al-Dakan A A, al-Tuffail M, Hannan M A
Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
Pharmacol Toxicol. 1995 Oct;77(4):288-92. doi: 10.1111/j.1600-0773.1995.tb01029.x.
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.
番泻叶制剂（用作植物性泻药的番泻叶浓缩物）的乙醇提取物在使用鼠伤寒沙门氏菌测试菌株TA98的Ames组氨酸回复突变试验中被发现无致突变性，同时它抑制了苯并[a]芘、山奈酚、黄曲霉毒素B1和甲基磺酸甲酯的致突变性。虽然番泻叶提取物完全抑制了像苯并[a]芘和山奈酚这类前致癌物（即代谢活化依赖性）的致突变性，但它仅使直接作用的诱变剂甲基磺酸甲酯的致突变活性降低了58%。诱变剂黄曲霉毒素B1在代谢活化系统存在的情况下，低浓度（1.0 - 4.0微克/平板）时每平板组氨酸回复突变体数量增加了25倍，而在高浓度（10.0 - 30.0微克/平板）时，在没有代谢活化的情况下被证明是弱诱变剂（每平板组氨酸回复突变体数量增加5倍）。番泻叶提取物在代谢活化存在的情况下完全抑制了低浓度黄曲霉毒素B1的诱变作用，但没有抑制高浓度且无代谢活化时产生的诱变作用。用苯并[a]芘、山奈酚和黄曲霉毒素B1得到的结果表明，番泻叶提取物的抗诱变作用可能主要归因于与前致癌物活化过程中涉及的代谢过程相互作用。然而，用甲基磺酸甲酯得到的结果表明，番泻叶中的成分也可能与直接诱变剂相互作用以产生一些抗诱变作用效果。粗番泻叶的乙醇提取物被发现有弱致突变性，它也抑制了（尽管比番泻叶制剂抑制程度小）苯并[a]芘的诱变作用，这表明抗诱变原理存在于这种复杂的植物材料本身。
