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• W2076617022 abstract "Down regulation of aryl sulfotransferase IV (AST IV) in promotion/progression of liver carcinogenesis byN-2-fluorenylacetamide (2-FAA) has been established. This study examined whether the C-9 oxidized metabolites of 2-FAA, which have recently been shown to promote diethylnitrosamine (DEN)-initiated liver carcinogenesis in male Sprague–Dawley rats, effect the above change. Hence, in DEN-initiated rats, the effects of promoting regimens of 9-OH-2-FAA or 9-oxo-2-FAA, 15 oral doses at 50 and 100 μmol/kg of body weight, were compared to those of 2-FAA at 50 μmol/kg of body weight and of the vehicle on the activity ofN-hydroxy(OH)-2-FAA sulfotransferase (ST), an isozyme of AST IV and AST IV expression and distribution. Relative to the vehicle, treatment with the fluorenyl compounds led to decreased levels in hepaticN-OH-2-FAA ST activity and development of hepatic nodules and tumors which had still lower levels of the ST activity than the respective remnant livers. At ∼8 months after treatment with the C-9-oxidized compounds at doses twice that of 2-FAA, the extents of decreases in the hepaticN-OH-2-FAA ST activity and cytosolic AST IV protein in tumors were comparable to those with 2-FAA. Immunocytochemical analysis showed close association of AST IV deficiency with neoplastic liver lesions. In comparison toN-OH-2-FAA, 9-OH-2-FAA had only low and 9-oxo-2-FAA lacked sulfate acceptor activity in the presence of male rat liver cytosol or AST IV. At 3.3-fold greater concentration thanN-OH-2-FAA, 9-oxo-2-FAA inhibited (27%) the sulfate acceptor activity ofN-OH-2-FAA in the presence of AST IV, which suggested interference by 9-oxo-2-FAA at the active site. Although the C-9-oxidized compounds do not appear to be substrates forN-OH-2-FAA ST, their ability to cause a decrease inN-OH-2-FAA ST activity and protein similar to that of 2-FAA supports their role in hepatocarcinogenesis. Whereas 9-OH-2-FAA had a 3.9-fold greater sulfate acceptor activity in the presence of female than male rat liver cytosol and inhibited dehydroepiandrosterone ST activity of female rat liver,N-OH-2-FAA and 9-oxo-2-FAA inhibited estrone ST activity of male rat liver, suggesting that the C-9-oxidized compounds as well asN-OH-2-FAA are substrates for STs other than AST IV." @default.
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• W2076617022 date "1997-04-01" @default.
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• W2076617022 title "Aryl Sulfotransferase IV Deficiency in Rat Liver Carcinogenesis Initiated with Diethylnitrosamine and Promoted withN-2-Fluorenylacetamide or Its C-9-Oxidized Metabolites" @default.
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• W2076617022 doi "https://doi.org/10.1006/exmp.1997.2211" @default.
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