Vitamin E and beta-carotene protect against ethanol combined with ischemiain an embryonic rat hippocampal culture model of fetal alcohol syndrome

Neurodevelopmental damage can occur as a result of in utero exposure to alc ohol. Oxidative stress processes are one of many proposed mechanisms though t to contribute to nervous system dysfunction characterized in fetal alcoho l syndrome (FAS). Therefore, this study examined neuroprotective effects of antioxidant supplementation during ethanol (EtOH) treatment (0, 200, 400, 800 or 1600 mg/dl) combined with concomitants of EtOH exposure: acute (2-h) ischemia (alSCH) and chronic (16-h) hypoglycemia (cHG). The antioxidants V itamin E and beta-carotene protected embryonic hippocampal cultures against 0-1600 mg/dl EtOH/alSCH/cHG treatments. In addition, neuronal viability, a s measured by MTT ((3,4,5-dimethylthiazol-2-yt)-2,5-diphenyl tetrazolium br omide; 5 mg/ml)), was equal to untreated cultures when supplemented with vi tamin E or p-carotene at 0-800 mg/dl or 0-200 mg/dl EtOH/alSCH/cHG, respect ively. These in vitro studies mirror potential in utero ethanol-exposed CNS conditions and may lead to therapeutic strategies targeted at attenuating neurodevelopmental FAS-related deficits. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.