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Alterations of hepatic drug metabolising system due to dimethylformamide (DMF)

K Fujishiro1, K Imazu, Y Makita

  • 1Occupational Health Training Center, University of Occupational and Environmental Health, Kitakyushu.

Fukuoka Igaku Zasshi = Hukuoka Acta Medica
|July 1, 1996
PubMed

Insights

Repeated N, N-dimethylformamide (DMF) exposure in rats altered liver drug metabolism, decreasing cytochrome P-450 and increasing glutathione enzymes. These changes occurred without significant increases in serum transaminase levels, suggesting a specific mechanism for DMF hepatotoxicity.

Area of Science:

  • Toxicology
  • Hepatology
  • Biochemistry

Background:

  • N, N-dimethylformamide (DMF) is an industrial solvent with potential toxic effects.
  • Understanding DMF's impact on liver function and metabolism is crucial for occupational safety.

Purpose of the Study:

  • To investigate the effects of repeated N, N-dimethylformamide (DMF) exposure on the liver and associated enzyme systems in rats.
  • To elucidate the mechanisms underlying DMF-induced hepatotoxicity.

Main Methods:

  • Wistar male rats were administered DMF (1.0 ml/kg) subcutaneously, three times weekly for two weeks.
  • Evaluated body weight, relative organ weights, hematology, serum transaminases (GOT, GPT), and hepatic enzyme activities (cytochrome P-450, b5, reductase, glutathione peroxidase, reductase, and S-transferase).

Main Results:

  • DMF exposure suppressed body weight gain and increased relative liver, spleen, and kidney weights.
  • Significant decreases in hepatic microsomal protein (30%) and cytochrome P-450 (38%) were observed.
  • Glutathione reductase (16%) and glutathione S-transferase (64%) activities significantly increased, while glutathione peroxidase remained unchanged. Serum transaminases showed no significant alterations.

Conclusions:

  • Repeated DMF exposure alters the hepatic drug-metabolizing system, specifically impacting cytochrome P-450 and glutathione metabolism.
  • The observed changes in enzyme activities, without elevated transaminases, suggest a distinct pathway for DMF hepatotoxicity.
  • These findings contribute to understanding the toxicological mechanisms of DMF in the liver.

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