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首页> 外文期刊>The clinical respiratory journal. >Genetic polymorphisms in antioxidative enzymes are associated to forced expiratory volume in 1 s (FEV1) in smokers independently of asthma.
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Genetic polymorphisms in antioxidative enzymes are associated to forced expiratory volume in 1 s (FEV1) in smokers independently of asthma.

机译：抗氧化剂中的遗传多态性与吸烟者在1 s内的呼气量（FEV1）相关，与哮喘无关。

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INTRODUCTION: In this study, we hypothesised that the genotypes coding for low antioxidative enzyme activity are associated with asthma and reduced lung function. METHODS: Using the European Community Respiratory Health Survey protocol, we enlisted 1091 Danish subjects in this cross-sectional study. Asthma phenotypes were defined as asthma symptoms in combination with steroid usage, bronchial hyperresponsiveness and atopy. These phenotypes and lung function were analysed with respect to glutathione peroxidase, GPX1 (Pro198Leu, rs1050450), manganese superoxide dismutase, SOD2 (Ala16Val, rs4880) and three glutathione S-transferases; GSTP1 (Ile105Val, rs1695), GSTT1 (gene copy number) and GSTM1 (gene copy number). RESULTS: We found no associations between these genotypes and the asthma phenotypes. For the 201 subjects identified as current smokers and recruited via random sampling, an association was seen between increasing number of genotypes coding for high antioxidative enzyme activity (GPX1 Pro/Pro, SOD2 Val/Val, GSTP1 Ile/Ile, GSTT1 two copies, GSTM1 two copies) and forced expiratory volume in 1 s (FEV1%) predicted. The increase in FEV1% predicted was 2.0% (95% confidence interval 0.3-3.8) per genotype. There was no identified significance for the inverse association between FEV1% predicted and number of genotypes coding for low antioxidative enzyme activity. CONCLUSION: The present study does not support the hypothesis that asthma is associated with genotypes of these major antioxidative enzymes. However, we speculate that since we see an impact of these genotypes on lung function in young adult smokers, polymorphisms in antioxidative enzymes may contribute to the range of susceptibility of smokers have to Chronic obstructive lung disease.
机译：引言：在这项研究中，我们假设编码低抗氧化酶活性的基因型与哮喘和肺功能下降有关。方法：使用欧洲共同体呼吸健康调查方案，我们在此横断面研究中招募了1091名丹麦受试者。哮喘的表型定义为哮喘症状与类固醇的使用，支气管高反应性和特应性相结合。分析了谷胱甘肽过氧化物酶，GPX1（Pro198Leu，rs1050450），锰过氧化物歧化酶，SOD2（Ala16Val，rs4880）和三种谷胱甘肽S-转移酶的这些表型和肺功能。 GSTP1（Ile105Val，rs1695），GSTT1（基因拷贝号）和GSTM1（基因拷贝号）。结果：我们发现这些基因型与哮喘表型之间没有关联。对于被确定为当前吸烟者并通过随机抽样招募的201名受试者，发现编码高抗氧化酶活性的基因型数量增加之间存在关联（GPX1 Pro / Pro，SOD2 Val / Val，GSTP1 Ile / Ile，GSTT1两份，GSTM1两份）和预计的1秒内呼气量（FEV1％）。每个基因型预测的FEV1％的增加为2.0％（95％置信区间0.3-3.8）。在预测的FEV1％与编码低抗氧化酶活性的基因型数量之间的负相关性没有确定的意义。结论：本研究不支持哮喘与这些主要抗氧化酶基因型相关的假说。但是，我们推测，由于我们看到了这些基因型对年轻成年吸烟者的肺功能的影响，因此抗氧化酶的多态性可能有助于吸烟者对慢性阻塞性肺疾病的易感性范围。

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