Add time:08/10/2019         Source:sciencedirect.com

The hepatic metabolism of the 16-androstene (cas 16506-82-4) steroids was investigated using isolated porcine hepatocytes. This study demonstrated that the liver is capable of producing both phase I and phase II steroid metabolites from 16-androstene steroid precursors. 16-Androstene metabolites were recovered by solid-phase extraction and identified by gas chromatography–mass spectrometry (GC–MS). When 5α-androstenone was provided as a substrate, both 3β- and 3α-androstenol were produced as well as a metabolite that showed evidence of hydroxylation. Incubations with the various 16-androstene steroids produced metabolic profiles which suggested that the major role of the liver is phase II conjugation. Sulfoconjugated 16-androstene steroids included androstadienol, 5α-androstenone, 3β-, 3α-androstenol, and possibly the hydroxylated metabolite of 5α-androstenone. It was determined that hydroxysteroid sulfotransferase (HST) is the likely candidate for the sulfoconjugation of the 16-androstene steroids within the liver. Despite the capacity of the hepatocytes to sulfoconjugate the 16-androstene steroids, the principle metabolites produced from incubations with 5α-androstenone, 3β-, and 3α-androstenol were glucuronide conjugates, accounting for approximately 68% of all phase II metabolism. These findings underline the importance of steroid conjugation and suggest that hepatic metabolism of the 16-androstene steroids may influence the levels of 5α-androstenone present in the circulation, and thus, capable of accumulating in fat.

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