The Japanese Journal of Veterinary Science
Online ISSN : 1881-1442
Print ISSN : 0021-5295
ISSN-L : 0021-5295
Cellular Injury and Lipid Peroxidation Induced by Hexavalent Chromium in Isolated Rat Hepatocytes
Shunji UENONobuyuki SUSAYoshinori FURUKAWAKatuhiro AIKAWAIori ITAGAKI
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JOURNAL FREE ACCESS

1989 Volume 51 Issue 1 Pages 137-145

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Abstract
In order to elucidate the relationship between cellular injury and lipid peroxidation induced by hexavalent chromium (CrVI), isolated rat hepatocytes treated with any one of scavengers of active oxygen species, antioxidants or antichromium agent were incubated with K2Cr2O7 as CrVI (1mM Cr). After the incubation, the development of lipid peroxidation was determined as thiobarbituric acid (TBA)-reacting materials in total lipid extracts from the incubated hepatocytes. Cellular injury was observed as a leakage of lactate dehydrogenase (LDH) from hepatocytes into incubation medium. The contents of reduced glutathione (GSH) in hepatocytes were also assessed. Results obtained were as follows: (1) CrVI facilitated lipid peroxidation in isolated hepatocytes after 20 min ofincubation. On the other hand, the cellular injury induced by CrVI was barely observed even after 60 min of incubation. (2) The CrVI-induced lipid peroxidation was inhibited by catalase and mannitol as scavengers of active oxygen species, or N, N'-diphenyl-p-phenylenediamine and α-tocopherol as antioxidants. However the cytotoxicity of CrVI could not be prevented by these chemicals. (3) CrVI depleted the contents of intracellular GSH and diminished the activities of glutathione reductase (GR) and glutathione-S-transferase (GST) except glutathione peroxidase. (4) The scavengers of active oxygen species and the antioxidants could not prevent the depletion of intracellular GSH induced by CrVI. (6) Ascorbic acid, antichromium agent, prevented all of the lipid peroxidation, the cellular injury and intracellular GSH depletion induced by CrVI. These results suggest that the cytotoxicity induced by CrVI is not necessarily correlated to the lipid peroxidation, and that the depletion of intracellular GSH induced by CrVI may be attributable to the direct oxidation of intracellular GSH and the inactivation of GR.
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© The Japanese Society of Veterinary Science
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