Studies relating to a fecal mutagen.
Studies relating to a fecal mutagen.
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与粪便诱变剂有关的研究。
DOI：
10.1093/ajcn/33.11.2511
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
P. Dion
中科院分区：
文献类型：
--
作者：
W. Bruce;P. Dion
人类粪便可能含有致突变化合物，可以通过化学致癌物的短期试验证明（1）。这一观察结果使我们进行了三种类型的研究：纯化诱变剂并鉴定其结构的化学研究，评估诱变剂对结肠癌起源的重要性的流行病学研究，以及确定饮食因素对诱变剂形成的重要性的营养研究。在这份报告中，我们审查的工作，集中在一个诱变剂，一种化学物质，是活跃的试验菌株鼠伤寒沙门氏菌TA-100没有微粒体激活。尚未完成的化学研究表明，可以用有机溶剂从粪便中提取诱变剂，并可以用色谱法广泛纯化（2; A。J. Varghese，P. C.土地和W。R.布鲁斯，手稿提交出版）。它对酸、热和紫外线不稳定，并与中心在340 nm处的紫外线吸收三重峰有关。来自10个个体的致突变组分具有相似的色谱特征和恒定的吸光度与致突变性比率，在我们的条件下，一个吸光度单位在试验板上产生3000个回复突变体（A. J. Varghese，P. C.土地和W。R.布鲁斯，手稿提交出版）。由于粪便中诱变剂的含量有限、粪便中干扰化学物质的复杂性以及纯化诱变剂的不稳定性，阻碍了对该化合物的完整化学鉴别。流行病学研究包括病例对照研究和有限的人口研究。比较了17例结肠癌患者和17例年龄匹配的对照痔疮患者的诱变剂水平。两组中具有可测量诱变剂水平的个体比例相同（表1）。虽然这一结果不支持诱变剂参与结肠癌起源的建议，但可能是在疾病过程中测量得太晚，或者两组不匹配。也就是说，产生诱变剂的人群可能容易患结肠癌和痔疮。在多伦多确实存在诱变剂形成的群体差异（2; P. W. Dion，E. B。See和W. R.布鲁斯，手稿正在准备中），尽管它们与这两种疾病都没有联系。诱变剂生产的人群差异，如何-
Human feces may contain mutagenic compounds that can be demonstrated with shortterm tests for chemical carcinogens (1). This observation has led us to three types of studies: chemical studies to purify the mutagens and to identify their structures, epidemiological studies to assess the importance of the mutagens for the origin of colon cancer, and nutritional studies to determine the importance of dietary factors on the formation of the mutagens. In this report we review work that has concentrated on one mutagen, a chemical that is active on testor strain Salmonella typhimurium TA-lOO without microsomal activation. The chemical studies, as yet incomplete, show that the mutagen can be extracted from feces with organic solvents and can be extensively purified by chromatographic methods (2; A. J. Varghese, P. C. Land and W. R. Bruce, manuscript submitted for publication). It is acid, heat, and UV labile and is associated with a UV absorbtion triplet centered at 340 nm. Mutagenic fractions from 10 individuals have similar chromatographic characteristics and a constant ratio of absorbance to mutagenicity, one absorbance unit yielding 3000 revertants on a test plate under our conditions (A. J. Varghese, P. C. Land and W. R. Bruce, manuscript submitted for publication). Complete chemical identification of this compound has been hampered by the limited amount of mutagen in feces, by the complexity of interfering chemicals in feces and the lability of the purified mutagen. The epidemiological studies have included a case-control study and limited population studies. The levels of mutagens in 17 patients with colon cancer and 17 age-matched, control patients with hemorrhoids have been compared. The fraction of individuals with measurable levels of mutagen was the same in the two groups (Table 1). While this result does not support the suggestion that the mutagen is involved in the origin of colon cancer, it is possible that the measurements were taken too late in the disease process or that the two groups were overmatched. That is the populations that produce mutagens may be prone to both colon cancer and hemorrhoids. Population differences in mutagen formation do exist in Toronto (2; P. W. Dion, E. B. Bright-See and W. R. Bruce, manuscript in preparation) though they have not been associated with either disease. Population differences in mutagen production have, how-