The role of neurotoxic esterase in the pathogenesis of delayed organophosphorus neurotoxicity.

摘要

In this comprehensive review of literature the organophosphorus induced-delayed neurotoxicity (OPIDN) pathogenesis, particularly the knowledge gained in recent years on the biochemical properties of neuropathy target esterase (NTE), are critically discussed in great detail. The discussion is oriented toward understanding how NTE is affected both in vitro and in vivo by neuropathic organophosphates (OPs), and the biochemical and physiological consequences correlated with such interactions. The understanding of these interactions has led to improvement in methods for predicting the neuropathic potential of OP compounds and for biomonitoring of neuropathic OP exposures. Discoveries have been reviewed regarding interactions that promote or potentiate OPIDN following its initiation with subthreshold doses of neuropathic OPs compounds. These findings have important implications, not only for the safety evaluation and regulation of OPs and other compounds that interact with NTE, but also for the acceptance of the role played by NTE in the biochemical mechanism of OPIDN.