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Genetic variation in antioxidant enzymes and lung function.

Amy R Bentley1, Stephen B Kritchevsky, Tamara B Harris

  • 1Center for Research in Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.

Free Radical Biology & Medicine
|March 6, 2012
PubMed
Summary

Genetic variations in antioxidant enzyme genes are linked to chronic obstructive pulmonary disease (COPD) susceptibility in smokers. Specific gene variants, like those in isocitrate dehydrogenase and peroxiredoxin, influence lung function decline in relation to smoking status.

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Area of Science:

  • Genetics
  • Pulmonology
  • Biochemistry

Background:

  • Chronic obstructive pulmonary disease (COPD) affects only a subset of cigarette smokers, indicating a need to identify genetic susceptibility factors.
  • Smoking-induced oxidative stress may compromise antioxidant defenses, with genetic variations in antioxidant enzymes potentially conferring vulnerability.
  • Previous candidate gene studies have not extensively explored the role of genetic variation in antioxidant enzyme networks concerning lung health.

Purpose of the Study:

  • To investigate the association between genetic variations in antioxidant enzyme genes and lung function phenotypes in diverse smoking populations.
  • To identify specific genetic variants and their interactions with smoking status that contribute to COPD susceptibility.

Main Methods:

  • Employed linear models to assess single-locus marker associations within a network of antioxidant enzyme genes.
  • Analyzed data from 2387 European American and African American participants in the Health, Aging, and Body Composition Study.
  • Utilized statistical corrections for multiple comparisons to identify significant associations, focusing on single nucleotide polymorphism (SNP) by smoking interactions.

Main Results:

  • Identified 15 statistically significant associations, all related to SNP-smoking interactions, after correcting for multiple comparisons.
  • Found significant associations for genes in the isocitrate dehydrogenase family (IDH3A, IDH3B, IDH2), notably rs6107100 (IDH3B) impacting FEV(1)/FVC ratio in African American smokers.
  • Observed a variant in PRDX5 (rs9787810) associated with reduced FEV(1) and FEV(1)/FVC ratio in European American current smokers.

Conclusions:

  • Sequence variations in genes encoding antioxidant enzymes contribute to smoking-related COPD susceptibility.
  • The identified genetic associations, particularly with isocitrate dehydrogenase and peroxiredoxin genes, suggest novel mechanisms underlying lung disease development.
  • These findings highlight potential new targets for research into COPD prevention and treatment strategies.