背景香烟烟导致了 DNA 损坏罐头原因航线房间 apoptosis 和死亡,它可以与长期的妨碍的肺的疾病(COPD ) 的发展被联系。然而,仅仅吸烟者的 20%-30% 开发 COPD,建议 DNA 修理的不同的度在吸烟者生产不同结果,即,他们的部分开发 COPD。我们总共在 DNA 修理基因 hOGG1 (Ser326Cys ) 和 XRCC1 (Arg399GIn ) ,独自或在 COPD.Methods 的联合,和危险性调查了在多型性之间的协会 201 个 COPD 病人和 309 控制被招募并且在年龄和性别匹配频率。hOGG1 和 XRCC1 遗传型被 COPD 的风险不是的 PCR 限制碎片长度多型性 analysis.Results 决定在有 Ser/Cys 和 Cys/Cys 遗传型的个人之中显著地不同与那些相比与 hOGG1 重量的单位 / 重量的单位遗传型。COPD 的风险不与有 XRCC1 Arg/Arg 遗传型的那些相比在有陷阱 / 陷阱遗传型的个人之中是显著地不同的,但是它显著地与 Arg/GIn 遗传型在个人之中被提高(调整机会比率(或)=1.55, 95% 信心间隔(C/) 1.05-2.29, P=0.029 ) 。对与 hOGG1 设置 / 设置遗传型与那些相比在当前的吸烟者吸地位的评价表明 COPD 的风险显著地与 Cys/Cys 遗传型在个人之中被提高(调整 OR=5.07, 95% CI 1.84-13.95, P=0.002 ) 。与那些相比与 XRCC1 Arg/Arg 遗传型, COPD 的风险显著地与 Arg/GIn 遗传型在个人之中被提高(调整 OR=2.77, 95% CI 1.52-5.07, P=0.001 ) 。对与 hOGG1 重量的单位 / 重量的单位遗传型与那些相比在轻吸烟者吸暴露的评价证明 COPD 的风险显著地与 Cys/Cys 遗传型在个人之中被提高(调整 OR=4.02, 95% CI 1.05-16.80, P=0.042 ) 。与那些相比与 XRCC1 Arg/Arg 遗传型, COPD 的风险显著地与陷阱 / 陷阱遗传型在个人之中被提高(调整 OR=4.48, 95% CI 1.35-14.90, P=0.014 ) 。在重吸烟者与那些相比与 XRCC1 Arg/Arg 遗传型, COPD 的风险显著地与 Arg/GIn 遗传型在个人之中被提高(调整 OR=2.55, 95% CI 1.42-4.58, P=0.002 ) 。hOGG1 Ser32
Background Cigarette-smoke induced DNA damage can cause airway cell apoptosis and death, which may be associated with the development of chronic obstructive pulmonary disease (COPD). However, only 20%-30% of smokers develop COPD, suggesting that different degrees of DNA repair produce different outcomes in smokers, i.e., part of them develop COPD. We investigated the association between polymorphisms in DNA repair genes hOGG1 (Ser326Cys) and XRCC1 (Arg399GIn), alone or in combination, and susceptibility of COPD. Methods Altogether 201 COPD patients and 309 controls were recruited and frequency-matched on age and sex. hOGG1 and XRCC1 genotypes were determined by PCR-restriction fragment length polymorphism analysis. Results The risk of COPD was not significantly different among individuals with Ser/Cys and Cys/Cys genotypes compared with those with hOGG1 Ser/Ser genotype. The risk of COPD was not significantly different among individuals with Gin/Gin genotype compared with those with XRCC1 Arg/Arg genotype, but it was significantly elevated among individuals with Arg/GIn genotype (adjusted odds ratios (OR)=1.55, 95% confidence intervals (CI) 1.05-2.29, P=0.029). Assessment of smoking status in current smokers compared with those with hOGG1 Ser/Ser genotype revealed that the risk of COPD was significantly elevated among individuals with Cys/Cys genotype (adjusted OR=5.07, 95% CI 1.84-13.95, P=0.002). Compared with those with XRCC1 Arg/Arg genotype, the risk of COPD was significantly elevated among individuals with Arg/GIn genotype (adjusted OR=2.77, 95% CI 1.52-5.07, P=-0.001). Assessment of smoking exposure in light smokers compared with those with hOGG1 Ser/Ser genotype showed that the risk of COPD was significantly elevated among individuals with Cys/Cys genotype (adjusted OR=4.02, 95% CI 1.05-16.80, P=0.042). Compared with those with XRCC1 Arg/Arg genotype, the risk of COPD was significantly elevated among individuals with Gin/Gin genotype (adjusted OR=4.48, 95% CI 1.35-14.