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Berzins, D. W., & Bundy, K. J. (2002). Bioaccumulation of lead in Xenopus laevis tadpoles from water and sediment. Environ Int, 28(1-2), 69–77.
Abstract: The overall objective of this research was to monitor the uptake kinetics of lead in an amphibian model and correlate metal content with embryo development. Based upon the concentration of lead found in the water and sediment of a Louisiana swamp adjacent to a Superfund site, a controlled laboratory experiment exploring lead uptake from water and sediment by Xenopus laevis tadpoles was conducted. For 5 weeks, tadpoles were exposed to water and a simulated sediment, kaolin, spiked with 1, 5, or 10 times the concentration of lead found in field water and sediment samples. Additionally, organisms were exposed to the 5 x condition for 3 and 6 weeks. The experimental controls consisted of unexposed tadpoles and ones exposed to lead originating from water or sediment exclusively. At the end of the exposure periods, developmental data, i.e., body weight and developmental stage, were recorded, and the tadpoles were analyzed for whole body lead concentration. Lead extraction was accomplished by dry ashing, and its amount was quantified polarographically. Results showed that lead inhibited the normal development of these amphibians, in a manner that generally was more severe as exposure level increased. The hindrance of tadpole development also coincided with an increase in whole body lead concentration at higher exposures. Temporally, at the 5 x exposure concentration, the mean lead level increased with time, but this difference was not statistically significant (P<.05). Additionally, control animals exposed to lead (either in water or in sediment) showed no statistical difference with regard to weight and lead uptake, indicating that lead originating from both water and sediment is incorporated into the tadpole. The controlled laboratory experimental protocol used here is thus capable of investigating the uptake of a single metal (Pb in this case) and determining its effect on the development of tadpoles while differentiating the significance of multiple sources of exposure.
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Peng, Y., Yang, P. - H., Guo, Y., Ng, S. S. M., Liu, J., Fung, P. C. W., et al. (2004). Catalase and peroxiredoxin 5 protect Xenopus embryos against alcohol-induced ocular anomalies. Invest Ophthalmol Vis Sci, 45(1), 23–29.
Abstract: PURPOSE: To study the molecular mechanisms underlying alcohol-induced ocular anomalies in Xenopus embryos. METHODS: 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 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. RESULTS: 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. In parallel, alcohol (0.1%-0.5%) dose dependently and significantly reduced the expression of several eye marker genes, of which TBX5, VAX2, and Pax6 were the most vulnerable. Overexpression of catalase and of cytosolic and mitochondrial peroxiredoxin 5 restored the expression of these alcohol-sensitive eye markers and significantly decreased the frequency of ocular malformation from 39% to 21%, 19%, and 13% respectively. All these enzymes reduced alcohol-induced ROS production, but only peroxiredoxin 5 inhibited RNS formation in the alcohol-treated embryos. CONCLUSIONS: The results suggest that oxidative and nitrosative stresses both contribute to alcohol-induced fetal ocular injury.
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