Protection of Xenopus laevis Embryos Against Alcohol-induced Delayed Gut Maturation and Growth Retardation by Peroxiredoxin 5 and Catalase

Alcohol dehydrogenase 1B genotype and fetal alcohol syndrome: a HuGE minireview

“…Restoration of Pax6 expression was sufficient to partially rescue the defects seen with ethanol exposure. [131][132][133] Overexpression of the antioxidants catalase or peroxiredoxin 5 partially protected against the ethanolmediated defects and restored Pax6 and other neural marker expression. Thus, polymorphisms in antioxidant genes that decrease oxidative stress, in addition to those in ROS-producing enzymes like CYP2E1, might be candidates to examine in relation to FAS.…”

Differential and Critical Roles of Reactive Oxygen Species and Reactive Nitrogen Species in Alcohol-Induced Gene Dysregulations and Birth Defects in <i>Xenopus</i> Embryos

“…Using the animal cap assay, we demonstrated that alcohol (0.1-0.5%) markedly suppressed the expression of several important genes for eye development, including a PAX gene (Pax6), a HOX gene (VAX2), and a T-box gene (TBX5) [14] . Alcohol also dose-dependently inhibited the expression of several genes crucial for gut development, of which Sox17, VegT, and Pax6 were particularly sensitive [29] . Moreover, we identified Pax6, Otx2, Sox3, Sox2, and NCAM as the neural developmental genes which were significantly downregulated after exposure to alcohol [23] ( fig.…”

“…Thus, the Xenopus is a good model for studying the effect of alcohol on growth and gut maturation because we can easily examine the looping pattern of the gut and the body length of the alcohol-treated embryos. In Xenopus embryos, transient alcohol exposure during the period of active gut development (between stages 13 and 22) produced tadpoles with a significant delay in gut maturation [29] . While the gut of all the control tadpoles reached developmental stages 45-46, the gut of the 0.5% alcohol-treated tadpoles was still at developmental stages 42-44 ( fig.…”

“…Our data showed that alcohol drastically increased the levels of ROS and RNS by more than 200 and 100%, respectively. The increase in ROS and RNS production, as well as the alcohol-induced dysmorphologies and dysregulation of developmental genes, could be effectively abrogated by overexpression of catalase and both mitochondrial and cytosolic/peroxisomal forms of PRDX5, indicating that both oxidative and nitrosative stresses are involved in the alcohol-induced birth defects [29] .…”

The Preventive Effect of Oral EGCG in a Fetal Alcohol Spectrum Disorder Mouse Model

“…Our previous studies showed that ethanol causes morphological changes in Xenopus laevis embryos (Peng et al, 2004a(Peng et al, ,b, 2005. We sought to extend this work by studying the effect of maternally administered ethanol on the morphology of mouse embryos.…”