Abstract:Chronic low-dose exposure to organophosphorus (OP) toxicants
is
correlated with an increase in the risk of impaired cognition and
neurodegenerative diseases. A mechanism to explain this relationship
is needed. We suggest that the formation of organophosphate-induced
high-molecular-weight protein aggregates that disrupt cell function
may be the missing link. It has been demonstrated that such aggregation
can be promoted by OP-labeled lysine. Alternatively, OP-labeled glutamate
may be the initiator. To test this… Show more
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