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Effects of quercetin on drug metabolizing enzymes and oxidation of 2', 7-dichlorofluorescin in HepG2 cells

School of Biochemistry, The University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK

N. Helsby

School of Biochemistry, The University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK

JK Chipman

School of Biochemistry, The University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK

1 The effects of quercetin on drug metabolising enzymes and oxygen radicals were studied in human HepG2 cells.

2 Cytotoxicity of quercetin in HepG2 cells was seen at 50 µM and above as evaluated by lactate dehydrogen ase (LDH) leakage, neutral red (NR) uptake, and 3-(4,5- dimethyl-thiazol-2yl)-2,5-diphenyl tetrazolium bro mide (MTT) reduction.

3 Quercetin inhibited activity of human cytochrome P- 450 towards ethoxycoumarin and ethylresorufin at relatively low substrate concentrations (0.1 µM and above).

4 In comparison to induction by the positive control (β- naphthoflavone; 1.0 µM), quercetin did not signifi cantly induce the metabolism of ethoxycoumarin or glutathione-S-transferase (GST) protein or activity.

5 Response elements for human CYP1A1, GSTa, xenobiotic response element (XRE), fos, HSP70, CRE, p53, NFB and DNA damage (GADD) in HepG2 cells were not activated by quercetin.

6 Quercetin exhibited antioxidant activity in HepG2 cells as evidenced by its ability to inhibit the oxidation of the fluorochrome dichlorofluorescin.

7 The results indicate a range of potential beneficial effects of quercetin with respect to the influence on carcinogen-metabolising enzymes, scavenging of re active oxygen species and a lack of stress response in HepG2 cells.

Key Words: quercetin • flavonoids • cytochrome P450 • reactive oxygen

Human & Experimental Toxicology, Vol. 16, No. 12, 700-708 (1997)
DOI: 10.1177/096032719701601202


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