Abstract
Maternal diabetes significantly increases the risk for birth defects. Studies using animal models indicate that oxidative stress may play a causative role. Oxidative stress can result from exposure to certain drugs, ionizing radiation and folic acid deficiency. Therefore, study of the mechanisms by which maternal diabetes affects embryogenesis may provide insight into general processes by which birth defects occur. Study of embryonic gene expression has demonstrated that maternal diabetes causes birth defects by disturbing expression of genes that control essential developmental processes, and that oxidative stress is involved. A model in which oxidative stress-induced deficient gene expression leads to congenital defects involving p53-dependent apoptosis is discussed.
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