## 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
The role of iron and glutathione in t-butyl hydroperoxide-induced damage towards isolated perfused rat livers
✍ Scribed by Maged Younes; Otfried Strubeit
- Publisher
- John Wiley and Sons
- Year
- 1990
- Tongue
- English
- Weight
- 505 KB
- Volume
- 10
- Category
- Article
- ISSN
- 0260-437X
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✦ Synopsis
Abstract
The hepatotoxic and lipid peroxidative potentials of t‐butyl hydroperoxide (t‐BuOOH) towards isolated perfused rat livers were investigated at doses of 1 and 3 mmol I^−1^. t‐BuOOH led to a concentration‐dependent release of cytosolic (glutamate‐pyruvate transaminase and lactate dehydrogenase) and mitochondrial (glutamate dehydrogenase) enzymes, an accumulation of calcium in the liver, a marked depletion of hepatic glutathione and an enhanced release of it into the perfusate, as well as an enhanced formation and release of malondialdehyde (MDA) by the liver. These effects were blocked in the presence of the potent iron chelator deferrioxamine, and enhanced in livers from iron‐overloaded as well as in livers from glutathione‐depleted rats. Our results indicate that the hepatotoxic and pro‐oxidant actions of organic hydroperoxides depend upon the presence of ionized iron as a catalyst of radical‐forming breakdown reactions, and are potentiated by impairment of glutathione‐dependent detoxification reactions.
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