Differential selectivity of cytochrome P450 inhibitors against probe substrates in human and rat liver microsomes

Br J Clin Pharmacol. 1998 Feb;45(2):107-14. doi: 10.1046/j.1365-2125.1998.00679.x.

Abstract

Aims: Chemical inhibitors of cytochrome P450 (CYP) are a useful tool in defining the role of individual CYPs involved in drug metabolism. The aim of the present study was to evaluate the selectivity and rank the order of potency of a range of isoform-selective CYP inhibitors and to compare directly the effects of these inhibitors in human and rat hepatic microsomes.

Methods: Four chemical inhibitors of human cytochrome P450 isoforms, furafylline (CYP1A2), sulphaphenazole (CYP2C9), diethyldithiocarbamate (CYP2E1), and ketoconazole (CYP3A4) were screened for their inhibitory specificity towards CYP-mediated reactions in both human and rat liver microsomal preparations. Phenacetin O-deethylation, tolbutamide 4-hydroxylation, chlorzoxazone 6-hydroxylation and testosterone 6beta-hydroxylation were monitored for enzyme activity.

Results: Furafylline was a potent, selective inhibitor of phenacetin O-deethylation (CYP1A2-mediated) in human liver microsomes (IC50 = 0.48 microM), but inhibited both phenacetin O-deethylation and tolbutamide 4-hydroxylation (CYP2C9-mediated) at equimolar concentrations in rat liver microsomes (IC50 = 20.8 and 24.0 microM respectively). Sulphaphenazole demonstrated selective inhibition of tolbutamide hydroxylation in human liver microsomes but failed to inhibit this reaction in rat liver microsomes. DDC demonstrated a low level of selectivity as an inhibitory probe for chlorzoxazone 6-hydroxylation (CYP2E1-mediated). DDC also inhibited testosterone 6beta-hydroxylation (CYP3A-mediated) in man and rat, and tolbutamide 4-hydroxylase activity in rat. Ketoconazole was a very potent, selective inhibitor of CYP3A4 activity in human liver (IC50 = 0.04 microM). Although inhibiting CYP3A in rat liver it also inhibited all other reactions at concentrations < or = 5 microM.

Conclusions: It is evident that CYP inhibitors do not exhibit the same selectivity in human and rat liver microsomes. This is due to differential selectivity of the inhibitors and/or differences in the CYP isoform responsible for metabolism in the different species.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chlorzoxazone / antagonists & inhibitors
  • Chlorzoxazone / metabolism
  • Cytochrome P-450 Enzyme Inhibitors*
  • Cytochrome P-450 Enzyme System / metabolism
  • Ditiocarb / pharmacology
  • Enzyme Inhibitors / pharmacology*
  • Humans
  • Ketoconazole / pharmacology
  • Kinetics
  • Male
  • Microsomes, Liver / drug effects*
  • Microsomes, Liver / metabolism
  • Phenacetin / antagonists & inhibitors
  • Phenacetin / metabolism
  • Rats
  • Rats, Wistar
  • Substrate Specificity
  • Sulfaphenazole / pharmacology
  • Testosterone / antagonists & inhibitors
  • Testosterone / metabolism
  • Theophylline / analogs & derivatives
  • Theophylline / pharmacology
  • Tolbutamide / antagonists & inhibitors
  • Tolbutamide / metabolism

Substances

  • Cytochrome P-450 Enzyme Inhibitors
  • Enzyme Inhibitors
  • Sulfaphenazole
  • Testosterone
  • Cytochrome P-450 Enzyme System
  • Tolbutamide
  • Ditiocarb
  • Theophylline
  • furafylline
  • Phenacetin
  • Chlorzoxazone
  • Ketoconazole