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Abstract
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.