A desert mushroom called Al-faga (Tirmania pinoyi) was sequentially extracted with boiling water, chloroform and ethanol under reflux conditions. The water extract was freeze-dried while the organic solvents were fully evaporated to obtain residues, which were redissolved in dimethylsulphoxide and then tested for mutagenicity in the Ames assay using the Salmonella tester strains TA98 and TA100. The aqueous extract failed to show any mutagenic activity while the chloroform extract proved to be mutagenic with and without metabolic activation. The ethanol extract was not mutagenic in the same tests. However, ethanol extract combined with known carcinogens like benzo[a]pyrene or 7,12-dimethyl-benz[a]anthracene (with metabolic activation) inhibited the carcinogen-induced mutagenicity in a dose-dependent manner. These results show that both mutagens and antimutagens may be extracted from a single food item by using different solvents.

Summary Experiments were performed on cultured Chinese hamster ovary cells exposed to haematoporphyrin derivative (HpD) The photosensitizing drug haematoporphyrin derivative (HpD) and light are demonstrating increasing promise in photodynamic therapy (PDT) for cancer (Dougherty, 1984 degenerative changes in mitochondria, ribosomes, endoplasmic reticulum and nuclear chromatin (Kato et al., 1984;Moan et al., 1982), and inhibits mitochondrial cytochrome c oxidase activity (Gibson & Hill, 1983). All effects were directly correlated with HpD dose and light exposure level.In the present work, the effect of sublethal doses of photoactivated HpD on DNA and protein synthesis and on progression through the cell cycle have been studied in cultured Chinese hamster ovary (CHO) cells.

Ethanol extract of Senokot tablets (Cassia senna concentrate used as vegetable laxative), was found to be non-mutagenic while it inhibited the mutagenicity of benzo[a]pyrene, shamma, aflatoxin B1 and methyl methanesulfonate in the Ames histidine reversion assay using the Salmonella typhimurium tester strain TA98. While the Senokot extract completely inhibited the mutagenicity of promutagens (i.e. metabolic activation dependent) like benzo[a]pyrene and shamma, it reduced the mutagenic activity of the direct acting mutagen methyl methanesulfonate by only 58%. The mutagen aflatoxin B1 showed a 25-fold increase in the number of histidine revertants per plate at low concentrations (1.0-4.0 micrograms/plate) in the presence of metabolic activation system while at high concentrations (10.0-30.0 micrograms/plate) it proved to be weakly mutagenic (with a 5-fold increase in the number of histidine revertants/plate) without metabolic activation. The Senokot extract completely inhibited the mutagenic effect of low concentrations of aflatoxin B1 in the presence of metabolic activation but not that resulting from higher concentrations without metabolic activation. The results obtained with benzo[a]pyrene, shamma and aflatoxin B1 indicated that the antimutagenic effects of Senokot extract could be largely due to an interaction with the metabolic process involved in the activation of procarcinogens. However, the results obtained with methyl methanesulfonate suggested that factors in Senokot may also interact with direct mutagens to produce some antimutagenic effects. An ethanol extract of crude senna leaves found to be weakly mutagenic also inhibited (though less than Senokot) the mutagenic effect of benzo[a]pyrene suggesting that the antimutagenic principle is present in the complex plant material itself.

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