Practice question

Embryos possess immature antioxidant defense systems with low catalase and superoxide dismutase activity. Ethanol oxidation by cytochrome P450 2E1 generates superoxide anion, hydrogen peroxide and hydroxyl radicals causing lipid peroxidation and mitochondrial permeability transition. Elevated ROS activates stress kinases JNK and p53 inducing intrinsic apoptosis pathway via Bax and cytochrome c release leading to caspase-mediated cell death in neural crest and neural tube. Antioxidant treatment reduces fetal alcohol defects in animal models. Cell death rather than increased proliferation underlies tissue hypoplasia from alcohol-induced oxidative stress resulting in loss of craniofacial precursors.