Polymorphisms and functional activity in SOD and catalase genes in smokers with COPD

¹ Division of Respiratory Medicine, Dept of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, China
² Princess Margaret Hospital, Hong Kong SAR, China
³ North District Hospital, Hong Kong SAR, China
⁴ United Christian Hospital, Hong Kong SAR, China
⁵ The Grantham Hospital, Hong Kong, SAR, China
⁶ Division of Respiratory Medicine, Dept of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong SAR, China; and Occupational and Environmental Lung Diseases Unit, Respiratory Division, Dept of Medicine, University of British Columbia, Vancouver, BC, Canada

^* To whom correspondence should be addressed. E-mail: address:.

	Abstract

Increased oxidative stress has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). This study investigated the risk of COPD and polymorphisms of manganese superoxide dismutase (MnSOD) gene at Ala16Val and catalase at C-262T, and the activity of erythrocyte SOD and catalase.

165 stable COPD patients of ever smokers (n=165) and healthy controls matched for age and pack-years smoked. Genotyping of MnSOD at Ala16Val and catalase gene at C-262T, and functional activities of SOD and catalase in erythrocytes were determined.

There were no significant differences in the distribution of the different genotypes or allele frequencies between patients and controls for both the MnSOD and catalase genes. Among healthy controls or COPD patients, no differences were observed in erythrocyte SOD and catalase activity irrespective of the genotypes. Significant higher activity of erythrocyte catalase was found in COPD patients compared with healthy controls. The TT genotype of the catalase gene and AlaAla genotype of the MnSOD gene were uncommon in our Chinese population.

The increase in erythrocyte catalase activity in Chinese patients with COPD probably indicates a dysfunction of oxidant/antioxidant defense system but it is unclear whether the increase is compensatory or a pathogenic factor.

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