Organophosphate compounds neuropathy

Chronic exposure to certain organophosphate compounds, including some organophosphate cholinesterase inhibitors, causes neuropathy associated with demyelination of axons. 

The subcommittee considered other possible toxicity end points, notably neurotoxicity, associated with GD exposure. Organophosphate compounds like GD may act directly on nerve cell receptors or, by inhibiting neural AChE, interfere with neuromuscular transmission and produce delayed-onset subjunctional muscle damage. In addition, some organophosphate compounds cause a neurotoxic effect (organophosphate-induced delayed neuropathy, or OPIDN) that is not associated with ChE inhibition. Emerging research in this area might indicate alternative... 

Exposure to some organophosphate cholinesterase inhibitors results in a delayed neuropathy characterized by degeneration of axons and myelin. This effect is not associated with the inhibition of acetylcholinesterase, but rather with the inhibition of an enzyme described as neuropathy target esterase (NTE) however, the exact mechanism of toxicity is not yet fully understood (Munro et al., 1994). For some organophosphate compounds, delayed neuropathy can be induced in experimental animals at relatively low exposure levels, whereas for others the effect is only seen following exposure to supralethal doses when the animal is protected from the acute toxic effects caused by cholinesterase inhibition. 

Organophosphate-induced delayed neuropathy is unrelated to the anticholinesterase (anti-ChE) effects of OP agents because many highly potent cholinergic OPs do not cause neuropathy, and other OP compounds such a.s tri-o-cresyl phosphate (which is not used as a pesticide) have only weak anti-ChE activity but are powerful inducers of neuropathy. The enzyme involved in organo-phosphatc-induced delayed neuropathy is neuropathy target esterase—lysophospholipase (Lush et al 1998 ... 

Certain organophosphates may also induce delayed polyneuropathy, usually 2-3 weeks after a single exposure. The symptoms are tingling of hands and feet, sensory loss, progressive muscle weakness, and ataxia. Also, certain organophosphorus compounds are poor inhibitors of AChE but may, however, bind to another esterase, known as neuropathy target esterase (NTE) and induce delayed neuropathy. 

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