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Ascorbic acid chronic alcohol consumption in the guinea pig.

R L Susick, G D Abrams, C A Zurawski

    Toxicology and Applied Pharmacology
    |June 30, 1986
    PubMed
    Summary

    High dietary vitamin C intake protected male guinea pigs from alcohol-induced liver damage. Supplementation significantly reduced liver enzymes and prevented hepatic steatosis and necrosis caused by chronic alcohol consumption.

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    Area of Science:

    • Biochemistry
    • Toxicology
    • Nutrition

    Background:

    • Chronic alcohol consumption is a significant public health concern, leading to various liver pathologies.
    • Ascorbic acid (vitamin C) is a vital antioxidant with potential protective roles against oxidative stress and tissue damage.

    Purpose of the Study:

    • To investigate the protective effects of a high-ascorbic-acid diet against alcohol-induced toxicity in male guinea pigs.
    • To assess the impact of dietary vitamin C levels on liver enzyme profiles and histological changes following chronic alcohol administration.

    Main Methods:

    • Male guinea pigs were divided into two dietary groups: high-ascorbic-acid and low-ascorbic-acid.
    • Alcohol was administered orally at 2.5 g/kg for up to 14 weeks.
    • Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured. Liver tissues were examined for steatosis and necrosis.

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    Main Results:

    • Animals on the low-ascorbic-acid diet receiving alcohol showed significant increases in AST (120%) and ALT (250%).
    • In contrast, animals on the high-ascorbic-acid diet with alcohol had only a 50% elevation in AST and no significant ALT increase.
    • Hepatic steatosis and necrosis were observed in the low-ascorbic-acid group but not in the high-ascorbic-acid group after 12-14 weeks of alcohol administration.

    Conclusions:

    • A high-ascorbic-acid diet confers significant protection against chronic alcohol-induced liver injury in male guinea pigs.
    • Adequate vitamin C intake may mitigate alcohol-related hepatotoxicity by reducing liver enzyme elevation and preventing histological damage.