Rowett Institute of Nutrition and Health, University of Aberdeen Aberdeen, UK.
Front Pharmacol. 2011 Mar 3;2:4. doi: 10.3389/fphar.2011.00004. eCollection 2011.
DNA damage is an essential component of the genesis of colonic cancer. Gut microbial products and food components are thought to be principally responsible for the damage that initiates disease progression. Modified Ames tests and Comet assays have been developed for measuring mutagenicity and genotoxicity. Their relevance to oncogenesis remains to be confirmed, as does the relative importance of different mutagenic and genotoxic compounds present in fecal water and the bacteria involved in their metabolism. Dietary intervention studies provide clues to the likely risks of oncogenesis. High-protein diets lead to increases in N-nitroso compounds in fecal water and greater DNA damage as measured by the Comet assay, for example. Other dietary interventions, such as non-digestible carbohydrates and probiotics, may lead to lower fecal genotoxicity. In order to make recommendations to the general public, we must develop a better understanding of how genotoxic compounds are formed in the colon, how accurate the Ames and Comet assays are, and how diet affects genotoxicity.
DNA 损伤是结直肠癌发生的一个重要组成部分。肠道微生物产物和食物成分被认为主要负责引发疾病进展的损伤。已经开发了修改后的艾姆斯试验和彗星试验来测量诱变和遗传毒性。它们与肿瘤发生的相关性仍有待证实，粪便水中存在的不同诱变和遗传毒性化合物以及参与其代谢的细菌的相对重要性也有待证实。饮食干预研究为肿瘤发生的可能风险提供了线索。例如，高蛋白饮食会导致粪便水中的 N-亚硝基化合物增加，并通过彗星试验测量到更大的 DNA 损伤。其他饮食干预，如不可消化的碳水化合物和益生菌，可能会导致粪便遗传毒性降低。为了向公众提出建议，我们必须更好地了解遗传毒性化合物在结肠中是如何形成的，艾姆斯试验和彗星试验的准确性如何，以及饮食如何影响遗传毒性。
