OPs with other proteins explains inter-individual differences in sensitivity to OP toxicity. These proteins themselves represent biomarkers of OP exposure and aid in the diagnosis. Some of these proteins may have a therapeutic potential as bioscavengers. In the wake of Gulf War syndrome (GWS) experience, additional advisory panels on the health risks of low-dose OP and CM exposure in warfare and measures to improve surveillance during military deployments have been put in place. The chapter also discusses the therapeutic management of OP pesticide poisoning.

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