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Mainstream and sidestream cigarette smoke-induced DNA adducts in C7Bl and DBA mice.

机译:C7B1和DBA小鼠中主流和支流香烟烟雾诱导的DNA加合物。

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摘要

Exposure to environmental tobacco smoke (ETS), which is largely composed of the sidestream cigarette smoke, has been implicated in increased incidence of cancer among nonsmokers. The present study was conducted to compare the potential of mainstream and sidestream cigarette smoke to induce DNA adducts in mice. Groups of female C57Bl and DBA mice were exposed twice daily for 65-70 weeks to mainstream or sidestream smoke from the University of Kentucky reference cigarettes (2R1) in a nose-only exposure system. Animals received a total particulate matter dose of about 16 and 6 mg/kg body weight/exposure and exhibited blood carboxyhemoglobin levels of about 16 and 34%, for mainstream and sidestream smoke-exposed groups, respectively. Pulmonary aryl hydrocarbon hydroxylase (AHH) activity was induced by about 2- to 3-fold in both mainstream and sidestream groups of C57Bl and in mainstream smoke-exposed group of DBA mice, but not in sidestream smoke-exposed DBA mice. An analysis of total DNA adduct levels by the 32P-postlabeling assay showed a significant (12- to 25-fold) increase in the magnitude of preexisting lung DNA adducts in both mainstream and sidestream smoke-exposed C57Bl and DBA mice. Smoke exposures did not affect the total preexisting DNA adducts in liver of either strain. It is concluded that both mainstream and sidestream smoke are capable of enhancing preexisting DNA adducts in the lungs of chronically smoke-exposed mice.
机译:暴露于主要由侧流香烟烟雾构成的环境烟草烟雾(ETS)与非吸烟者癌症发病率的增加有关。进行本研究以比较主流和侧流香烟烟雾在小鼠中诱导DNA加合物的潜力。在仅鼻暴露系统中,将雌性C57B1和DBA小鼠组每天两次暴露于肯塔基大学参考香烟(2R1)的主流烟气或侧流烟中,持续65-70周。对于主流和侧流烟气暴露组,动物接受的总颗粒物剂量约为16和6 mg / kg体重/暴露,并且血液中的羧基血红蛋白水平分别约为16%和34%。在C57B1的主流和侧流组中以及在DBA小鼠的主流烟气暴露组中,肺芳基烃羟化酶(AHH)活性被诱导约2-3倍,而在侧流烟气暴露的DBA小鼠中没有被诱导。通过32P后标记测定法对总DNA加合物水平的分析表明,在主流和侧流烟暴露的C57B1和DBA小鼠中,现有肺DNA加合物的量显着增加(12至25倍)。烟暴露不影响任一菌株肝脏中总的预先存在的DNA加合物。结论是,主流烟气和侧流烟气都能够增强慢性烟气暴露小鼠的肺中预先存在的DNA加合物。

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