June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Genetic variation of superoxide dismutases in patients with primary open-angle glaucoma
Author Affiliations & Notes
  • Dragana Celojevic
    Institute of Neuroscience & Physiology, University of Gothenburg, Gothenburg, Sweden
  • Staffan Nilsson
    Institute of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden
  • Anne Petersen
    Institute of Neuroscience & Physiology, University of Gothenburg, Gothenburg, Sweden
  • Gunnar Tasa
    Institute of General and Molecular Pathology, University of Tartu, Tartu, Estonia
  • Erkki Juronen
    Institute of General and Molecular Pathology, University of Tartu, Tartu, Estonia
  • Madeleine Zetterberg
    Institute of Neuroscience & Physiology, University of Gothenburg, Gothenburg, Sweden
  • Footnotes
    Commercial Relationships Dragana Celojevic, None; Staffan Nilsson, None; Anne Petersen, None; Gunnar Tasa, None; Erkki Juronen, None; Madeleine Zetterberg, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 6207. doi:
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    • Get Citation

      Dragana Celojevic, Staffan Nilsson, Anne Petersen, Gunnar Tasa, Erkki Juronen, Madeleine Zetterberg; Genetic variation of superoxide dismutases in patients with primary open-angle glaucoma. Invest. Ophthalmol. Vis. Sci. 2013;54(15):6207.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Oxidative stress has been described as an underlying pathogenetic mechanism in retinal ganglion cell apoptosis, which is a hallmark of primary open-angle glaucoma (POAG). Superoxide dismutases (SODs) are enzymes involved in the protection against oxidative stress by detoxification of superoxide. In this study, we investigated a number of disease-associated single nucleotide polymorphisms (SNPs) in the copper-zinc-containing SOD1 and SOD3, and in the manganese superoxide dismutase SOD2, in POAG patients.

Methods: The study included 239 patients with POAG and 185 controls, all of Estonian origin, recruited at two ophthalmic clinics in Tartu, Estonia. Eleven SNPs, either functional, disease-associated or tag SNPs in SOD1, SOD2 and SOD3 were genotyped using TaqMan Allelic Discrimination. Haplotype analysis was performed on the SNPs in SOD2.

Results: Using binary logistic regression in an additive model, the rs2842980 SNP in SOD2 was significantly associated with POAG diagnosis (p=0.03) at a univariate level. None of the studied SNPs showed an association with risk of POAG in a multivariate analysis, including age and current smoking as covariates. Analysis of SOD2 haplotypes did not show any association with risk of POAG.

Conclusions: If oxidative stress is an important mechanism in POAG-related retinal ganglion cell death, genetic variations in SOD1, SOD2 and SOD3 are not major contributors in the pathogenesis.

Keywords: 539 genetics • 634 oxidation/oxidative or free radical damage  
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