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首页> 外文期刊>Human and Experimental Toxicology >Cell proliferation kinetics and genotoxicity in lymphocytes of smokers living in Mexico City.
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Cell proliferation kinetics and genotoxicity in lymphocytes of smokers living in Mexico City.

机译：居住在墨西哥城的吸烟者的淋巴细胞中的细胞增殖动力学和遗传毒性。

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Genotoxicity caused by tobacco smoke was assessed in peripheral blood lymphocytes of smokers living in Mexico City by determining sister chromatid exchange (SCE), cell proliferation kinetics (CPK), replication index (RI) and mitotic index (MI). Nicotine levels, and its major metabolite cotinine, were also estimated in urine samples using gas-chromatography-mass spectrometry to quantify smoking intensity. The outcome of the analysis and the comparison of the 77-smoker group with a non-smoking control group showed that moderate and heavy smokers exhibited significant differences (P < 0.001 and P < 0.05, respectively) in CPK, with an underlying delay in the cellular cycle; similarly, RI was significantly different in these groups (P < 0.001 and P < 0.0001, respectively). There were significant correlations (P < 0.05) between age and number of years the subject had been smoking, as well as between RI and nicotine and cotinine levels and between CPK (M1, M2 and M3) and nicotine and cotinine levels. Smokers were classified for the analysis according to the nicotine levels (it is in relation to number of cigarettes smoked per day) found in urine (ng/mL) as: light (10-250), moderate (251-850) and heavy (851-4110). Significant differences in CPK were found (P < 0.05) between moderate and heavy smokers and non-smokers. Significant differences in RI were found between moderate (P < 0.001) and heavy smokers (P < 0.0001) and non-smokers, but not for the light smoking group. MI was determined in 57 of the smokers, whereas SCE frequency was only recorded in 34 smokers. Both parameters yielded no significant differences, nor correlations with any of the assessed variables. In conclusion, cytokinetic and cytostatic effects were mainly detected in heavy and moderate smokers. Cell cycle delay and RI decrease were found in all ;healthy' smokers. The nicotine and cotinine exposure (causing oxidative damage to DNA) may have implications in the decrease in cell replication due to direct damage to DNA and/or a decrease in the DNArepair mechanisms. Alternatively, nicotine and cotinine may possibly induce apoptosis.
机译：通过确定姐妹染色单体交换（SCE），细胞增殖动力学（CPK），复制指数（RI）和有丝分裂指数（MI），评估了居住在墨西哥城的吸烟者外周血淋巴细胞中由烟草烟雾引起的基因毒性。还使用气相色谱-质谱法对尿液样本中的尼古丁含量及其主要代谢产物可替宁进行了定量，以量化吸烟强度。分析的结果以及将77名吸烟者与非吸烟对照组进行比较的结果表明，中度和重度吸烟者的CPK表现出显着差异（分别为P <0.001和P <0.05），并且潜在的延迟是细胞周期同样，这些组的RI显着不同（分别为P <0.001和P <0.0001）。受试者年龄和吸烟年龄之间，RI与尼古丁和可替宁水平之间以及CPK（M1，M2和M3）与尼古丁和可替宁水平之间存在显着相关性（P <0.05）。根据尿液中的尼古丁含量（与每天抽烟的数量有关），对吸烟者进行分类以进行分析（ng / mL）：轻（10-250），中（251-850）和重（ 851-4110）。中度和重度吸烟者与非吸烟者之间的CPK差异显着（P <0.05）。在中度吸烟者（P <0.001）和重度吸烟者（P <0.0001）与不吸烟者之间发现RI的显着差异，而在轻度吸烟组中则没有。在57位吸烟者中确定了心梗，而在34位吸烟者中仅记录了SCE频率。两个参数均未产生显着差异，也未与任何评估变量相关。总之，主要在重度和中度吸烟者中发现了细胞动力学和细胞抑制作用。所有健康的吸烟者均发现细胞周期延迟和RI降低。尼古丁和可替宁的暴露（对DNA造成氧化性损伤）可能由于直接对DNA的损伤和/或DNA修复机制的降低而对细胞复制的减少产生影响。或者，尼古丁和可替宁可能会诱导细胞凋亡。

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