Abstract:The level of TSOD, Cu/Zn-SOD, and Mn SOD isoenzyme activity decreased with age in LECs of patients with age-related cataract. A significant difference in the level of TSOD and Cu/Zn-SOD isoenzyme activity between different types of cataract was observed. The activity of all 3 SOD isoenzymes was highest in cortical cataracts.
“…Sorte et al [3] found that LEC DNA damage in cortical cataracts was significantly higher than that in nuclear and posterior subcapsular cataracts. Rajkumar et al [28] found the level of superoxide dismutase activity higher in the cortical cataract. However, most previous studies have also observed no difference in 8-HOdG, antioxidative enzymes and oxidative stress products in the three subtypes of ARC [4,5,29].…”
Background: Oxidative DNA damage may be one of the etiologies of age-related cataract (ARC). We quantified DNA damage in lens epithelial cells (LECs) and peripheral blood lymphocytes of ARC. Methods: A total of 64 patients with different types of ARC and 23 control subjects were enrolled. Fresh LECs and peripheral lymphocytes were collected and DNA damage was evaluated by alkaline comet assay. The percentage of DNA in the tail of comets (%Tail DNA) and the olive tail moment (OTM) were calculated by CASP software. Results: The results showed the %Tail DNA and OTM in LECs and lymphocytes in the overall cataract patient group were significantly higher than those in the control subjects. The %Tail DNA and OTM of LECs and lymphocytes showed no differences among cortical, nuclear and posterior subcapsular cataracts. The %Tail DNA and OTM in LECs were significantly lower than those in lymphocytes but a significant correlation of the DNA damage was found between them. Conclusion: We concluded that DNA damage in lens and peripheral blood lymphocytes increased in ARC. The results imply that local and systemic oxidative DNA damage might play certain roles in ARC pathogenesis.
“…Sorte et al [3] found that LEC DNA damage in cortical cataracts was significantly higher than that in nuclear and posterior subcapsular cataracts. Rajkumar et al [28] found the level of superoxide dismutase activity higher in the cortical cataract. However, most previous studies have also observed no difference in 8-HOdG, antioxidative enzymes and oxidative stress products in the three subtypes of ARC [4,5,29].…”
Background: Oxidative DNA damage may be one of the etiologies of age-related cataract (ARC). We quantified DNA damage in lens epithelial cells (LECs) and peripheral blood lymphocytes of ARC. Methods: A total of 64 patients with different types of ARC and 23 control subjects were enrolled. Fresh LECs and peripheral lymphocytes were collected and DNA damage was evaluated by alkaline comet assay. The percentage of DNA in the tail of comets (%Tail DNA) and the olive tail moment (OTM) were calculated by CASP software. Results: The results showed the %Tail DNA and OTM in LECs and lymphocytes in the overall cataract patient group were significantly higher than those in the control subjects. The %Tail DNA and OTM of LECs and lymphocytes showed no differences among cortical, nuclear and posterior subcapsular cataracts. The %Tail DNA and OTM in LECs were significantly lower than those in lymphocytes but a significant correlation of the DNA damage was found between them. Conclusion: We concluded that DNA damage in lens and peripheral blood lymphocytes increased in ARC. The results imply that local and systemic oxidative DNA damage might play certain roles in ARC pathogenesis.
“…Recently, epidemiological studies have indicated that apart from elevated intraocular pressure (IOP) and age, the risk of POAG might also be associated with ethnic origin, the presence of diabetes mellitus and most significantly, genetic predisposition [8,9,10]. In addition, oxidative stress is a very dangerous condition that can lead to the development of glaucoma, together with many other diseases [11,12]. Oxidative stress is defined as a shift in the pro-oxidant antioxidant balance in favor of the former caused by the production of inter alia reactive oxygen species (ROS) [13].…”
The development of glaucoma may be connected with a long-term exposure to oxidative stress caused by free radical (ROS). The main aim of this work was an analysis of associations of Cat-262C/T, GPX1 Pro198Leu and SOD1 35 A/C gene polymorphisms of antioxidant enzymes with a risk of open-angle glaucoma (POAG) in a Polish population. DNA samples collected from 209 patients with POAG and 191 healthy controls were used in this study. Polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). We found that the +35A/C polymorphisms of SOD1 were not associated with a risk of POAG. We found that C/T genotype (1-GPX1Pro198Leu, 2-Cat C262T) is associated with increased risk of open angle glaucoma (1-OR = 2.24; 95% CI: 1.46-3.44; p = 0.0001, 2-OR = 2.16; 95% CI: 1.35-3.34; p = 0.001). We also found that T/T genotype is a risk factor for progression of POAG (1-OR = 3.86; 95% Cl: 1.36-10.96; p = 0.007, 2-OR = 6.37; 95% CI: 1.39-29.28; p = 0.007). Finally our data suggest that gene polymorphisms of GPX1 Pro198Leu and CAT C262T may have a protective role in the development of primary open-angle glaucoma in a Polish population.
“…Rajkumar et al demonstrated increased SOD activity in lens capsule samples from cortical cataract patients and the activity declined gradually with age in all samples; the highest levels of SOD were found in samples from patients 50 years of age or younger [20]. However, conflicting data on SOD activity levels also exist and there are studies showing decreased SOD activity levels in erythrocytes, sera and lenses from cataract patients compared to controls [21–23].…”
BackgroundIt has been suggested that the higher prevalence of cataract in women is caused by a withdrawal effect of oestrogen at menopause. In vitro studies have demonstrated protection of serum oestradiol (E2) against oxidative stress through upregulation of antioxidant enzymes, including superoxide dismutase (SOD). The purpose of the present study was to investigate E2 levels and SOD erythrocyte activity in patients with age-related cataract.MethodsThe studied subjects consisted of 103 patients with age-related cataract and 22 controls. Cataracts were classified as nuclear, cortical, or posterior subcapsular. Blood samples were collected and data on smoking, hormonal use, diabetes and age at menarche/menopause was obtained for all individuals. Serum oestradiol analyses were performed with radioimmunoassay (RIA) and SOD activity was measured in erythrocyte lysates.ResultsA negative correlation between age and E2 concentration was seen in a linear regression analysis. No correlation was seen between SOD activity and age or gender and no correlation between E2 levels and SOD activity was found using multiple linear regression. The mean level of E2 for all male subjects was 50.1 ± 16.3 pmol/L, significantly higher compared to 13.8 ± 11.8 pmol/L for postmenopausal women.ConclusionThe present study does not support a role for E2-induced effects on SOD in cataract formation. The findings of higher E2 levels in men than in postmenopausal women may suggest that decreased oestrogen at menopause is partially responsible for the gender-related difference in cataract prevalence. However, the latter can only be verified through prospective randomized trials using hormonal replacement therapy.
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