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      Possible Involvement of Nitric Oxide in the Progression of Diabetic Retinopathy


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          Abnormal nitric oxide (NO) synthesis has been implicated in the pathogenesis of diabetes mellitus. The aim of our study was to elucidate the relationship between the stages of diabetic retinopathy (DR) and the NO levels in aqueous humor and plasma. Using the chemiluminescence assay, we measured the concentrations of NO in aqueous humor and plasma samples obtained during intraocular surgery from 45 diabetic patients and 19 nondiabetic cataract patients. The patients with diabetes were classified into 4 groups: proliferative DR (PDR) with active neovascularization (active PDR; 9 cases), PDR with quiescent neovascularization (regressed PDR; 6 cases), background DR (BDR; 16 cases) and no DR (14 cases). We found that the aqueous NO levels (mean ± SE) of the active PDR group (83.2 ± 13.9 µ M) were significantly higher than those of the BDR group (45.8 ± 6.0 µ M, p = 0.049) and the diabetics without DR (33.3 ± 5.2 µ M, p = 0.011), and, although not statistically significantly, they were also higher than those of the regressed PDR group (52.1 ± 10.3 µ M, p = 0.224). However, no significant differences were observed between any of the diabetic subgroups in the plasma NO levels (p = 0.345). We therefore concluded that NO present in the ocular tissues may play important roles in the progression of DR.

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          Most cited references9

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          Nitric oxide synthases: roles, tolls, and controls.

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            Nitric oxide neurotoxicity.

            Derangements in glutamate neurotransmission have been implicated in several neurodegenerative disorders including, stroke, epilepsy, Huntington's disease, Alzheimer's disease, and amyotrophic lateral sclerosis (ALS). Activation of the N-methyl-D-aspartate (NMDA) receptor subtype of glutamate receptors results in the influx of calcium which binds calmodulin and activates neuronal nitric oxide synthase (nNOS), to convent L-arginine to citrulline and nitric oxide (NO). NO has many roles in the central nervous system as a messenger molecule, however, when generated in excess NO can be neurotoxic. Excess NO is in part responsible for glutamate neurotoxicity in primary neuronal cell culture and in animal models of stroke. It is likely that most of the neurotoxic actions of NO are mediated by peroxynitrite (ONOO-), the reaction product from NO and superoxide anion. In pathologic conditions, peroxynitrite and oxygen free radicals can be generated in excess of a cell antioxidant capacity resulting in severe damage to cellular constituents including proteins, DNA and lipids. The inherent biochemical and physiological characteristics of the brain, including high lipid concentrations and energy requirements, make it particularly susceptible to free radical and oxidant mediated insult. Increasing evidence indicates that many neurologic disorders may have components of free radical and oxidative stress induced injury.
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              Nitric oxide, a novel biologic messenger.


                Author and article information

                S. Karger AG
                October 2003
                20 August 2003
                : 217
                : 5
                : 342-346
                Departments of aOphthalmology and bMedical Research and Education, Taipei Veterans General Hospital and National Yang-Ming University, cInstitute of Clinical Medicine, National Yang-Ming University, dInstitute of National Chinese Medicine, Taipei, eDepartment of Ophthalmology, Taoyuan Veterans Hospital, Taiwan, ROC
                71349 Ophthalmologica 2003;217:342–346
                © 2003 S. Karger AG, Basel

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                : 04 November 2000
                : 21 March 2003
                Page count
                Figures: 1, Tables: 1, References: 35, Pages: 5
                Original Paper

                Vision sciences,Ophthalmology & Optometry,Pathology
                Diabetic retinopathy,Nitric oxide,Aqueous humor,Plasma,Chemiluminescence


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