While oxidative stress as an underlying cause of many neurological diseases is well documented [25,26], the role of alcohol-induced oxidative stress in the CNS is largely unknown. Recent high-throughput neuroproteomic studies of protein expression profiles indicated increased levels of ammonia and ROS in the CNS of alcoholics [27]. Chronic alcohol administration resulted in microencephaly and neuronal loss in juvenile mice [28] and impacted behavior [29] through modulation of neuronal nitric oxide synthase, suggesting the involvement of oxidative stress. Protective effects of vitamin E on neuronal loss against alcohol-induced oxidative product in neonatal rat hippocampus [30] and decrease in glutathione level in fetal cortical neurons suggest the role of alcohol-mediated oxidative stress in the CNS [31].
