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Mutagenesis:首次发现二手烟可引发人类细胞出现DNA损伤

来源:生物谷 2013-06-23 15:13

2013年6月22日 讯 /生物谷BIOON/ --近日,来自美国劳伦斯柏克莱国家实验室(Lawrence Berkeley National Laboratory,LBNL)研究人员通过研究首次揭示了二手烟可以导致人类细胞出现明显的遗传损伤。相关研究成果刊登于国际杂志Mutagenesis上。同时研究者也发现,慢性二手烟的暴露比急性暴露危害更大,引发的DNA损伤更为严重。

研究者Lara Gundel表示,这是我们首次研究揭示二手烟可以引发遗传物质出现突变现象,烟草所特殊的亚硝胺类物质,如NNA、NNK和NNN等,其是潜在的致癌物质,其可以随着吸烟过程附着在衣服或者地毯表面,这对于人类,尤其是儿童是非常危险的。

这项研究中,研究者使用两种测定方法,彗星试验和长扩增子定量PCR试验测定了二手烟引发的基因毒性,发现二手烟可以引发DNA链的破裂以及氧化性的DNA损伤,这将引发基因突变;而且基因毒性和疾病的发生直接相关,其是很多吸烟、二手烟引发的许多类型癌症的一种关键机制。

在进行这项研究之前,研究者并不清楚二手烟引发疾病的分子机制,研究者Hang说,相比被动吸烟二手烟中含有较少量的化合物,因此这就提供了一定的实验证据来证实其引发的基因毒性。如今这项研究揭示了二手烟或许对人类非常有危害性,研究者发现在慢性二手烟样品中发现的有毒化合物的浓度比急性样品中多很多;二手烟引发的累积效应非常明显。

下一步研究者将寻找NNA和DNA之间反映的分子机理,NNA是一种烟草特殊亚硝胺类物质,其并没有在新释放的二手烟中发现,其相比NNK和NNN研究较少。在这项研究中,研究显示暴露于二手烟中可以增加个体疾病发生的风险,这或许为科学家开发新型策略预防其引发的危害提供帮助和希望。(生物谷Bioon.com)

Thirdhand smoke causes DNA damage in human cells

Bo Hang1,*, Altaf H. Sarker1, Christopher Havel2, Saikat Saha3, Tapas K. Hazra3, Suzaynn Schick2, Peyton Jacob III2, Virender K. Rehan4, Ahmed Chenna5, Divya Sharan1, Mohamad Sleiman6, Hugo Destaillats6 and Lara A. Gundel6

Exposure to thirdhand smoke (THS) is a newly described health risk. Evidence supports its widespread presence in indoor environments. However, its genotoxic potential, a critical aspect in risk assessment, is virtually untested. An important characteristic of THS is its ability to undergo chemical transformations during aging periods, as demonstrated in a recent study showing that sorbed nicotine reacts with the indoor pollutant nitrous acid (HONO) to form tobacco-specific nitrosamines (TSNAs) such as 4-(methylnitrosamino)-4-(3-pyridyl)butanal (NNA) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The goal of this study was to assess the genotoxicity of THS in human cell lines using two in vitro assays. THS was generated in laboratory systems that simulated short (acute)- and long (chronic)-term exposures. Analysis by liquid chromatography–tandem mass spectrometry quantified TSNAs and common tobacco alkaloids in extracts of THS that had sorbed onto cellulose substrates. Exposure of human HepG2 cells to either acute or chronic THS for 24h resulted in significant increases in DNA strand breaks in the alkaline Comet assay. Cell cultures exposed to NNA alone showed significantly higher levels of DNA damage in the same assay. NNA is absent in freshly emitted secondhand smoke, but it is the main TSNA formed in THS when nicotine reacts with HONO long after smoking takes place. The long amplicon–quantitative PCR assay quantified significantly higher levels of oxidative DNA damage in hypoxanthine phosphoribosyltransferase 1 (HPRT) and polymerase β (POLB) genes of cultured human cells exposed to chronic THS for 24h compared with untreated cells, suggesting that THS exposure is related to increased oxidative stress and could be an important contributing factor in THS-mediated toxicity. The findings of this study demonstrate for the first time that exposure to THS is genotoxic in human cell lines.

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