Superoxide dismutases, lung function and bronchial responsiveness in a general population

Oxidative stress is an important causative factor in the onset and progression of smoking-related lung diseases, such as chronic obstructive pulmonary disease (COPD). Superoxide dismutases (SODs) can prevent an increase in oxidative burden. A total of 1,390 subjects from the prospective Vlagtwedde–Vlaardingen cohort were genotyped for two single nucleotide polymorphisms (SNPs) inSOD2and four SNPs inSOD3, which were further analysed for associations with the presence of bronchial hyperresponsiveness (BHR; provocative concentration causing a 10% fall in the forced expiratory volume in one second (FEV1; PC10≤8 mg·mL−1of histamine), COPD (defined as Global Initiative for Chronic Obstructive Lung Disease stage II or higher), lung function level and the longitudinal course of FEV1. The intronic C5774T SNP ofSOD2was significantly associated with the presence of COPD and BHR in the total population. The T/T genotype for this polymorphism and the Val/Val genotype for theSOD2Ala16Val substitution were risk factors for BHR in individuals without COPD. TheSOD3Arg213Gly substitution was associated with slower FEV1decline in never-smokers exclusively, and theSOD3G(−4466)T SNP was associated with a lower vital capacity level. BothSOD2polymorphisms are associated with bronchial hyperresponsiveness, a risk factor for chronic obstructive pulmonary disease, whileSOD2C5774T additionally confers a risk for chronic obstructive pulmonary disease in the total population. The current authors furthermore confirm previously reported associations ofSOD3single nucleotide polymorphisms with lung function in the general population.