The antioxidants vitamin E and beta-carotene protect against ethanol-induced neurotoxicity in embryonic rat hippocampal cultures

Fetal alcohol syndrome is characterized by numerous nervous system anomalie s with the developing hippocampus being highly vulnerable. Other conditions can result from maternal ethanol consumption including oxidative stress. C ritical antioxidants, such as vitamin E, can be decreased and antioxidative defenses altered. Gestational day 18 rat hippocampal cultures were exposed to ethanol ranging from 400 to 2400 mg/dl (16 h). MTT assays assessed neur otoxicity. Viability was decreased dose dependently. Supplementation with v itamin E or beta-carotene afforded neuroprotection against all ethanol conc entrations. Vitamin E completely ameliorated neuronal loss following 400 an d 800 mg/dl ethanol. Vitamin E increased survival to 95%, 79%; 66%, and 75% during 1600, 1800, and 2000 and 2400 mg/dl ethanol compared to nonethanol treatment. Vitamin E increased viability by 38%, 23%, 12%, and 29% at 1600, 1800, 2000, and 2400 mg/dl compared to non-vitamin E-supplemented, ethanol treatment. beta-Carotene completely ameliorated cell loss from 400 mg/dl e thanol and increased survival by 18% at 1600 mg/dl and 12% at 2000 mg/dl. T his study demonstrates in vitro antioxidative neuroprotection against devel opmental ethanol exposure and suggests that nutritional therapies incorpora ting antioxidants may help protect against deleterious fetal effects from m aternal alcohol abuse. (C) 1999 Elsevier Science Inc. All rights reserved.