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Hydroxyl radical generation by microsomes after chronic ethanol consumption.

E Dicker, A I Cederbaum

    Alcoholism, Clinical and Experimental Research
    |June 1, 1987
    PubMed
    Summary

    Chronic ethanol consumption increases hydroxyl radical production in rat liver microsomes, particularly with iron compounds. This suggests a role for oxygen radicals in ethanol-induced liver damage.

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    Ethanol inhibits the JAK-STAT signaling pathway in freshly isolated rat hepatocytes but not in cultured hepatocytes or HepG2 cells: evidence for a lack of involvement of ethanol metabolism.

    Clinical biochemistry·2001

    Area of Science:

    • Biochemistry
    • Toxicology
    • Hepatology

    Background:

    • Chronic ethanol consumption is linked to liver injury.
    • Oxidative stress, involving oxygen radicals, is implicated in ethanol toxicity.
    • Iron metabolism and its role in ethanol-induced liver damage require further investigation.

    Purpose of the Study:

    • To investigate the effect of chronic ethanol feeding on hydroxyl radical (.OH) generation by rat liver microsomes.
    • To determine the influence of iron and other oxidative stress-inducing compounds (paraquat, menadione) on .OH production.
    • To elucidate the mechanisms underlying .OH generation in ethanol-treated rats.

    Main Methods:

    • Microsomes were isolated from chronic ethanol-fed rats and pair-fed controls.
    • .OH generation was measured in the presence of iron compounds (ferric-chloride, ferric-ADP, ferric-EDTA), paraquat, and menadione.

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  • The role of hydrogen peroxide (H2O2) and superoxide dismutase (SOD) was assessed using catalase and SOD inhibition studies.

    • Main Results:

    • Ethanol-fed rat microsomes exhibited a 2-fold increase in .OH production, especially with iron compounds.
    • Paraquat and menadione increased .OH generation similarly in both ethanol-fed and control groups.
    • Catalase inhibited .OH generation, indicating H2O2 as the precursor, while SOD had no significant effect.

    Conclusions:

    • Elevated .OH generation by microsomes, particularly with iron, following chronic ethanol consumption may contribute to ethanol-induced hepatotoxicity.
    • Ethanol treatment enhances the interaction of iron with microsomes, leading to increased oxidative stress.
    • Further research into hepatic iron metabolism and ethanol's effects on iron disposition is crucial for understanding the role of oxygen radicals in ethanol's actions.