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Lipid peroxidation in isolated hepatocytes from rats ingesting ethanol chronically

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Summary

Isolated hepatocytes from rats consuming ethanol (8.5 g/kg) daily produce malondialdehyde in significantly higher amounts than liver cells from control animals. The release of LDH and the uptake of trypan blue in both types of hepatocytes do not differ during the incubation period of 2 h. GLDH, however, is only set free into the medium from liver cells of ethanol drinking rats, indicating that mitochondrial alterations are involved.

Bomotrichloromethane (CBrCl3) promotes lipid peroxidation in hepatocytes from ethanol drinking rats in a much higher degree than in cells from control rats. The cell damage induced by CBrCl3 and indicated by a release of LDH and GLDH from the hepatocytes and their uptake of trypan blue is also much more pronounced in liver cells from ethanol drinking animals.

The stronger action of CBrCl3 cannot be explained by an enhanced microsomal metabolism, because no increase of drug metabolizing enzymes could be observed. The relatively low ethanol consumption did not influence body growth and liver weight and did not evoke any triglyceride accumulation.

The normal balance between processes favouring lipid peroxidations and reactions protecting the liver cells seems to be shifted to a state during alcohol intake which promotes formation of radicals.

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Remmer, H., Albrecht, D. & Kappus, H. Lipid peroxidation in isolated hepatocytes from rats ingesting ethanol chronically. Naunyn-Schmiedeberg's Arch. Pharmacol. 298, 107–113 (1977). https://doi.org/10.1007/BF00508617

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