Molecular mechanisms for the regulation of aryl sulfotransferase IV expression during 2-acetylaminofluorene-induced hepatocarcinogenesis in rat.
The dietary administration of 2-acetylaminofluorene to male rats to induce hepatocarcinogenesis causes a reversible as well as persistent down-modulation of N-hydroxy-2AAF sulfotransferase activity. Studies are presented which indicate that several molecular mechanisms may be involved in the down-regulation of sulfotransferase activity and expression. These include carcinogen-mediated inactivation of sulfotransferase mRNA or protein, interference with hormonal regulation of sulfotransferase expression, and, mutation of the sulfotransferase gene.
Ringer
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Biomedical Division, S.R. Noble Foundation, Inc., Ardmore, OK.
Yerokun
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T
Khan
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D015073:2-Acetylaminofluorene / Q000008:administration & dosage / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D015536:Down-Regulation; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects*; D006728:Hormones / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000201:enzymology*; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced*; D008297:Male; D009154:Mutation / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D015238:Sulfotransferases / Q000235:genetics* / Q000378:metabolism
D006728:Hormones; D012333:RNA, Messenger; D015073:2-Acetylaminofluorene; D015238:Sulfotransferases; C077557:tyrosine-ester sulfotransferase