May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Retinal Cell Damage Due to Oxidative Stress in Diabetic Retinopathy
Author Affiliations & Notes
  • H. Sato
    Ophthalmology & Visual science,
    Yamagata University, Yamagata, Japan
  • S. Sato
    Ophthalmology & Visual science,
    Yamagata University, Yamagata, Japan
  • R. Kawasaki
    Ophthalmology & Visual science,
    Yamagata University, Yamagata, Japan
  • T. Yamamoto
    Ocular cellular engineering,
    Yamagata University, Yamagata, Japan
  • T. Yamashita
    MITSUBISHI–KAGAKU Bio–Clinical Laboratories, Tokyo, Japan
  • H. Yamashita
    Ophthalmology & Visual science,
    Yamagata University, Yamagata, Japan
  • Footnotes
    Commercial Relationships  H. Sato, None; S. Sato, None; R. Kawasaki, None; T. Yamamoto, None; T. Yamashita, None; H. Yamashita, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 443. doi:
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      H. Sato, S. Sato, R. Kawasaki, T. Yamamoto, T. Yamashita, H. Yamashita; Retinal Cell Damage Due to Oxidative Stress in Diabetic Retinopathy . Invest. Ophthalmol. Vis. Sci. 2005;46(13):443.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Background and Purpose:Oxidative stress exerts serious insults on retinal cells. In this study, the cell damage due to oxidative stress along with the progression of retinopathy was evaluated by measuring the expression levels of 8–Hydroxy–2’–deoxyguanosine (8–OHdG= the bio–marker of cell damage due to oxidative stress) and other bio–markers in vitreous of diabetic eyes. Methods:The vitreous specimens were obtained during surgeries from 59 eyes (7 eyes of diabetic macular edema without new vessels (DME), 26 eyes with proliferative diabetic retinopathy(PDR), 26 eyes with idiopathic macular hole or epiretinal membrane(the control)), after securing the written permission from the subjects. This study has been approved by the Ethical Committee of Yamagata University Faculty of Medicine. The concentration of 8–OHdG, interleukin–6 (IL–6) and vascular endothelial growth factor(VEGF) (the latter 2 factors as markers of retinopathy severity) were measured by enzime–linked immunosorbentassay. To measure the expression level of nitric oxide (NO) as a marker of oxidative stress, Nox level was measured by Griess method instead of NO. Results:The expression levels of VEGF and IL–6 were significantly higher in the DME and the PDR eyes than in the control (P=0.016 and P=0.006,respectively). There was no significant difference of the vitreous levels of IL–6 or VEGF between in the DME and the PDR eyes (p=0.2361,p=0.0985 respectively). The expression levels of 8–OHdG and NOx were significantly higher in the DME and the PDR eyes than in the control. There was no significant difference of the vitreous levels of 8–OHdG or NOx between in the DME and in the PDR eyes (p=0.7456). Conclusions:The retinopathy severity, oxidative stress level and retinal cell damage in the diabetic macular edema eyes without new vessel formation was almost similar to the proliferative stage. Anti–oxidant agents are good candidates of therapeutic agents for diabetic macular edema.

Keywords: diabetic retinopathy • oxidation/oxidative or free radical damage • cytokines/chemokines 
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