Contribution of phenolic and quinonoid structures in the mutagenicity of the edible mushroom Agaricus bisporus.

The objectives of this work were to establish the contribution of agaritine in the mutagenicity of ethanolic extracts from Agaricus bisporus and to examine the possible involvement of phenolic and quinonoid compounds in the mutagenic response to mushrooms. The mutagenic profile of agaritine in the Ames test, in the absence of an activation system, was different from that of the mushroom ethanolic extracts. Incorporation of rat hepatic cytosolic fractions as the activation system increased the mutagenicity of the mushroom ethanolic extracts in Salmonella typhimurium strain TA 104 but did not influence the mutagenicity of agaritine. It was concluded that agaritine is not the principal mutagenic component in the mushroom. The cytosol-induced mutagenicity of the mushroom extracts required NADPH, and was inhibited by dicoumarol and menadione. Moreover, the mutagenic response in the presence of cytosolic fractions was inhibited by superoxide dismutase, catalase, glutathione and dimethyl sulfoxide, thus implicating reactive oxygen species. Finally, tyrosinase, the enzyme converting mushroom phenols to quinones, increased the mutagenicity of the mushroom extracts. Collectively, the above results indicate that phenolic and quinonoid compounds, presumably through the generation of reactive oxygen species, may play a significant role in the mutagenicity of mushroom extracts.