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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.
Insights
Organophosphorus compounds cause chronic toxicity affecting long axons. This toxicity results from protein phosphorylation, not the loss of esterase activity.
Area of Science:
- Neurotoxicology
- Biochemistry
Background:
- Organophosphorus compounds induce chronic neurotoxicity, a "dying-back" process impacting long axons.
- The initial step involves protein phosphorylation.
Purpose of the Study:
- To investigate the relationship between protein phosphorylation, esterase activity, and organophosphorus-induced neurotoxicity.
Main Methods:
- Focuses on the phosphorylation of a specific protein with phenyl phenylacetate hydrolyzing activity.
- Examines the effect of phosphorylation on esterase activity.
Main Results:
- Phosphorylation of the target protein occurs.
- Esterase activity is inhibited by this phosphorylation, likely at the active site.
- The toxic effect is directly linked to phosphorylation, independent of esterase activity loss.
Conclusions:
- Protein phosphorylation is a critical initial event in organophosphorus compound neurotoxicity.
- The toxicity mechanism is related to the phosphorylation event itself, not solely the inhibition of esterase function.