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Differential modulation of the genotoxicity of food carcinogens by naturally occurring monomeric and dimeric polyphenolics

AuthorsCatterall, Fenton; Souquet, Jean-Marc; Cheynier, Veronique; Pascual-Teresa, Sonia de CSIC ORCID ; Santos-Buelga, Celestino; Clifford, Michael N.; Ioannides, Costas
Issue Date2000
CitationEnvironmental and Molecular Mutagenesis 35(2): 86-89 (2000)
AbstractNaturally occurring dimeric polyphenolics and their gallate esters were isolated from grape seeds, almond fruits, and apple skin, and their ability to modulate the mutagenicity of food carcinogens was studied in the Ames test, and compared to that of the monomeric green tea flavonols, (+)-catechin and (−)-epicatechin. Neither the monomeric nor the dimeric polyphenols and their galloylated derivatives influenced the mutagenic activity elicited by the indirectly acting food carcinogens benzo[a]pyrene and 2-amino-3-methylimidazo-[4,5-f]quinoline (IQ), in the presence of a hepatic activation system derived from Aroclor 1254–treated rats; the only exception was the B7 dimer, which, at concentrations above 1 μM, suppressed the mutagenicity of IQ. None of the polyphenolics modulated the mutagenic activity elicited by the directly acting carcinogen N′-methyl-N′-nitro-nitrosoguanidine (MNNG). In contrast, all the dimeric polyphenols and the galloylated metabolites, at concentrations over 1 μM, potentiated the mutagenic activity induced by the indirectly acting carcinogen N-nitrosopyrrolidine, in the presence of an activation system derived from isoniazid-treated rats. In conclusion, dimeric polyphenols and galloylated derivatives of plant origin are unlikely to influence the initiation stage of the carcinogenicity of chemicals through mechanisms that involve inhibition of their cytochrome P450–mediated bioactivation or scavenging of the reactive, genotoxic intermediates.
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