In vivo and in vitro evidence concerning the role of lipid peroxidation in the mechanism of hepatocyte death due to carbon tetrachloride

Cell Biochem Funct. 1991 Apr;9(2):111-8. doi: 10.1002/cbf.290090208.

Abstract

Isolated rat hepatocytes exposed to CCl4 showed a stimulated formation of malonaldehyde after only 30-60 min incubation. Conversely, the onset of hepatocyte death was a relatively late event, being significant only after 2-3 h of treatment. A cause-effect relationship between the two phenomena has been demonstrated by using hepatocytes isolated from rats pretreated with alpha-tocopherol. Comparable results were obtained in vivo where supplementation with alpha-tocopherol 15 h before CCl4 dosing induced a partial or complete protection against the drug's necrogenic effect, depending on the concentration of the haloalkane used. Moreover, the vitamin supplementation prevented the CCl4-induced increase of liver total calcium content, probably by blocking alterations in the liver cell plasma membranes due to lipid peroxidation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium Chloride / metabolism
  • Carbon Tetrachloride / toxicity*
  • Cell Survival / drug effects*
  • Lipid Peroxidation / drug effects*
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / pathology
  • Male
  • Malondialdehyde / metabolism
  • Necrosis
  • Rats
  • Rats, Inbred Strains
  • Vitamin E / pharmacology

Substances

  • Vitamin E
  • Malondialdehyde
  • Carbon Tetrachloride
  • Calcium Chloride