Hepatotoxicity induced by various therapeutic agents, industrial chemicals and environmental polIutants is a well-recognized phenomenon. These chemicals are known to cause liver damage that is localized to either periportal or centrilobular regions of the liver lobule (1-3). Depending on dose, durat
The role of iron in t-butyl hydroperoxide-induced lipid peroxidation and hepatotoxicity in rats
✍ Scribed by Maged Younes; Alexander Wess
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 404 KB
- Volume
- 10
- Category
- Article
- ISSN
- 0260-437X
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✦ Synopsis
Abstract
Treatment of rats with 100 mg kg^−1^ t‐butyl hydroperoxide led to an enhanced ethane exhalation as a marker of in vivo lipid peroxidation, as well as a moderate hepatoxicity as evidenced by a rise in plasma activities of liver‐specific enzymes (glutamate‐pyruvate transaminase and sorbitol dehydrogenase) and an increase in hepatic calcium content. Furthermore, a depletion of hepatic glutathione by 17% was observed. Apart from the loss of glutathione, all these effects were antagonized by pretreatment of rats with the potent iron chelator deferrioxamine and potentiated by pretreatment with low concentrations of FeSO~4~ having no pro‐oxidant activity per se; this was also the case in rats under conditions of iron overload (experimental haemochromatosis). These data indicate a close relationship between t‐butyl hydroperoxide‐induced lipid peroxidation and its hepatotoxicity, and point out the importance of iron in catalysing reinitiation (propagation) reactions of lipid peroxidation in vivo.
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