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Environmental tobacco smoke is just as damaging to DNA as mainstream smoke.

机译:环境烟草烟雾对DNA的危害与主流烟雾一样。

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摘要

This study demonstrates the ability of tar isolated from environmental tobacco smoke (ETS) to nick DNA in mammalian cells. Solutions of ETS tar behave similarly to aqueous solutions of cigarette tar from mainstream smoke. Both solutions contain the tar semiquinone radical, and this radical associates with the DNA in viable rat alveolar macrophages. Solutions of tar from ETS cause single-strand DNA breaks in rat thymocytes in proportion to the amount of tar present, until a plateau is reached. ETS tar solutions, like mainstream tar solutions, produce hydrogen peroxide. Hydrogen peroxide appears to be an essential component of the mechanism by which both ETS tar and mainstream tar cause DNA damage in rat thymocytes, as catalase substantially protects against DNA damage. Glutathione also protects against DNA nicking by both ETS and mainstream tar solutions by scavenging radicals and/or oxidants. The chelator diethylenetriamine pentaacetic acid also provides partial (40%) protection. The studies demonstrate that the water-soluble components of ETS tar can enter cells, associate with, and then nick DNA.
机译:这项研究证明了从环境烟草烟雾(ETS)中分离出的焦油具有在哺乳动物细胞中切割DNA的能力。 ETS焦油溶液的行为与主流烟气中的香烟焦油水溶液相似。两种溶液均含有焦油半醌自由基,并且该自由基与活的大鼠肺泡巨噬细胞中的DNA缔合。来自ETS的焦油溶液会导致大鼠胸腺细胞中的单链DNA断裂,与存在的焦油量成比例,直至达到平稳。与主流焦油溶液一样,ETS焦油溶液也会产生过氧化氢。过氧化氢似乎是ETS焦油和主流焦油均引起大鼠胸腺细胞DNA损伤的机制的重要组成部分,因为过氧化氢酶可基本上防止DNA损伤。谷胱甘肽还可以清除自由基和/或氧化剂,从而防止ETS和主流焦油溶液对DNA形成切口。螯合剂二亚乙基三胺五乙酸还提供部分(40%)保护。研究表明,ETS焦油的水溶性成分可以进入细胞,与DNA结合并形成缺口。

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