![]() In parallel, alcohol (0.1%–0.5%) dose dependently and significantly reduced the expression of several eye marker genes, of which TBX5, VAX2, and Pa圆 were the most vulnerable. Exposure of Xenopus embryos to alcohol during eye development produced marked gross ocular anomalies, including microphthalmia, incomplete closure of the choroid fissure, and malformation of the retina in 40% of the eyes examined. To investigate the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in fetal alcohol syndrome (FAS)–associated ocular injury, two antioxidant enzymes, catalase and peroxiredoxin 5, were overexpressed in the two blastomeres of the two-cell stage Xenopus embryos. Xenopus embryos were exposed to various concentrations (0.1%–0.5%) of alcohol, and the subsequent effects in eye development and in eye marker gene expression were determined. To study the molecular mechanisms underlying alcohol-induced ocular anomalies in Xenopus embryos. ![]()
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