NDLI: Toxicity of the heterocyclic amine batracylin: investigation of rodent N-acetyltransferase activity and potential contribution of cytochrome P450 3A

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Effects of parasitism and pesticide exposure on characteristics and functions of hemocyte populations in the freshwater snail Lymnaea palustris (Gastropoda, Pulmonata)

Toxicity of the heterocyclic amine batracylin: investigation of rodent N-acetyltransferase activity and potential contribution of cytochrome P450 3A

Hydroquinone inhibits PMA-induced activation of NFκB in primary human CD19+ B lymphocytes

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Cell Biology and Toxicology : Volume 15

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Cell Biology and Toxicology : Volume 13

Toxicity of the heterocyclic amine batracylin: investigation of rodent N-acetyltransferase activity and potential contribution of cytochrome P450 3A

Content Provider	Springer Nature Link
Author	Stevens, G.J. Burkey, J.L. McQueen, C.A.
Copyright Year	2000
Abstract	The heterocyclic amine, batracylin (BAT), is genotoxic and several lines of evidence suggest that acetylation is one step in the formation of a DNA-damaging product. The variation in susceptibility to BAT toxicity observed between rats and mice has also been linked to the acetylated product. BAT N-acetyltransferase (NAT) activity was determined in rat and mouse hepatic cytosols. Formation of acetylbatracylin (ABAT) was 6 times greater in F-344 hepatic samples compared to either mouse strain, while hepatic BAT NAT activities were similar in C57B1/6 and A/J mice. No deacetylation of ABAT was detected. In contrast, 2-aminofluorene NAT activity in C57B1/6 hepatic cytosol was twice that of the A/J strain and activities in both strains of mice were greater than in rat. Deacetylation of 2-acetylaminofluorene was detected in both species with enzyme activities in C57B1/6>A/J>F-344. Hepatocytes from the F-344 rats, the species most sensitive to BAT toxicity, were used to investigate the contribution of other biotransformation reactions to BAT cytotoxicity. Leakage of cellular lactate dehydrogenase was greater in hepatocytes from male rats than from females, increased on in vivo exposure to dexamethasone, and decreased in the presence of troleandomycin, suggesting that CYP3A-mediated biotransformation of BAT is involved in the formation of a cytotoxic product. When phenol red, a substrate for UDP-glucuronsyltransferase (UDPGT), was absent from the medium, BAT cytotoxicity was reduced. These data are consistent with a role for NAT, CYP, and UDPGT in the biotransformation of BAT.
Starting Page	31
Ending Page	39
Page Count	9
File Format	PDF
ISSN	07422091
Journal	Cell Biology and Toxicology
Volume Number	16
Issue Number	1
e-ISSN	15736822
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2000-01-01
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Pharmacology/Toxicology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Health, Toxicology and Mutagenesis Toxicology

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