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J Agric Food Chem. 2008 Jan 23;56(2):577-83. Epub 2007 Dec 20.

Metabolic conversion of dietary quercetin from its conjugate to active aglycone following the induction of hepatocarcinogenesis in fisher 344 rats.

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Department of Biosystems Science, Graduate School of Science and Technology, Kobe University, Rokkodai, Nada, Kobe 657-8501, Japan.


Quercetin exhibits a potent anticarcinogenic activity. However, ingested quercetin circulates as the glucuronide/sulfate conjugates, which are less active compared to the aglycone in healthy individuals. This study aimed to develop further understandings of the cancer-preventing mechanism with dietary quercetin. According to a two-stage hepatocarcinogenesis model with N-diethylnitrosamine (DEN) and phenobarbital (PB), preneoplasms were induced specifically in the liver of Fisher 344 rats. In the liver, glutathione S-transferase placental form (GST-P) positive foci were produced 14 weeks later. beta-Glucuronidase activity increased significantly in the liver by 1.2-fold in the DEN/PB group compared to the activity in a saline group. In the kidney, thymus, lung, heart, and plasma, the activities were similar between both groups. When quercetin was dosed intragastrically 15 min before sacrifice, the aglycone level of quercetin in liver was significantly 1.9-fold higher in the DEN/PB group than in the saline group. On the other hand, quercetin was dosed to rats 3 times a week for 14 weeks. The treatment kept the aglycone level of quercetin at a significantly higher level and tended to suppress the formation of GST-P positive foci. The increase in beta-glucuronidase activity with carcinogenesis induction became insignificant following the frequent doses of quercetin. It was considered that quercetin aglycone played a preventative role and, thus, the conjugates were converted to the active aglycone by beta-glucuronidase that was induced by the generation of preneoplasms.

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