THE ROLE OF NEUROTOXIC ESTERASE (NTE) IN THE PREVENTION AND POTENTIATION OF ORGANOPHOSPHORUS-INDUCED DELAYED NEUROTOXICITY (OPIDN)

The first step in the initiation of organophosphorus-induced delayed n europathy (OPIDN) is proposed to be the phosphorylation of an enzyme f ound in the nervous system called neurotoxic esterase (neuropathy targ et esterase, NTE). It has been known for over twenty years that non-ne uropathic inhibitors of NTE exist and can actually prevent OPIDN when given before a neuropathic organophosphate (OP). Within the last three years it has become evident that another outcome is possible followin g in vivo interaction between neuropathic and non-neuropathic NTE inhi bitors. When administered after OP exposure, non-neuropathic inhibitor s can intensify or potentiate signs of OPIDN in adult chickens. Additi onally, whereas developing chickens are typically resistant to the eff ects of neuropathic OPs, resistant age groups will develop OPIDN when exposure to a neuropathic OP is followed by the non-neuropathic NTE in hibitor phenylmethylsulfonyl fluoride. As in the case of prevention, s tudies of the potentiation of OPIDN may yield insight into mechanisms involved in the pathogenesis of delayed neurotoxicity. A brief review of current knowledge regarding the role of NTE in both the prevention and potentiation of OPIDN is presented.