Lack of an Inducible Effect of Dietary Soy Isoflavones on the mRNA Abundance of Hepatic Cytochrome P-450 Isozymes in Rats

  • KISHIDA Taro
    Department of Biological Resources, Faculty of Agriculture, Ehime University
  • NAGAMOTO Manabu
    Department of Biological Resources, Faculty of Agriculture, Ehime University
  • OHTSU Yohhei
    Department of Biological Resources, Faculty of Agriculture, Ehime University
  • WATAKABE Miho
    Department of Biological Resources, Faculty of Agriculture, Ehime University
  • OHSHIMA Daisuke
    Department of Biological Resources, Faculty of Agriculture, Ehime University
  • NASHIKI Kunitaka
    Department of Biological Resources, Faculty of Agriculture, Ehime University
  • MIZUSHIGE Takafumi
    Department of Biological Resources, Faculty of Agriculture, Ehime University
  • IZUMI Tohru
    Research and Development Division, Kikkoman Corporation
  • OBATA Akio
    Research and Development Division, Kikkoman Corporation
  • EBIHARA Kiyoshi
    Department of Biological Resources, Faculty of Agriculture, Ehime University

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Modulation of the activity and content of cytochrome P-450 (CYP) in hepatic microsomes may be important to human health since these enzymes activate and inactivate a wide range of xenobiotics and food components. Regulation of the inducibility of most CYPs involves transcriptional regulation and post-transcriptional mRNA stabilization. We examined in the present study the effect of dietary soy isoflavone (0–300 mg of isoflavone/kg of diet) on the mRNA abundance of rat hepatic CYP1A1, CYP1A2, CYP2B1/2, CYP2C11, CYP2E1, CYP3A1, CYP3A2 and CYP4A1 by quantitative competitive RT-PCR and real-time monitored RT-PCR. A fermented soy extract containing 155 mg/g of genistein, 127 mg/g of daidzein, and other minor isoflavones was used as the isoflavone source. The dietary soy isoflavone had no affect on the hepatic mRNA abundance of these CYPs. The results by both methods were well matched and indicate that the dietary soy isoflavone did not cause the induction of CYPs by transcriptional step-up regulation or post-transcriptional mRNA stabilization.

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