N-acetylation of drugs. Pharmacogenetic studies in rabbits selected for their acetylator characteristics.
Studies on acetylation of sulfadiazine, isoniazid, and p-aminobenzoic acid in selected lines of slow and rapid acetylator rabbits are described. Pedigree analysis of rabbits classified as slow or rapid sulfadiazine acetylators confirmed previous studies that the rate of sulfadiazine elimination (acetylation) is genetically controlled, with rapid elimination dominant over slow elimination of the drug. Pharmacokinetic studies in rabbits of specified sulfadiazine acetylator genotypes with isoniazid and p-aminobenzoic acid show that the rate of isoniazid elimination is under the same genetic control as is sulfadiazine, whereas the rate of p-aminobenzoic acid elimination is not. A new drug acetylation polymorphism, which controls the rate of enzymatic acetylation of p-aminobenzoic acid in peripheral blood cells and which is related to the sulfadiazine acetylation polymorphism, is described.
N-acetylation of drugs. Pharmacogenetic studies in rabbits selected for their acetylator characteristics. Studies on acetylation of sulfadiazine, isoniazid, and p-aminobenzoic acid in selected lines of slow and rapid acetylator rabbits are described. Pedigree analysis of rabbits classified as slow or rapid sulfadiazine acetylators confirmed previous studies that the rate of sulfadiazine elimination (acetylation) is genetically controlled, with rapid elimination dominant over slow elimination of the drug. Pharmacokinetic studies in rabbits of specified sulfadiazine acetylator genotypes with isoniazid and p-aminobenzoic acid show that the rate of isoniazid elimination is under the same genetic control as is sulfadiazine, whereas the rate of p-aminobenzoic acid elimination is not. A new drug acetylation polymorphism, which controls the rate of enzymatic acetylation of p-aminobenzoic acid in peripheral blood cells and which is related to the sulfadiazine acetylation polymorphism, is described.