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Abstract

Rodent models of the human isoniazid-acetylator polymorphism.

R H Tannen and W W Weber
Drug Metabolism and Disposition September 1979, 7 (5) 274-279;
R H Tannen
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W W Weber
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Abstract

Inbred strains and subpopulations of rats, laboratory mice, and deer mice were examined for individual variation in the ability to metabolize several arylamines (p-aminobenzoic acid, sulfamethazine, aniline, alpha-naphthylamine, and aminofluorene) by N-acetylation. Individual differences within species were found to be dependent upon the tissue source of N-acetyltransferase activity and the acetyl acceptor employed. Long-Evans rats possessed about 2-fold more p-aminobenzoic acid N-acetyltransferase activity in blood and liver than Sprague-Dawley rats; no strain differences could be found with sulfamethazine. Nine strains of laboratory mice (Mus musculus) were found to have considerable liver p-aminobenzoic acid N-acetyltransferase activity but only slight activity towards sulfamethazine. No strain differences were apparent in regard to liver N-acetyltransferase activity. Blood p-aminobenzoic acid N-acetyltransferase activity was distinctly polymorphic in laboratory mice; of the nine strains tested, only A/J mice did not have this activity. Partially inbred deer mice (Peromyscus maniculatus) showed a narrower phenotypic range than random-bred stock from which they were obtained, which suggests the existence of distinct subpopulations with respect to N-acetylation capacity. Presumptive evidence for multiple forms of N-acetyltransferase in liver and blood was obtained through a study of substrate specificity.

 

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Drug Metabolism and Disposition
Vol. 7, Issue 5
1 Sep 1979
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Abstract

Rodent models of the human isoniazid-acetylator polymorphism.

R H Tannen and W W Weber
Drug Metabolism and Disposition September 1, 1979, 7 (5) 274-279;

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Abstract

Rodent models of the human isoniazid-acetylator polymorphism.

R H Tannen and W W Weber
Drug Metabolism and Disposition September 1, 1979, 7 (5) 274-279;
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