Alcohol-Generated Free Radicals and Birth Defects: Functions and Mechanisms

摘要

Maternal alcohol consumption during pregnancy is known to cause fetal anomalies and represents a major public health issue worldwide. Using our established Xenopus embryo model, we have shown that alcohol exposure results in tadpoles with fetal alcohol syndrome-like morphological defects, and induces the production of reactive oxygen species and reactive nitrogen species. In this study, we determined the global gene expression changes in the alcohol-treated embryos using microarray. We found that several important genes involved in embryonic development, oxidative stress and DNA damage are differentially expressed. These results provide invaluable information for us to elucidate the underlying molecular mechanisms leading to alcohol-induced birth defects.