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Related Experiment Videos

Species differences in enzymes controlling reactive epoxides.

H R Glatt, F Oesch

    Archives of Toxicology. Supplement. = Archiv Fur Toxikologie. Supplement
    |January 1, 1987
    PubMed
    Summary
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    Mice exhibit lower microsomal epoxide hydrolase activity, suggesting a role for epoxides in mouse liver carcinogenesis. However, this low activity alone doesn't explain high tumor susceptibility in certain mouse strains.

    Area of Science:

    • Toxicology
    • Carcinogenesis
    • Metabolic Biochemistry

    Background:

    • Epoxides are reactive intermediates in metabolism that can be carcinogenic.
    • Epoxide hydrolase activity varies across species and influences detoxification.
    • Mice show lower microsomal epoxide hydrolase activity compared to other mammals, prompting investigation into its role in liver carcinogenesis.

    Purpose of the Study:

    • To investigate the role of epoxides and epoxide hydrolase activity in mouse liver carcinogenesis.
    • To determine if carcinogens are metabolized into reactive epoxides or if they alter epoxide metabolism.
    • To examine sex-based and strain-based differences in liver tumor susceptibility in relation to epoxide metabolism.

    Main Methods:

    • Assessed epoxide-metabolizing enzyme activities in liver subcellular preparations from 11 mammalian species and various mouse strains.

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  • Tested mutagenicity of phenobarbital, DDT, lindane, and benzo(a)pyrene in Salmonella typhimurium using liver preparations.
  • Measured activities and inducibilities of monooxygenase, epoxide hydrolase, and glutathione transferase in male and female mice.

    • Main Results:

    • Microsomal epoxide hydrolase activity was significantly lower in mice than in other species.
    • Phenobarbital, DDT, and lindane were not mutagenic; a DDT metabolite showed mutagenicity under specific conditions.
    • Benzo(a)pyrene metabolism and related enzyme activities did not explain sex-based differences in tumor susceptibility.
    • No significant differences in hepatic microsomal epoxide hydrolase activity were found between high and low tumor susceptibility mouse strains.

    Conclusions:

    • Lower microsomal epoxide hydrolase activity in mice may contribute to liver carcinogenesis, but is not the sole critical factor for high tumor susceptibility.
    • Differences in benzo(a)pyrene metabolism do not account for sex-based variations in liver tumor susceptibility.
    • While not the primary determinant, the low epoxide hydrolase activity in mice might potentiate susceptibility to certain carcinogens.