Post-initiation effects of chlorophyllin and indole-3-carbinol in rats given 1,2-dimethylhydrazine or 2-amino-3-methyl- imidazo.
Post-initiation effects of chlorophyllin and indole-3-carbinol in rats given 1,2-dimethylhydrazine or 2-amino-3-methyl- imidazo.
复制标题
给予 1,2-二甲基肼或 2-氨基-3-甲基-咪唑的大鼠中叶绿素和吲哚-3-甲醇的后引发效应。
DOI：
10.1093/carcin/22.2.309
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发表时间：
2001
期刊：
影响因子：
4.7
通讯作者：
Dashwood,RH
中科院分区：
文献类型：
--
作者：
Xu,M;Orner,GA;Bailey,GS;Stoner,GD;Horio,DT;Dashwood,RH
叶绿酸（CHL）是叶绿素的水溶性衍生物，叶绿素是绿色和叶菜中普遍存在的色素，而吲哚-3-甲醇（I3 C）存在于十字花科蔬菜如卷心菜、花椰菜和花椰菜中。在大鼠开始与1，2-二甲基肼（DMH），CHL和I3 C据报道，促进或增强结肠肿瘤的发病率时，他们被管理后，或期间和之后的致癌物暴露，分别。起始后给予的相同化合物抑制由杂环胺如2-氨基-3-甲基咪唑[4，5-f]喹啉（IQ）诱导的结肠异常隐窝的形成，但在后面的研究中未检查肿瘤抑制。在本研究中，雄性F344大鼠在为期1年的研究的前5周内接受IQ或DMH治疗; IQ在饮食中给予（0.03%），而DMH每周一次通过皮下注射（20 mg/kg体重）给药。从IQ或DMH末次给药后1周开始直至处死，大鼠在饮用水中接受0.001、0.01或0.1%（w/v）CHL或在饮食中接受0.001、0.01或0.1% I3 C。与单独给予致癌物的对照组相比，0.1%I3C处理抑制了IQ诱导的结肠肿瘤的多样性，CHL以剂量相关的方式抑制IQ诱导的肝脏肿瘤的发生率。0.001%CHL能显著增加DMH诱导的结肠肿瘤的发生率，而对IQ诱导的结肠肿瘤无影响。这些结果表明，致癌物的选择以及肿瘤调节剂的剂量可以是重要的决定因素的事件发生在启动后暴露于CHL或I3 C。根据目前的研究结果和文献中的数据，CHL和I3 C有可能作为肿瘤促进剂或抗癌剂，这取决于试验种属、引发剂和暴露方案。
Chlorophyllin (CHL) is a water-soluble derivative of chlorophyll, the ubiquitous pigment in green and leafy vegetables, whereas indole-3-carbinol (I3C) is present in cruciferous vegetables such as cabbage, broccoli and cauliflower. In rats initiated with 1,2-dimethylhydrazine (DMH), CHL and I3C reportedly promoted or enhanced the incidence of colon tumors when they were administered after, or during and after the carcinogen exposure, respectively. The same compounds given post-initiation inhibited the formation of colonic aberrant crypts induced by heterocyclic amines, such as 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), but tumor suppression was not examined in the latter studies. In the present investigation, male F344 rats were treated with IQ or DMH during the first 5 weeks of a 1 year study; IQ was given in the diet (0.03%), whereas DMH was administered once a week bys.c.injection (20 mg/kg body wt). Beginning 1 week after the last dose of IQ or DMH until sacrifice, rats received 0.001, 0.01 or 0.1% (w/v) CHL in the drinking water or 0.001, 0.01 or 0.1% I3C in the diet. Compared with controls given carcinogen alone, 0.1% I3C treatment suppressed the multiplicity of IQ-induced colon tumors, and CHL inhibited in a dose-related manner the incidence of IQ-induced liver tumors. However, 0.001% CHL increased significantly the multiplicity of DMH-induced colon tumors while having no effect on the colon tumors induced by IQ. These results indicate that both the choice of carcinogen as well as the dose of the tumor modulator can be important determinants of the events that occur during post-initiation exposure to CHL or I3C. Based on the present findings and data in the literature, it is possible for CHL and I3C to act as tumor promoters or anticarcinogens, depending upon the test species, initiating agent and exposure protocol.