Background
This project investigated whether or not EtOH‐induced reductions in the levels of long‐chain polyunsaturated membrane fatty acids could be attenuated by exogenous exposure to either α‐tocopherol, γ‐tocopherol, or diallyl sulfide (DAS).
Methods
At 0 days of development, fertile chicken eggs were injected with a single dose of either saline supplemented with various concentrations of EtOH, α‐ or γ‐tocopherol and EtOH, or DAS and EtOH. At 18 days of development, brains were isolated and subjected to membrane analyses.
Results
When exposed to EtOH, concentrations ranging from 0–60.50 μm/Kg egg, dose‐dependent decreases in the levels of brain 18:0, 18:1 (n‐9), 18:2 (n‐6), 18:3 (n‐3), and 20:4 (n‐6) were observed. These ethanol–induced changes in membrane fatty acid composition correlated with ethanol‐induced reductions in brain mass, brain protein levels, acetylcholine esterase (AChE) activities and correlated with increased lipid hydroperoxide levels. Exposure to either 2.5 μm α‐tocopherol/Kg egg and 6.050 mm EtOH/Kg egg, or 2.5 μm α‐tocopherol/ Kg egg and 6.050 mm EtOH/Kg egg attenuated EtOH‐induced changes in membrane fatty acid composition, brain mass, brain protein levels, AChE activities, and lipid hydroperoxide levels. Embryonic exposure to the cytochrome p450‐2E1 inhibitor, diallyl sulfide (DAS), also attenuated EtOH‐induced decreases in long‐chain, unsaturated membrane fatty acids. However, embryonic exposure to DAS promoted abnormally low brain mass.
Conclusion
EtOH‐induced reductions in the levels of brain long‐chain polyunsaturated fatty acid are caused by lipid peroxidation. Teratology 62:26–35, 2000. © 2000 Wiley‐Liss, Inc.