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R. A. Kowluru, M. Kanwar; Continued Damage to the Retinal Microvasculature and Progression of Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3644.
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Re-institution of good glycemic control (GC) in diabetic patients fails to reverse retinopathy, and the pre-existing damage at the time of intervention is considered a primary factor in determining the outcome of the GC. This study is to investigate the role of peroxynitrite in the failure of retinopathy to reverse after re-establishment of GC, and to determine the effect of GC on the activity of the enzyme responsible for scavenging superoxide, MnSOD.
Streptozotocin diabetic rats remained in poor glycemic control (PC, GHb>12.0%) for 6 months followed by GC (GHb about 6%) for 6 additional months. Trypsin-digested retinal microvessels were used for immuno-localization of nitrotyrosine (a measure of peroxynitrite) and for evaluating histopathology; and the retina was used to estimate MnSOD activity and total antioxidant capacity.
Re-institution of GC after 6 months of PC had no significant effect on nitrotyrosine-positive retinal capillary cells and on the number of acellular capillaries; the values were similar in PC-GC and PC groups. In the same rats MnSOD activity and the total antioxidant capacity of the retina remained subnormal 6 months after cessation of PC.
Accumulation of peroxynitrite in the retinal microvasculature, the site of histopathology, is not easily reversed after termination of PC, and superoxide scavenging is hampered. Continued peroxynitrite accumulation in the retinal capillaries could be, in part, responsible for the resistance of diabetic retinopathy to overturn after re-establishment of GC.
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