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Genistein Induction of Human Sulfotransferases in HepG2 and Caco‐2 Cells
Author(s) -
Chen Yue,
Huang Chaoqun,
Zhou Tianyan,
Chen Guangping
Publication year - 2008
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2008.00316.x
Subject(s) - genistein , isoflavones , caco 2 , enzyme inducer , sulfotransferase , enzyme , biochemistry , retinoic acid , western blot , chemistry , xenobiotic , phytoestrogens , biology , gene , endocrinology , cell , estrogen
Sulfotransferases are phase II drug‐metabolizing enzymes. While the induction of sulfotransferases by hormones and endogenous molecules is relatively well known, induction by xenobiotics is not well studied. Isoflavones are naturally occurring phyto‐oestrogens, mainly existing in soy food products. They have been described as health‐promoting, disease‐preventing dietary supplements and as agents with cancer‐preventive activities. Recently, isoflavones have been reported to interact with nuclear receptors, including those that are known to mediate the induction of drug‐metabolizing enzymes. In the present investigation, the isoflavone genistein was shown to be a xenobiotic inducer of human sulfotransferases in transformed human liver cells (HepG2) and colon carcinoma cells (Caco‐2). Enzymatic activity assay, Western blot, and real‐time reverse transcription–polymerase chain reaction (RT‐PCR) results demonstrated that genistein significantly induced protein and mRNA expression of human simple phenol sulfotransferase (hSULT1A1) and human dehydroepiandrosterone sulfotransferase (hSULT2A1) in HepG2 and Caco‐2 cells. The induction was time‐dependent and dose‐dependent. Western blot results agreed well with real‐time RT‐PCR results, suggesting that induction occurred at the gene transcription level. This isoflavone is the first nutritionally related phyto‐oestrogen shown to induce human sulfotransferases in HepG2 and Caco‐2 cells.