Carcinogenic activity of cigarette smoke gas phase and its modulation by beta-carotene and N-acetylcysteine.
Carcinogenic activity of cigarette smoke gas phase and its modulation by beta-carotene and N-acetylcysteine.
复制标题
香烟烟雾气相的致癌活性及其通过β-胡萝卜素和N-乙酰半胱氨酸的调节。
DOI：
10.1093/toxsci/kfi043
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Witschi,Hanspeter
中科院分区：
文献类型：
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作者：
Witschi,Hanspeter
雄性A/J型小鼠每天6小时，每周5天，连续6个月暴露在完全的烟草烟雾中，或者暴露在通过HEPA过滤器过滤的烟草烟雾中，HEPA过滤器可以去除99%以上的颗粒物。在空气中再待四个月后，将动物处死，计算肺肿瘤的数量，以计算其多样性和发病率。对室内气氛的分析表明，在过滤后的烟雾中，多环芳烃和烟草烟雾特定亚硝胺的浓度从低于18%降至甚至无法检测到未过滤烟雾中原始测量值的水平。醛和其他挥发性有机化合物，如1,3-丁二烯、苯或丙烯醛的浓度降至未过滤烟雾的50%至90%左右。一些潜在的致癌金属在过滤后的烟雾中达到了77%到全烟中不到1%的水平。暴露在过滤烟雾环境中的小鼠与暴露在完全烟雾环境中的小鼠几乎具有相同的肺肿瘤多样性和发病率，显著高于暴露在空气中的对照组。饲粮中含有0.5% β-胡萝卜素或0.4% n -乙酰半胱氨酸具有一定的化学预防作用。初步认为1,3-丁二烯可能是烟草烟雾致癌小鼠肺肿瘤发生的重要因素。
Male strain A/J mice were exposed for six hours a day, five days a week for six months to either full tobacco smoke or to tobacco smoke drawn through a HEPA filter that removed more than 99% of particulate matter. After another four months in air, the animals were sacrificed and lung tumors were counted for calculation of multiplicities and incidences. Analysis of the chamber atmospheres showed that in the filtered smoke the concentrations of polycyclic aromatic hydrocarbons and tobacco smoke specific nitrosamines were reduced to from below 18% to even nondetectable levels of the original values measured in the unfiltered smoke. Aldehydes and other volatile organic compounds such as 1,3-butadiene, benzene, or acrolein were reduced to about 50 to 90% of the concentrations found in unfiltered smoke. Some potentially carcinogenic metals reached levels in filtered smoke ranging from 77% to less than 1% found in full smoke. The mice exposed to the filtered smoke atmosphere had practically identical lung tumor multiplicities and incidence as had the animals exposed to full smoke, significantly higher than in air exposed controls. Diets containing 0.5% β-carotene or 0.4% N-acetylcysteine afforded some chemoprevention. It was tentatively concluded that 1,3-butadiene might be an important contributor to lung tumorigenesis in this mouse model of tobacco smoke carcinogenesis.