Effects of Methanol and Chloramphenicol on CCl4 Toxicity

  • Jane B. Owens
  • Michael J. Brabec
Part of the Advances in Experimental Medicine and Biology book series (AEMB)

Abstract

The mechanism of CCl4 toxicity is unknown, although lipid peroxidation has been implicated in the development of the pathology. Methanol (MeOH) is a well known potentiator of CC14 toxicity (mechanism unknown), while chloramphenicol (CAP) antagonizes the toxicity possibly by inhibiting cytochrome P-450; (Dolci and Brabec, 1978). By use of both an antagonist and a potentiator of CC14 toxicity, it may be possible to selectively disturb and identify the various processes that produce damage in the hepatocyte after exposure to CC14. In the following experiments, serum enzyme levels, hepatic glutathione levels, glucose-6-phosphatase (G6Pase) activity, and lipid peroxidation in hepatic microsomes of CC14-intoxicated rats were measured after treatment with CAP; MeOH, and CAP and MeOH in combination.

Keywords

Lipid Peroxidation Serum Enzyme Hepatic Microsome Mitochondrial Protein Synthesis Serum Enzyme Level 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. Ames, B. N., 1966, Assay of inorganic phosphate, total phosphate and phosphatases, in “Methods In Enzymology”, Vol. VII, E. F. Neufield and V. Ginsburg, ed., Academic Press, New York.Google Scholar
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Copyright information

© Springer Science+Business Media New York 1982

Authors and Affiliations

  • Jane B. Owens
    • 1
  • Michael J. Brabec
    • 1
  1. 1.Department of Environmental and Industrial HealthThe University of MichiganAnn ArborUSA

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