Lipid Peroxidation was Involved in the Memory Impairment of Carbon Monoxide-induced Delayed Neuron Damage

Abstract

Carbon monoxide (CO)-induced delayed neuron damage is the serious complication, but the underlying mechanisms are poorly understood. This study was designed to investigate the time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; and anti-reactive oxygen species anti-ROS) in nerve tissues for the possible mechanisms exploration. Adult rats were treated with CO by peritoneal injection, and sacrificed after day 0, 1, 3, 7, 14 and 21 of treatment. The results showed that the step-down latency progressively shortened while the numbers of error increased. Comparing with the level of day 0, MDA levels in serum, cerebral cortex and hippocampus significantly increased on day 1, 3 and 7. The level of GSH increased firstly but then decreased. The activities of GR, GSH-Px, and anti-ROS decreased in serum, cerebral cortex and hippocampus of rats after day 1, 3, 7, 14 and 21. Thus, we concluded that CO-mediated delayed neuron damage might be associated with elevation of lipid peroxidation and reduction of antioxidative status. The time-dependent changes of lipid peroxidation and antioxidative status in serum, cerebral cortex and hippocampus, at least in part, are involved in the toxic effects of CO poisoning on neuron.