April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Can Hyperglicemia Induced Oxidative Stress and Inflammation With Genetic Influence Lead to Diabetic Retinopathy?
Author Affiliations & Notes
  • P. DeSouza-Ramalho
    Ophthalmology-Genetics,
    Lisbon University, Lisboa, Portugal
  • A. Pereira da Silva
    Genetics Laboratoty, Metabolic Unit,
    Lisbon University, Lisboa, Portugal
  • P. Pego
    Genetics Laboratoty, Metabolic Unit,
    Lisbon University, Lisboa, Portugal
  • M. Bicho
    Genetics Laboratoty, Metabolic Unit,
    Lisbon University, Lisboa, Portugal
  • Footnotes
    Commercial Relationships  P. DeSouza-Ramalho, None; A. Pereira da Silva, None; P. Pego, None; M. Bicho, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 1371. doi:
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      P. DeSouza-Ramalho, A. Pereira da Silva, P. Pego, M. Bicho; Can Hyperglicemia Induced Oxidative Stress and Inflammation With Genetic Influence Lead to Diabetic Retinopathy?. Invest. Ophthalmol. Vis. Sci. 2009;50(13):1371.

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

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Abstract

Purpose: : Diabetic Retinopathy neurovascular degenerative complication of systemic disease is one of the main causes of blindness in adults. Its pathogenesis is not fully understood. There is growing evidence that inflammation/oxidative stress are the main factors involved in STZ induced diabetic rats with blood retinal barrier breakdown and vascular/neuronal apoptosis. To assess the role of inflammation/oxidative stress/genetic influence we studied blood markers and genetic phenotypes in diabetics with and without retinopathy and controls.

Methods: : Transmembrane Reductase (TMR), Erythropoietin (EPO), Low molecular weight acid phosphatase (ACP1) and Haptoglobin (Hp) genetic phenotypes (3 phenotypes: 2-2, 2-1, 1-1) were studied in 60 type 2 diabetics and 44 non diabetic controls. Diabetics of both sexes with mean age of 64.2 ± 64 years and the controls were age and sex matched.TMR (mmol/l cell/h)and ACP1 (µmol/g/hb) studied by spectophotometry,EPO by ELISA,"" Haptoglobin phenotypes in the serum by polyacrylamide gel electrophoresis.

Results: : TMR activity high in retinopathy 5.29±2.11vs 4.11±1.51 controls. p=0.016.EPO levels high in retinopathy patients:15.15±11.14 vs 9.47±6.57 vs controls p=0.043.ACP1 values high: 360.99± 41.81 vs 188.63 ± 43.17,with retinopathy vs controls, p=0.001.Hp 2-2 phenotypes high incidence in diabetics with retinopathy (41.7%)Hp 2-1 high incidence in diabetics without retinopathy (70.3%), p=0.0.28Hp 2-2 high levels of EPO 28.38 mIU/ml compared to Hp 1-1, 2-1 with 10.07 mIU/ml.Correlation between TMR and EPO.

Conclusions: : This study with high TMR,EPO,ACP1 activity and Hp genetic phenotypes related markers in diabetic retinopathy supports the role of inflammation/ oxidative damage and genetic influence in the process of retinopathy. Other inflammatory/oxidative stress molecules studied,like MHR(methemoglobine reductase), EpOx (epinephrine oxidase) and ACE (angiotensin converting enzyme) gives additional support to this hypothesis with therapeutic implications. Further studies are required to understand the mechanisms of Diabetic Retinopathy.

Keywords: clinical laboratory testing • inflammation • diabetic retinopathy 
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