الفهرس 
AcknowledgementOnly 14 pages are availabe for public view
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Abstract
Organophosphorus ester-induced delayed neurotoxicity or OPIDN has been characterized as a clinical syndrome of human and domestic animals for just over 55 years. This OPIDN is characterized pathologically by distal axonal degeneration and secondary demyelination of the central
v
and peripheral axons (Cavanagh, 1964). OPIDN originates from a distinctive biochemical lesion of the nerve axon produced by phosphorylation of a specific protein receptor called neurotoxic esterase or neuropathy target esterase, NTE (Johnson, 1982). This phosphorylation which may result from either acute or chronic exposure to some organophos-phorus compounds by oral, dermal or inhalation routes, appears to trigger a delayed reaction over a period of 1 to 3 weeks that eventually may produce inco-ordination, >ataxia, spasticity and a flacid paralysis developing distally in the hind limbs and eventually spreading to the fore limbs (Cavanagh, 1964 and Metcalf, 1984). Phosphory¬lation of NTE appears to be a necessary step in producing OPIDN, but inhibition alone is insufficient. A second time-dependent reaction involving transfer of a side-chain from the phosphorylated protein to another site (aging) must also occur (Clothier and Johnson, 1979 and 1980). The organophosphorus insecticide leptophos, 0-methyl 0-( 4-b.romo-2 , 5-dichlorophenyl) phenylphosphonothloate, is one of the most well known compounds