Vitamin E protects developing rat hippocampus and cerebellum against ethanol-induced oxidative stress and apoptosis

It has been suggested that developmental alcohol-induced brain damage is mediated through increases in
oxidative stress. Current research suggests that antioxidant therapy may afford some level of protection
against the toxicity of alcohol and alcoholic beverage in cellular and genomic levels. Seven day pregnant
wistar rats were randomly divided into three groups: control, ethanol and vitamin E treated alcoholic
groups. Apoptosis, lipid peroxidation and protein oxidation amounts, as well as, catalase and superoxide
dismutase (SOD) activities were compared in male offspring hippocampus and cerebellum in the end of
lactation. Offspring from ethanol-exposed animals showed significant increase in apoptosis, protein carbonyl
and lipid hydroperoxide (LPO) in hippocampus and cerebellum than controls. Vitamin E treatment
significantly decreased apoptosis in ethanol group and restored the increased protein carbonyl and LPO
contents and catalase activity to the level of controls. Our findings strongly support oxidative nature of
alcohol-induced cellular stress in developing hippocampus and cerebellum, prove that oxidative stress
induced cell apoptosis plays a crucial role in pathogenic consequences, and imply that a strong protective
effect could be achieved using vitamin E as an antioxidant.