title: Mitochondrial complex I inhibition as a possible mechanism of chlorpyrifos induced neurotoxicity.
abstract: 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.
  
  
  OBJECTIVE
  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.
authors.affiliation: Toxicology Department; ; Medical Experimental Research Center (MERC)-Mansoura University;
authors.forename: Mohamed
authors.initials: M
authors.lastname: Salama
authors.affiliation: Toxicology Department;
authors.forename: Doaa
authors.initials: D
authors.lastname: El-Morsy
authors.affiliation: Medical Experimental Research Center (MERC)-Mansoura University;
authors.forename: Mohamed
authors.initials: M
authors.lastname: El-Gamal
authors.affiliation: Toxicology Department;
authors.forename: Osama
authors.initials: O
authors.lastname: Shabka
authors.affiliation: Clinical pharmacology department, Menoufia Medical School, Menoufia University, Egypt.
authors.forename: Wael My
authors.initials: WM
authors.lastname: Mohamed
keywords: CI; CPF; Esterases; Mitochondria; OPIDN; OPs