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

¹ Dept of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands
² Dept of Pulmonology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands

^* To whom correspondence should be addressed. E-mail: H.M.Boezen{at}epi.umcg.nl.

	Abstract

Oxidative stress is an important causative factor in the onset and progression of smoking-related lung diseases like chronic obstructive pulmonary disease (COPD). Superoxide Dismutases (SODs) can prevent an increase in oxidative burden.

1,390 subjects from the prospective Vlagtwedde–Vlaardingen cohort were genotyped for 2 Single Nucleotide Polymorphisms (SNPs) in SOD2 and 4 SNPs in SOD3, that were further analyzed for associations with the presence of bronchial hyperresponsiveness (BHR; PC₁₀8 mg·ml^-1 of histamine), COPD (defined as GOLD stage II), lung function level and the longitudinal course of FEV₁.

The intronic C5774T SNP of SOD2 was 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 the SOD2 Ala16Val substitution were risk factors for BHR in individuals without COPD. The SOD3 Arg213Gly substitution was associated with slower FEV₁ decline in never smokers exclusively, and the SOD3 G(-4466)T SNP was associated with a lower Vital Capacity level.

Both SOD2 polymorphisms are associated with BHR, a risk factor for COPD, while SOD2 C5774T additionally confers a risk for COPD in the total population. We furthermore confirm previously reported associations of SOD3 SNPs with lung function in the general population.

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