ArticleDrug metabolism and disposition: the biological fate of chemicals2008
Systemic functional expression of N-acetyltransferase polymorphism in the F344 Nat2 congenic rat.
Article in Drug metabolism and disposition: the biological fate of chemicals, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Non-coding and intergenic genetic variants of human arylamineFrontiers in pharmacology · 2023Review
- Acetylator Genotype-Dependent Dyslipidemia in Rats Congenic forToxicology reports · 2020Article
- Deficiency of N-acetyltransferase increases the interactions of isoniazid with endobiotics in mouse liver.Biochemical pharmacology · 2017Article
- Article
- Folate-Dependent Hydrolysis of Acetyl-Coenzyme A by Recombinant Human and Rodent Arylamine N-Acetyltransferases.Biochemistry and biophysics reports · 2015Article
- Accuracy of various human NAT2 SNP genotyping panels to infer rapid, intermediate and slow acetylator phenotypes.Pharmacogenomics · 2012Article
- Lack of association of the N-acetyltransferase NAT1*10 allele with prostate cancer incidence, grade, or stage among smokers in Finland.Biochemical genetics · 2011Article
- Codominant expression of N-acetylation and O-acetylation activities catalyzed by N-acetyltransferase 2 in human hepatocytes.The Journal of pharmacology and experimental therapeutics · 2010Article
- Effect of N-acetyltransferase 2 polymorphism on tumor target tissue DNA adduct levels in rapid and slow acetylator congenic rats administered 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine or 2-amino-3,8-dimethylimidazo-[4,5-f]quinoxaline.Drug metabolism and disposition: the biological fate of chemicals · 2009Article
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4 authors at 1 institution in 1 country.
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Abstract
Rat lines congenic for the rat N-acetyltransferase 2 [(RAT)Nat2] gene were constructed and characterized. F344 (homozygous Nat2 rapid) males were mated to Wistar Kyoto (homozygous Nat2 slow) females to produce heterozygous F1. F1 females were then backcrossed to F344 males. Heterozygous acetylator female progeny from this and each successive backcross were identified by rat Nat2 genotyping and mated with F344 rapid acetylator males. After 10 generations of backcross mating, heterozygous acetylator brother/sister progeny were mated to produce the homozygous rapid and slow acetylator Nat2 congenic rat lines. p-Aminobenzoic acid (selective for rat NAT2) and 4-aminobiphenyl N-acetyltransferase activities were expressed in all tissues examined (liver, lung, esophagus, stomach, small intestine, colon, pancreas, kidney, skin, leukocytes, and urinary bladder in male and female rats and in breast of female and prostate of male rats). NAT2 expression in rat extrahepatic tissues was much higher than that in liver. In each tissue, activities were Nat2-genotype-dependent, with the highest levels in homozygous rapid acetylators, intermediate levels in heterozygous acetylators, and lowest in homozygous slow acetylators. Sulfamethazine (selective for rat NAT1) N-acetyltransferase activities were observed in all tissues examined in both male and female rats except for breast (females), bladder, and leukocytes. In each tissue, the activity was Nat2 genotype-independent, with similar levels in homozygous rapid, heterozygous, and homozygous slow acetylators. These congenic rat lines are useful for investigating the role of NAT2 genetic polymorphisms in susceptibility to cancers related to arylamine carcinogen exposures.
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