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Serum Alcohol Dehydrogenase and Aldehyde Dehydrogenase Activity in the Course of Hepatitis C

Wojciech Jelski, Anna Strumnik, Karolina Orywal

    Clinical Laboratory
    |February 7, 2017
    PubMed

    Insights

    Hepatitis C patients show significantly increased levels of alcohol dehydrogenase (ADH) isoenzymes I and II in their serum. This elevation in ADH activity is linked to liver cell damage caused by the Hepatitis C virus (HCV).

    Area of Science:

    • Hepatology
    • Clinical Biochemistry
    • Virology

    Background:

    • Hepatitis C virus (HCV) infection impacts 170 million globally, a primary cause of chronic liver disease.
    • Liver cell damage in HCV is indicated by elevated serum enzyme activities, including alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).
    • ADH and ALDH are crucial for metabolizing various substances and are predominantly found in the liver.

    Purpose of the Study:

    • To investigate alcohol dehydrogenase (ADH) activity and its isoenzymes in hepatitis C patients.
    • To assess the total aldehyde dehydrogenase (ALDH) activity in the serum of individuals with hepatitis C.

    Main Methods:

    • Serum samples from 50 hepatitis C patients and 50 healthy controls were analyzed.
    • Spectrofluorometric methods measured ADH isoenzymes I and II, and total ALDH activity.
    • Photometric methods determined total ADH activity and ADH isoenzymes III and IV.

    Main Results:

    • A statistically significant 2.5-fold increase in ADH I and a 2-fold increase in ADH II activity were observed in hepatitis C patients.
    • Elevated ADH isoenzyme activities correlated well with alanine and aspartate aminotransferase levels.
    • Total ADH activity showed a moderate increase, confirming the heightened activity of ADH classes I and II.

    Conclusions:

    • Class I and II alcohol dehydrogenase isoenzymes are significantly elevated in the serum of hepatitis C patients.
    • This increase is likely due to the release of these enzymes from liver cells damaged by the Hepatitis C virus.
    Abstract

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