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M.A. Ihnat, D.W. Green, R.C. Kaltreider, M.R. Leeper, A. Sismey, K. Ross, L. Piconi, A. Ceriello; Differential Antioxidant Response in ARPE–19 Cells and Human Retinal Pericytes in Response to Chronic High as Compared to Oscillating Normal/High Glucose Levels . Invest. Ophthalmol. Vis. Sci. 2005;46(13):416.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To examine the antioxidant response and oxidative stress generation in two critical retinal cell types exposed to stable or oscillating high glucose, mimicking chronic hyperglycemia or postprandial changes in glucose, with or without AGE–modified albumin (AGE–Alb). Methods: ARPE–19 cells and human retinal pericytes in culture exposed for 14 days to high constant or oscillating glucose with or without AGE–Alb. Activity of total superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) were measured. Levels of 8–OH–dG and 3–nitrotyrosine (NT) were assayed using ELISA and western blot. Results: High constant glucose exposure resulted in significant increases in SOD activity with little effect on GPx and catalase levels in the ARPE–19 cells. Oscillating glucose, on the other hand, had no effect on the activity levels of SOD, GPx, or catalase in the ARPE–19 cells. In cells exposed to oscillating glucose, levels of both 8–OH–dG and NT were increased as compared to either high constant or normal glucose. Trends observed in the ARPE–19 cells were also observed in the pericytes with the exception that absolute levels of SOD were much lower in the pericytes. The addition of AGE–Alb to any treatment group did not result any additional antioxidant effect with the exception of normal glucose plus AGE–Alb resulting in increased SOD activity. Conclusions: In two retinal cell types, oscillating glucose exposure resulted in decreased antioxidant response and increased levels of markers of reactive oxygen (8–OH–dG) and reactive nitrogen (NT) species as compared with stable high glucose levels. This implies that the increased oxidative stress associated with the postprandial state in diabetes might be due in part to a reduced antioxidant response and that a balance between reactive oxygen species production and detoxification exists in the diabetic retina.
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