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Related Experiment Videos

Procainamide N-acetyltransferase: modulation by clofibrate and a microsomal form.

E S Kang1, P R Deaton, D Epstein

  • 1Department of Pediatrics, University of Tennessee, Memphis 38163.

General Pharmacology
|January 1, 1989
PubMed
Summary

Clofibrate treatment alters rat liver N-acetyltransferase activity, affecting procainamide detoxification. While high substrate concentrations show reduced specific activity, physiological levels reveal increased total enzyme activity and a distinct microsomal form.

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Area of Science:

  • Pharmacology
  • Biochemistry
  • Toxicology

Background:

  • N-acetyltransferase (NAT) is crucial for detoxifying xenobiotics like procainamide.
  • This enzyme is primarily located in the cytoplasmic fraction of rat liver cells.
  • Clofibrate is known to modulate various liver enzyme activities.

Purpose of the Study:

  • To investigate the effect of clofibrate treatment on rat liver N-acetyltransferase (NAT) activity.
  • To characterize the kinetic properties of NAT under varying substrate concentrations.
  • To identify potential differences between cytoplasmic and microsomal NAT forms.

Main Methods:

  • Rats were treated with clofibrate.
  • Liver fractions (cytoplasmic and microsomal) were isolated.

Related Experiment Videos

  • N-acetyltransferase activity was measured using procainamide and acetyl CoA as substrates at different concentrations.
  • Protein concentrations were determined.

    • Main Results:

    • Clofibrate treatment reduced specific NAT activity at high procainamide (100 microM) and acetyl CoA (10 or 100 microM) concentrations.
    • Despite reduced specific activity, total NAT activity remained unchanged due to a 44% increase in cytoplasmic protein.
    • At physiological substrate concentrations (10 microM), total NAT activity significantly increased (P < 0.05).
    • A distinct microsomal NAT activity was observed, unaffected by acetyl CoA concentration, unlike the cytoplasmic form.

    Conclusions:

    • Clofibrate modulates rat liver N-acetyltransferase activity, impacting procainamide detoxification.
    • The enzyme's response varies with substrate concentration, suggesting complex regulatory mechanisms.
    • The presence of a distinct, acetyl CoA-independent microsomal NAT form warrants further investigation.