Thorax 61:394-399 doi:10.1136/thx.2005.048512
  • Chronic obstructive pulmonary disease

Functional variants of antioxidant genes in smokers with COPD and in those with normal lung function

  1. R P Young1,
  2. R Hopkins2,
  3. P N Black1,
  4. C Eddy1,
  5. L Wu1,
  6. G D Gamble1,
  7. G D Mills4,
  8. J E Garrett3,
  9. T E Eaton2,
  10. M I Rees5
  1. 1Department of Medicine, University of Auckland, Auckland, New Zealand
  2. 2Respiratory Services, Green Lane Hospital, Auckland, New Zealand
  3. 3Department of Respiratory Medicine, Middlemore Hospital, South Auckland, New Zealand
  4. 4Department of Respiratory Medicine, Waikato Hospital, Hamilton, New Zealand
  5. 5School of Medicine, University of Wales Swansea Singleton Park, Swansea, UK
  1. Correspondence to:
    Dr R Young
    Department of Medicine, Auckland Hospital, Private Bag 92024, Auckland, New Zealand; roberty{at}
  • Received 2 September 2005
  • Accepted 6 February 2006
  • Published Online First 7 February 2006


Background: Chronic obstructive pulmonary disease (COPD) is predominantly the consequence of chronic smoking exposure, but its development may be influenced by genetic variants that affect lung remodelling, inflammation, and defence from oxidant stress. A study was undertaken to determine whether genetic variants within genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase may be associated with the development of impaired lung function.

Methods: In a case-control study, the allele and genotype frequencies of functional polymorphisms from SOD1 (CuZnSOD), SOD2 (MnSOD), SOD3 (extracellular SOD), and catalase (CAT) were compared in chronic smokers with normal lung function (resistant smokers) and in those with COPD.

Results: Significantly higher frequencies of the G allele and CG/GG genotype of the 213 SOD3 polymorphism were found in resistant smokers (odds ratios (ORs) 4.3 (95% CI 1.5 to 13.3) and 4.2, 95% CI 1.4 to 13.3), Bonferroni corrected p = 0.02 and p = 0.02, respectively) than in those with COPD. There were no differences between the COPD and resistant smokers for the SOD1, SOD2, or CAT polymorphisms tested.

Conclusions: The 213Gly variant of the SOD3 gene may, through antioxidant or anti-inflammatory effects, confer a degree of resistance in some smokers to the development of COPD.


  • Published Online First 7 February 2006

  • This study was supported by grants from the University of Auckland, Lottery Grants of New Zealand, Auckland Medical Research Foundation, Paykel Trust and Health Research Council of New Zealand.

  • Competing interests: none declared.