## 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 an
Controversial role of intracellular iron in the mechanisms of chemically-induced hepatotoxicity
✍ Scribed by Badr, Mostafa Z.
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 498 KB
- Volume
- 9
- Category
- Article
- ISSN
- 0887-2082
No coin nor oath required. For personal study only.
✦ Synopsis
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, duration, and route of exposure, the resultant liver injury may regress or progress and becomes irreversible (1). Mechanisms involved in this selective, localized toxicity have been the target of extensive research efforts, and many studies produced conflicting results. As depicted in Figure 1, although many investigators implicate iron and lipid peroxidation in this process (4-9), others dispute such assertions (10-12).
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