Changes of lipid peroxidation in carbon disulfide-treated rat nerve tissues and serum.

To further elucidate the mechanism and determine the biomarker of neuropathy induced by carbon disulfide (CS(2)), we performed a longitudinal observational study of reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GSH-Px), catalase (CAT), superoxide dismutase (SOD) and total antioxidative capacity (T-AOC) in rat cerebral cortex, hippocampus, spinal cord and serum after 0, 2, 4, 8 and 12 weeks of CS(2) administration. CS(2) exposure was found to markedly increase ROS and MDA levels in cerebral cortex, hippocampus, spinal cord and serum of rats in both time and symptom-dependent manners. Although SOD activities slightly increased, there was a decrease in the GSH contents and GSH-Px, CAT activities in cerebral cortex, hippocampus, spinal cord and serum after 2, 4, 8 or 12 weeks' CS(2) intoxication and at gait score of 2, 3, or 4. The activities of T-AOC also decreased in all three nerve tissues and serum as time went on and symptom developed. Furthermore, significant correlations between LPO and gait abnormality were observed as symptom developed. Oxidation stress also resulted in Ca(2+) concentrations and calmodulin (CaM) levels increases in cerebral cortex, hippocampus and spinal cord. Thus, CS(2) intoxication was associated with elevation of lipid peroxidation (LPO) and reduction of antioxidant status, and the time and symptom-dependent changes of these indexes in rats' nerve tissues and serum suggested that ROS and concomitant LPO, at least in part, were involved in CS(2)-induced neuropathy.