Neuropathy target esterase (NTE) and organophosphorus-induced delayed polyneuropathy (OPIDP): recent advances

The identification of neuropathy target esterase (NTE) as the site for initiation of organophosphorus-induced delayed polyneuropathy (OPIDP) has led to informative acute and chronic neurotoxicity tests (adopted by OECD and EPA), to structure/activity and in vitro/in vivo predictions, and to a sound basis for extrapolations to man. Purification of the sodium dodecyl sulphate (SDS)-denatured 155-kDa sub-unit of NTE has enabled partial sequencing and molecular biological studies. A MAb to the chicken brain sub-unit and PAbs to synthetic peptides have been raised: preliminary experiments suggest that one is effective for immunohistochemistry of frozen tissue. cDNA libraries are being screened with synthetic oligonucleotides, polymerase chain reaction (PCR)-developed primers, and with Ab in order to obtain cloned NTE. Previous studies of NTE in vivo have not revealed its normal physiological function or the route from inhibition to degeneration of axons, but the current progress in molecular biology of NTE is applicable to study of the function of normal and organophosphorus (OP)-modified NTE in cultured neural cells.