Mitochondrial complex I inhibition as a possible mechanism of chlorpyrifos induced neurotoxicity

BACKGROUND Organophosphates (OPs) represent the most widely used class of pesticides. Although perceived as low toxicity compounds compared to the previous organochlorines, they still possess neurotoxic effects both on acute and delayed levels. Delayed neurotoxic effects of OPs include OPIDN and OPICN. The mechanisms of these delayed effects have not been totally unraveled yet. One possible contributor for neurotoxicity is mitochondrial complex I (CI) inhibition. PURPOSE in the present study we evaluated the contributing role of (CI) inhibition in chlorpyrifos (CPF) induced delayed neuropathy in hens. METHODS Experimented birds received 150 mg/kg of CPF, and evaluated behaviorally and biochemically. RESULTS CPF treated hens received 150 mg/kg and developed signs of delayed neurotoxicity, which were verified by NTE inhibition. These effects were paralleled by CI inhibition and decrease in ATP level. CONCLUSIONS The data confirms the possible role of CI inhibition in CPF induced delayed neuropathy.