PT  - JOURNAL ARTICLE
AU  - R. P. Bowler
AU  - J. Hokanson
AU  - M. Taylor
AU  - S. Levy
AU  - E. M. Canaham
AU  - E. Regan
AU  - C. Wheeler
AU  - M. Nicks
AU  - E. Chan
AU  - J. D. Crapo
TI  - Extracellular superoxide dismutase (EC-SOD) as a protective factor for risk of chronic obstructive pulmonary disease
AID  - 10.1183/09059180.00010117
DP  - 2006 Dec 01
TA  - European Respiratory Review
PG  - 200--201
VI  - 15
IP  - 101
4099  - http://err.ersjournals.com/content/15/101/200.short
4100  - http://err.ersjournals.com/content/15/101/200.full
SO  - EUROPEAN RESPIRATORY REVIEW2006 Dec 01; 15
AB  - Tobacco smoke contains a high concentration of oxidants and is the primary cause of chronic obstructive pulmonary disease (COPD). Extracellular superoxide dismutase (EC-SOD) is the major antioxidant enzyme in the extracellular space of the lung and is part of the lung defense against these oxidants. We hypothesized that EC-SOD is a risk factor for COPD. We found that EC-SOD plasma levels were significantly higher (p<0.001) in 337 patients with COPD (147±7 ng·ml−1) versus 343 controls (96±9 ng·ml−1) and that lower FEV1s were associated with lower EC-SOD levels. To identify whether the EC-SOD gene was associated with COPD, we resequenced a subset of 188 subjects and identified 33 novel SNPs. Two of these SNPs (rs8192287 and rs8192288) were associated with a reduced odds of having COPD (OR 0.05 and 0.34; P<0.05). Haplotype analysis using a total of 5 EC-SOD SNPs (Table 1⇓) further identified a protective haplotype (TTCGC) that was found in 11.4% of controls, but only 2.1% of subjects with COPD (P<0.001). These data indicate that EC-SOD genotype may partially predict whether smokers are resistant to the effects smoking.