Biological targets and phase II metabolism of chemopreventive licorice compounds. Biological targets and phase II metabolism of chemopreventive licorice.

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Biological targets and phase II metabolism of chemopreventive licorice compounds. Biological targets and phase II metabolism of chemopreventive licorice compounds. A, The GI-specific compound, LicA, is a Michael acceptor that can covalently modify Keap1 to upregulate the detoxification enzyme, NQO1, in MCF-10A and liver cells (21) as well as in liver tissue. LicA is also an AhR antagonist that can downregulate P450 1A1/1B1-mediated estrogen oxidative metabolism (11). In this animal model (ACI rats), GG and GI increased P450 1A1 gene expression (CYP1A1) in mammary tissue (Fig. 5B). In addition, GI also decreased P450 1B1 gene expression (CYP1B1) in the mammary gland as indicated with arrows. B, LicA is mainly metabolized to various glucuronides by UDP-glucuronosyltransferases (UGT; Supplementary Fig. S2). As a Michael acceptor, LicA also forms GSH conjugates. In the liver and serum, LicA sulfate conjugates catalyzed by sulfotransferases (SULT) were detected as minor metabolites (Supplementary Fig. S2). Shuai Wang et al. Cancer Prev Res 2018;11:819-830 ©2018 by American Association for Cancer Research