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      • Record: found
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      Possible Involvement of Nitric Oxide in the Progression of Diabetic Retinopathy

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          Abstract

          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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              • Record: found
              • Abstract: not found
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              Nitric oxide, a novel biologic messenger.

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                Author and article information

                Journal
                OPH
                Ophthalmologica
                10.1159/issn.0030-3755
                Ophthalmologica
                S. Karger AG
                0030-3755
                1423-0267
                2003
                October 2003
                20 August 2003
                : 217
                : 5
                : 342-346
                Affiliations
                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
                Article
                71349 Ophthalmologica 2003;217:342–346
                10.1159/000071349
                12913324
                c1484aa5-d24c-4883-878e-88bf9cd89c0a
                © 2003 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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

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

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