10.22376/ijpbs.2019.10.1.p1-12 Volume 4 Issue 1 2013 (January - March) The objective of the study was to see if oxidative damage is involved in organophosphorus-induced delayed neurotoxicity (OPIDN) and its subsequent alleviation through antioxidants. A total of 72 hens aged 56 weeks were divided into 4 groups (n=18).Group 1 sham, Groups 2, 3 and 4 were administered chlorpyrifos (CPS) @ 350mg/kg BW s.c. in divided doses over a period of 24 hrs. To prevent death due to cholinergic toxicity, atropine and 2-PAM were administered. In group 3, vit. E was administered @ 50mg/kg p.o 10 days prior to administration of CPS and in group 4 phenytoin @ 50mg /kg p.o.was administered for 5 days prior to CPS. Signs of OPIDN were scored. Acetyl cholinesterase (AchE) activity in distal spinal cord served as a biomarker of exposure. Sciatic nerve total calcium was estimated, since Ca lessThan sup greaterThan 2+ lessThan /sup greaterThan is implicated in generation of ROS and in phosphorylation of proteins. Thiobarbituric acid reacting substances (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD) and catalase were estimated to assess lipid peroxidation. CPS produced signs of OPIDN that were reversed on 10th day. There was a decline in AChE activity. Oxidative stress with CPS was manifested by a significant rise in TBARS, increased activity of SOD, catalase and decline in glutathione levels. The above parameters were significantly lowered with prior administration of vitamin E. Phenytoin offered mild protection to the birds. Hence, it is concluded that oxidative stress could be one of the mechanisms of OPIDN and antioxidants might provide a viable therapeutic regimen for alleviation of OPIDN. KAVITHA K, KALA KUMAR B AND GOPALA REDDY A Chlorpyrifos, phenytoin, OPIDN,oxidative stress, ROS, Vit E, 207-220