Purpose: Age-related macular degeneration (AMD) is a major cause of blindness in developed countries. Oxidative mechanisms may play a key role in the aetiology of AMD. The main aim of this study was to investigate antioxidative markers in the pathogenesis of AMD.
Methods: A total of 510 subjects including 240 patients with AMD (mean age 77.9 ± 8.5 year) and 270 controls (mean age 74.0 ± 10.4 year) were allowed in this study. We measured activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and examined their association with the SNPs of respective genes (SOD1 + 35A/C, CAT C-262T and GPx Pro197Leu). Restriction fragment length polymorphism (RFLP) technique was used to determine the selected gene polymorphisms. Sixty subjects including 30 patients with AMD (mean age 69.4 ± 9.3) and 30 controls (mean age 64.6 ± 8.2) were enrolled to determine the activity of antioxidant enzymes by spectrometry method.
Results: A significant decrease in enzymes, SOD (p = 0.011), CAT (p = 0.002) and GPx (p ≤ 0.001) in AMD patients compared to controls, was indicated. The risk of susceptibility to AMD was significantly higher in patients with AMD who had Pro197Leu C/T genotype of GPx (OR = 2.78; 95% CI = 1.78-4.35). The A/C genotype and the C allele frequencies of A/C polymorphism of SOD1 gene significantly reduce the risk of AMD (OR=0.48; 95% CI 0.27; 0.85).
Conclusion: In conclusion, our data showed that insufficient antioxidant capacity may have an important role in age-related macular degeneration. The polymorphism of GPx Pro197Leu may reduce the ability to scavenge free radicals in retina and contribute to the development of AMD.
Keywords: age-related macular degeneration; antioxidant enzyme; genetic polymorphism; the polish population.
© 2016 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.