Abstract
Previous studies demonstrated that embryonic exposure to ethanol (EtOH) promoted a reduction in brain mass, a reduction in brain neuron densities, and a reduction in membrane long-chain polyunsaturated fatty acids (PUFAs) in embryonic chick brains. These EtOH-induced reductions in brain membrane PUFAs may be the result of lipid peroxidation because embryonic exposure to exogenous - or γ-tocopherol partially attenuated EtOH-induced reductions in membrane PUFAs. In this paper, we report that embryonic exposure to exogenous - or γ-tocopherol attenuated EtOH-induced decreases in endogenous levels of -tocopherol in both embryonic chick brains and liver. Embryonic exposure to exogenous - or γ-tocopherol also partially attenuated EtOH-induced reductions in brain neuron densities within the cerebral hemispheres of embryonic chick brains. Finally, embryonic exposure to exogenous - or γ-tocopherol also partially attenuated EtOH-induced reductions in long-chain PUFAs in 2-day old neonatal chick brains.