Chronic exposure to allyl chloride (AC) is known to produce a central-peripheral distal axonopathy. To access the biomarker of exposure and elucidate the mechanism of neuropathy induced by AC, we performed a longitudinal observational study of malondialdehyde (MDA), anti-reactive oxygen species (anti-ROS), glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) in rats serum and sciatic nerve after 0, 3, 6, 9 and 12 weeks of AC administration. AC was administrated to Wistar rats by gavage at a single dosage of 200 mg/kg/per dose (three times per week). Rats were sacrificed after 0, 3, 6, 9 and 12 weeks of AC treatment, serum and sciatic nerves were quickly collected at 4 degrees C. The results showed that MDA levels in serum (115.4 and 126.2%) and sciatic nerve (130.5 and 145.3%) significantly increased (p<0.05) on 3rd week of AC treatment and at gait score of 2, and further changes of MDA levels were observed after 6, 9 and 12 weeks and at gait score of 3 and 4. While a decrease (p<0.05) in the activities of CAT on 6th week of AC intoxication and at gait score of 2 was observed in serum (81.2 and 72.8%) and sciatic nerve (71.7 and 70.7%). The other antioxidants also decreased in serum and sciatic nerve after 3, 6 and 9, 12 weeks' intoxication and at gait score of 2, 3 and 4. Significant (p<0.05) positive correlations were observed between serum and sciatic nerve in MDA levels (r=0.9162 and 0.9551, respectively) and CAT (r=0.9410 and 0.9557, respectively) activities as time went on and symptoms developed. Thus, AC intoxication was associated with elevation of lipid peroxidation and reduction of antioxidative status, and the time dependent changes of these indexes in Wistar rats' serum and sciatic nerve occurred. The misbalance of lipid peroxidation and antioxidation status might be one of mechanisms of toxic neuropathy induced by AC. MDA and CAT could be served as the biomarkers of AC exposure to afford the early diagnosis of AC-induced toxic neuropathy.