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Time course of the carbon tetrachloride-induced decrease in mitochondrial aldehyde dehydrogenase activity.

J J Hjelle, J H Grubbs, D G Beer

    Toxicology and Applied Pharmacology
    |February 1, 1983
    PubMed
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    Carbon tetrachloride (CCl4) rapidly inhibits low Km mitochondrial aldehyde dehydrogenase (ALDH) within 6 hours, earlier than previously thought. This finding offers insights into CCl4

    Area of Science:

    • Biochemistry
    • Toxicology
    • Enzymology

    Background:

    • Hepatic microsomal enzymes, including cytochrome P-450, are known targets of carbon tetrachloride (CCl4) toxicity.
    • Less is understood regarding the rapid effects of CCl4 on nonmicrosomal enzymes.
    • Mitochondrial low Km aldehyde dehydrogenase (ALDH) isozyme is a known target, typically showing inhibition 24 hours post-CCl4 exposure.

    Purpose of the Study:

    • To investigate the rapidity of CCl4-induced inhibition of the low Km mitochondrial aldehyde dehydrogenase (ALDH) isozyme.
    • To compare the time course of CCl4 effects on mitochondrial ALDH with known effects on microsomal enzymes like cytochrome P-450.
    • To explore the potential of sensitive enzymes as early biomarkers for CCl4-induced biochemical damage.

    Main Methods:

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  • Administration of a single intragastric dose of CCl4 (1 ml/kg) to experimental subjects.
  • Measurement of hepatic enzyme activities, including low Km mitochondrial ALDH, cytochrome P-450 content, alcohol dehydrogenase, and low Km cytosolic ALDH at various time points (6, 12, and 24 hours) post-dosing.
  • Comparison of enzyme activities in CCl4-treated subjects to control groups.

    • Main Results:

    • Significant reduction in low Km mitochondrial ALDH activity observed as early as 6 and 12 hours after CCl4 administration.
    • Lowest values for both cytochrome P-450 content and low Km mitochondrial ALDH activity occurred at 6 hours post-CCl4, showing 44% and 37% of control, respectively.
    • Alcohol dehydrogenase activity decreased at 12 hours, while low Km cytosolic ALDH activity remained unaffected by CCl4 treatment.

    Conclusions:

    • The CCl4-induced decline in mitochondrial low Km ALDH activity occurs much earlier than previously reported, preceding other observed mitochondrial damage.
    • The rapid inhibition of mitochondrial ALDH suggests it may serve as a sensitive early indicator of CCl4 toxicity.
    • Studying early-affected enzymes like low Km ALDH can elucidate the relationship between rapid CCl4 effects (e.g., lipid peroxidation) and subsequent damage to nonmicrosomal components.