C47T polymorphism in manganese superoxide dismutase (MnSOD), antioxidant intake and survival

Jeanine M. Genkinger, Elizabeth A. Platz, Sandy C. Hoffman, Paul Strickland, Han Yao Huang, George W. Comstock, Kathy J. Helzlsouer

Research output: Contribution to journalArticlepeer-review

Abstract

Introduction and objective: Manganese superoxide dismutase (MnSOD), an enzyme that catalyzes superoxide radical quenching, is hypothesized to protect against premature aging. A C47T transition in the MnSOD gene may affect the enzyme's distribution to the mitochondrion, a site of high oxidative stress. We examined the association between this polymorphism and survival. Methods: Individuals who donated a blood sample to the CLUE I and II campaigns in 1974 and 1989, respectively, and completed a food frequency questionnaire in 1989 (N = 6151) were included in the analysis. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models. Mortality follow-up extended from 1989 to 2002. Results: MnSOD genotype distributions were 27% CC (wildtype homozygotes), 50% CT (heterozygotes) and 23% TT (variant homozygotes). TT and CT genotypes compared to the CC genotype were not associated with all-cause or cardiovascular disease mortality. A slight, but non-statistically significant higher risk of cancer mortality was observed for the CT (HR = 1.13, 95% CI: 0.86-1.49) and TT (HR = 1.24, 95% CI: 0.90-1.70) genotypes compared to CC genotype (p-trend = 0.19). Conclusion: We did not observe an association between the C47T polymorphism in the MnSOD gene and survival. These null associations were not modified by fruit and vegetable intake, cigarette smoking status, or body mass index.

Original languageEnglish (US)
Pages (from-to)371-377
Number of pages7
JournalMechanisms of Ageing and Development
Volume127
Issue number4
DOIs
StatePublished - Apr 2006

Keywords

  • Disease
  • Mortality
  • Oxidation
  • Polymorphism

ASJC Scopus subject areas

  • Aging
  • Developmental Biology

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