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Benzidine glucuronidation in dog liver

S R Babu1, V J Wongsurawat, T V Zenser

  • 1VA Medical Center, St. Louis, MO.

Carcinogenesis
|May 1, 1993
PubMed
Summary
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Dog liver microsomes facilitate benzidine N-glucuronidation, a key step in aromatic amine-induced bladder cancer. Estriol and catechol estrones inhibit this process, potentially impacting carcinogenesis in vivo.

Area of Science:

  • Biochemistry
  • Toxicology
  • Carcinogenesis

Background:

  • Dogs serve as a model for aromatic amine-induced bladder cancer.
  • Hepatic N-glucuronidation is a proposed pathway in carcinogenesis initiation.

Purpose of the Study:

  • To evaluate benzidine N-glucuronidation in dog liver microsomes and slices.
  • To investigate the kinetic properties and inhibition of this metabolic pathway.

Main Methods:

  • Utilized dog liver microsomes and liver slices for benzidine N-glucuronidation assays.
  • Employed detergents (Emulgen 911, CHAPS) to enhance microsomal activity.
  • Determined kinetic parameters (Km, Vmax) and inhibition constants (Ki) for various chemicals.

Main Results:

Related Experiment Videos

  • Detergent treatment increased microsomal UDP-glucuronosyltransferase activity 3- to 6-fold.
  • Kinetic analysis revealed Km of 0.142 mM and Vmax of 0.65 nmol/mg protein/min.
  • Estriol, 2-aminofluorene, and 4-aminobiphenyl inhibited benzidine N-glucuronidation with varying mechanisms.

Conclusions:

  • Benzidine N-glucuronidation is a significant metabolic pathway in dogs.
  • Inhibition by estriol and catechol estrones suggests a role in aromatic amine-induced carcinogenesis.