| Current research has suggested that antioxidant therapy may prevent or ameliorate some effects of alcohol exposure during development. This study examined the effectiveness of antioxidant treatment in alleviating biochemical, neuroanatomical, and behavioral effects of neonatal alcohol exposure. Neonatal rats were administered alcohol (5.25 g/kg) by intragastric intubation on postnatal days (PD) 7, 8, and 9. A subset of alcohol-exposed pups were co-administered a high dose of vitamin E (2000 mg/kg). Controls consisted of a non-treated group, a group given the administration procedure only, and a group given the administration procedure plus the vitamin E dose. In the first cohort of animals, spatial learning was evaluated by performance in the Morris water maze beginning at postnatal day 22, and CA1 cell loss was assessed by unbiased cell counting from brains of postnatal day 30 rats. In the second cohort, protein carbonyl formation was measured by Western blot in hippocampal and liver tissue taken two hours after alcohol administration on PD9. Ethanol-exposed animals showed impaired spatial navigation, a decreased number of CA1 pyramidal cells, and higher protein carbonyl formation in the hippocampus than other groups. The ethanol-exposed animals that also received vitamin E did not differ from controls in spatial navigation. However, the vitamin E-treatment alleviated the increase in protein carbonyls and the reduction in CA1 pyramidal cells seen in the ethanol-exposed group. These results suggest that oxidative stress may be a contributing factor in FAS and that antioxidant therapy may be beneficial in preventing some effects of alcohol exposure. However, antioxidant therapy does not appear to be sufficient to prevent the behavioral impairments associated with FAS, suggesting that additional mechanisms beyond oxidative stress also contribute to the disorder. |
