Lipid Peroxidation, Protein Thiols and Calcium Homeostasis in Bromobenzene-Induced Liver Damage
Previous studies from our laboratory1 have shown that bromobenzene or iodobenzene administration to mice results in the development of lipid peroxidation when the hepatic glutathione (GSH) depletion reaches critical values. Liver necrosis behaves similarly and strictly correlates with the extent of lipid peroxidation. The treatment of the intoxicated animals with Trolox C (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), a lower homolog of vitamin E, completely prevented both lipid peroxidation and necrosis, while not changing at all the extent of the covalent binding of bromobenzene metabolites to liver protein. This would suggest that lipid peroxidation is an important factor in the pathogenesis of the bromobenzene-induced liver cell death.
KeywordsLipid Peroxidation Calcium Uptake Calcium Homeostasis Mitochondrial Fraction Protein Thiol
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- 2.G. Bellomo, S. A. Jewell, M. T. Smith, H. Thor, and S. Orrenius, Perturbation of Ca2+ homeostasis during hepatocyte injury, in: “Mechanisms of Hepatocyte Injury and Death,” D. Keppler, H. Popper, L. Bianchi, and W. Reutter, eds., MTP Press Limited, Lancaster (1984).Google Scholar