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  • Title: Genotoxicity of quercetin in cultured mammalian cells.
    Author: van der Hoeven JC, Bruggeman IM, Debets FM.
    Journal: Mutat Res; 1984 Apr; 136(1):9-21. PubMed ID: 6717476.
    Abstract:
    The naturally occurring flavonol, quercetin, was investigated concerning its ability to induce SCEs and HGPRT-deficient mutants in V79 Chinese hamster cells, and HGPRT- and TK-deficient mutants in mouse lymphoma L5178Y cells. V79 cells were exposed to quercetin in monolayer, under exponential growing condition, in suspension in the presence of liver homogenate, and in co-cultivation with primary chick embryo hepatocytes. No induction of HGPRT-deficient mutants was observed. Furthermore, under standard conditions, no relevant increase in the number of SCEs could be detected. If, however, the cells were exposed simultaneously to quercetin and BrdUrd, a greater than 3-fold increase in the number of SCEs was observed. This induction was dose-related for both quercetin and BrdUrd. Treatment of L5178Y cells with quercetin did not result in an increase in HGPRT-deficient mutants. At the TK locus a weak increase in the number of TK-deficient mutants was found. Addition of liver homogenate abolished this effect. The inability of quercetin to induce SCEs and point mutations in mammalian cells, and the fact that the clastogenic effect of quercetin, whereby it induces TK-deficient mutants in mouse lymphoma L5178Y cells, is abolished by the addition of liver homogenate, may explain the negative outcome of the majority of carcinogenicity studies on quercetin in mammals.
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