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Related Experiment Videos

Transient decrease of liver cytosolic glutathione S-transferase activities in rats given 1,2-dibromoethane or CCl4.

B Botti, M T Moslen, N M Trieff

    Chemico-Biological Interactions
    |December 1, 1982
    PubMed
    Summary

    Hepatotoxicity from 1,2-dibromoethane (DBE) and carbon tetrachloride (CCl4) in rats rapidly alters liver enzyme activity. Both toxins transiently decrease cytosolic glutathione S-transferase activity, suggesting potential irreversible inhibition.

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    Area of Science:

    • Biochemistry
    • Toxicology
    • Enzymology

    Background:

    • Glutathione S-transferases (GSTs) are crucial detoxification enzymes.
    • Hepatotoxins like 1,2-dibromoethane (DBE) and carbon tetrachloride (CCl4) can impact GST activity.
    • Understanding these interactions is vital for assessing liver damage and developing protective strategies.

    Purpose of the Study:

    • To investigate the in vivo effects of DBE and CCl4 on rat liver cytosolic and microsomal glutathione S-transferase (GST) activities.
    • To characterize the time course and kinetic changes in GST activity following exposure to these toxins.
    • To explore the potential mechanisms underlying GST inhibition by DBE and CCl4.

    Main Methods:

    • Administration of DBE and CCl4 to fasted male rats.

    Related Experiment Videos

  • Assay of liver cytosolic and microsomal GST activities using substrates like chloro-2,4-dinitrobenzene (CDNB) and 3,4-dichloronitrobenzene (DCNB).
  • Measurement of liver glutathione (GSH) concentrations.
  • Kinetic analysis (Vmax, Km) of GST inhibition.

    • Main Results:

    • Both DBE and CCl4 increased microsomal GST activity towards CDNB within 2 hours.
    • Cytosolic GST activities towards CDNB and DCNB were selectively and transiently decreased.
    • DBE exposure diminished GSH levels, while CCl4 did not; cytosolic GST activity decreased within 15 min for CCl4 but not DBE.
    • Kinetic studies revealed decreased apparent Vmax without altered Km, suggesting non-competitive or irreversible inhibition.

    Conclusions:

    • DBE and CCl4 induce rapid alterations in hepatic GST isozyme activities.
    • The observed decrease in cytosolic GST activity may result from covalent modification by reactive metabolites.
    • These findings highlight the complex interaction between hepatotoxins and the cellular defense system, impacting detoxification pathways.