Catalase and Peroxiredoxin 5 Protect Xenopus Embryos against Alcohol-Induced Ocular Anomalies

Abstract

The results suggest that oxidative and nitrosative stresses both contribute to alcohol-induced fetal ocular injury.

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

“…In zebrafish embryos, alcohol reduced the visual acuity, produced smaller eyes, and impaired the migration of the prechordal plate, which is required for the development of the ventral brain [12,13] . Similar to other animal models, exposure of Xenopus embryos to alcohol (0.1-0.5%) also led to marked defects in the eye development [14] . The most pronounced defect is the disappearance of the pigmented layers at the ventral site of the eye ( fig.…”

“…In contrast, embryos at neural developmental stages (stages [13][14][15][16][17][18][19][20][21][22] were highly vulnerable to alcohol-induced neurotoxicity and they exhibited a significant reduction in head size after transient alcohol exposure [23,24] . As illustrated in figure 1 b and c, alcohol dose-dependently produced tadpoles with microcephaly (indicated by a reduction in the horizontal distance between the two eyes) and growth retardation (indicated by a reduction in the body length).…”

“…Total RNA was isolated and reverse transcribed, and then PCR was performed using primers specific for various developmental genes. 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] .…”

Mitochondrial Energy Metabolism and Redox Signaling in Brain Aging and Neurodegeneration

“…3) are involved in the enzymatic degradation of H 2 O 2 ; Prx5 can also reduce ONOO - (69,183). Trx2 is highly efficient at reducing disulfides in proteins (163), thus impacting cellular functions such as antioxidant defenses and the redox control of transcription and signal transduction (8,101).…”

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.…”