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Home > Medicine & Health Science textbooks > Pre-clinical medicine: basic sciences > Anatomy > Sorbitol Dehydrogenase Does Not Contribute to the Ischemia/Reperfusion-Induced Oxidative Stress and Retinal Injury: (English)
Sorbitol Dehydrogenase Does Not Contribute to the Ischemia/Reperfusion-Induced Oxidative Stress and Retinal Injury: (English)

Sorbitol Dehydrogenase Does Not Contribute to the Ischemia/Reperfusion-Induced Oxidative Stress and Retinal Injury: (English)

          
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About the Book

This dissertation, "Sorbitol dehydrogenase does not contribute to the ischemia/reperfusion-induced oxidative stress and retinal injury" by Man-kit, Tong, 湯文傑, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Diabetic retinopathy (DR) was characterized by numerous hyperglycemia-dependent cellular and pathological changes in the retina, including retinal ischemia/reperfusion (I/R) injury. To determine the role of the 2nd enzyme of polyol pathway in relation with the pathogenesis in ischemic retinopathy, SDH deficient mice, C57BL/LiA, that lacked SDH activity, was used to study the pathogenesis of diabetic retinopathy, which also included I/R injury. Wild type and SDH-deficient mice were subjected to I/R injury by transiently occluding middle cerebral artery for two hours and twenty-two hour of reperfusion. The rationale of this study was to investigate the effect by blocking the conversion of sorbitol to fructose by SDH null mutation (SDH -/-), leading to accumulation of sorbitol level and reduction of oxidative stress, as demonstrated by the polyol pathway. Results: After induction with transient MCAO, there was increase in the thickness of OLM to ILM ipsilateral SDH+/+ compared with contralateral SDH+/+ (from 84 +/- 1 to 96 +/- 2 μm) while that of ipsilateral SDH-/- compared with contralateral SDH -/- (from 77 +/- 2 to 90 +/- 2 μm) suggested that there was edema after ischemic reperfusion injury. The result showed that there was increased cellular edema in ipsilateral retina of both SDH +/+ and SDH -/- retina after transient MCAO. The level of immunoreactivity against Aquaporin-4 and nitrotyrosine in studying the presence of oxidative stress; glutamine synthetase and glutamate in studying the toxicity of astrocyte glutamate; sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) in studying the regulation Ca2+ homeostasis was determined using immunohistochemistry. For all the antibodies, there was similar immunoreactivity level between the contralateral side of both SDH+/+ and SDH -/- mice. For the SDH+/+ group, there was increase in signal in the ipsilateral retina in comparison with the contralateral one. On the other hand, for the SDH-/- group, similar result was observed. There was increase in signal and it was found more in the ipsilateral retina in comparison with the contralateral retina. Finally, in the ipsilateral retina of both SDH +/+ and SDH -/- mice, increased immunoreactivity was found in both but their difference was not statistically significant. This concluded that SDH deletion and subsequent accumulation of sorbitol metabolites did not contribute significantly in the role of pathogenesis of ischemic retinopathy especially in mice after I/R injury. DOI: 10.5353/th_b5071282 Subjects: Sorbitol Dehydrogenases Oxidative stress Diabetic retinopathy Retina - Diseases - Pathogenesis


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Product Details
  • ISBN-13: 9781360998626
  • Publisher: Open Dissertation Press
  • Publisher Imprint: Open Dissertation Press
  • Height: 279 mm
  • No of Pages: 102
  • Spine Width: 5 mm
  • Width: 216 mm
  • ISBN-10: 1360998624
  • Publisher Date: 26 Jan 2017
  • Binding: Paperback
  • Language: English
  • Series Title: English
  • Weight: 259 gr


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