Side effects of organophosphorus compounds: delayed neurotoxicity

Abstract

Many organophosphorus compounds produce a chronic toxicity that has been classified as a dying-back process in which the long axons are particularly affected. Recent evidence indicates that an essential first step in the production of the lesion is the phosphorylation of a protein that is able to hydrolyse substrates such as phenyl phenylacetate. The esterase activity of the protein is inhibited by this phosphorylation, presumably at the active site. However, the toxic effect is related only to phosphorylation and not to loss of esterase activity.