Investigation of Testosterone, Androstenone, and Estradiol Metabolism in HepG2 Cells and Primary Culture Pig Hepatocytes and Their Effects on 17 beta HSD7 Gene Expression

文献类型： 外文期刊

第一作者： Chen, Gang

作者： Chen, Gang;Li, Sicong;Chen, Ailiang;Yang, Shuming;Dong, Xinxing;Bai, Ying;Fang, Meiying;Zamaratskaia, Galia;Doran, Olena

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期刊名称：PLOS ONE （ 影响因子：3.24； 五年影响因子：3.788 ）

ISSN： 1932-6203

年卷期： 2012 年 7 卷 12 期

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收录情况： SCI

摘要： Steroid metabolism is important in various species. The accumulation of androgen metabolite, androstenone, in pig adipose tissue is negatively associated with pork flavor, odour and makes the meat unfit for human consumption. The 17 beta-hydroxysteroid dehydrogenase type 7 (17 beta HSD7) expressed abundantly in porcine liver, and it was previously suggested to be associated with androstenone levels. Understanding the enzymes and metabolic pathways responsible for androstenone as well as other steroids metabolism is important for improving the meat quality. At the same time, metabolism of steroids is known to be species- and tissue-specific. Therefore it is important to investigate between-species variations in the hepatic steroid metabolism and to elucidate the role of 17 beta HSD7 in this process. Here we used an effective methodological approach, liquid chromatography coupled with mass spectrometry, to investigate species- specific metabolism of androstenone, testosterone and beta-estradiol in HepG2 cell line, and pig cultured hepatocytes. Species- and concentration-depended effect of steroids on 17 beta HSD7 gene expression was also investigated. It was demonstrated that the investigated steroids can regulate the 17 beta HSD7 gene expression in HepG2 and primary cultured porcine hepatocytes in a concentration-dependent and species- dependent pattern. Investigation of steroid metabolites demonstrated that androstenone formed a 3'-hydroxy compound 3 beta-hydroxy-5 alpha-androst-16-ene. Testosterone was metabolized to 4-and-rostene-3,17-dione. Estrone was found as the metabolite for beta-estradiol. Inhibition study with 17 beta HSD inhibitor apigenin showed that apigenin didn't affect androstenone metabolism. Apigenin at high concentration (50 mu M) tends to inhibit testosterone metabolism but this inhibition effect was negligible. Beta-estradiol metabolism was notably inhibited with apigenin at high concentration. The study also established that the level of testosterone and b-estradiol metabolites was markedly increased after Co-incubation with high concentration of apigenin. This study established that 17bHSD7 is not the key enzyme responsible for androstenone and testosterone metabolism in porcine liver cells.

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