Induction of peroxisomal enzymes and palmitoyl-CoA hydrolase in rats treated with cholestyramine and nicotinic acid.
Male Wistar rats were given 200 mg/kg/day nicotinic acid or 1000 mg/kg/day cholestyramine by stomach tube for ten days. Peroxisomal palmitoyl-CoA oxidation (cyanide-insensitive) and the activities of palmitoyl-CoA hydrolase and urate oxidase were significantly increased in the total liver homogenate. Subcellular fractionation showed enhanced enzyme activities after drug treatment mainly in the peroxisome-containing fractions. The increase in urate oxidase activity and its subcellular distribution suggest that the tested drugs induce core-containing peroxisomes. The findings are similar to those previously reported with low doses of peroxisome-proliferating hypolipidemic drugs and with acetylsalicylic acid, a drug which is structurally similar to nicotinic acid. Since cholestyramine is not absorbed, its influence on hepatic enzymes probably occurs indirectly as a consequence of enhanced catabolism of cholesterol.
D000818:Animals; D002792:Cholestyramine Resin / Q000494:pharmacology*; D004790:Enzyme Induction / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D008297:Male; D008830:Microbodies / Q000187:drug effects / Q000201:enzymology*; D009525:Niacin / Q000494:pharmacology*; D009929:Organ Size / Q000187:drug effects; D010170:Palmitoyl-CoA Hydrolase / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains; D013869:Thiolester Hydrolases / Q000096:biosynthesis*; D014503:Urate Oxidase / Q000096:biosynthesis
D002792:Cholestyramine Resin; D009525:Niacin; D014503:Urate Oxidase; D013869:Thiolester Hydrolases; D010170:Palmitoyl-CoA Hydrolase