Increased nadh oxidase activity in the retina of the BBZ/WOR diabetic rat

E. Ann Ellis, Maria B. Grant, Frederick T. Murray, Martha B. Wachowski, Dennis L. Guberski, Paul S. Kubilis, Gerard A. Lutty

Research output: Contribution to journalArticle

103 Scopus citations

Abstract

This morphological study demonstrates a role for endothelial cells in generating reactive oxygen species in early stages of retinopathy in the BBZ/Wor rat, an obese, noninsulin dependent model of diabetes. Hyperglycemia induced pseudohypoxia results in an imbalance in cytosolic NADH/NAD+. In the oxygen-rich environment of the retina, NADH oxidase generates superoxide radical which is dismutated to hydrogen peroxide. Localization of hydrogen peroxide by the cerium NADH oxidase enzyme activity cytochemical localization technique shows a statistically significant increase of peroxide localization in the central retina of diabetic rats as compared to age-matched, nondtabetic controls. Endothelial cell dysfunction, indicated by leakage of endogenous serum albumin, coincided with areas of NADH oxidase activity localization. In diabetic rats there are increased levels of fibronectin in areas of hydrogen peroxide localization. This in vivo, morphological study is the first demonstration of oxidative injury and endothelial cell dysfunction in the retina of a spontaneous, noninsulin dependent model of diabetes.

Original languageEnglish (US)
Pages (from-to)111-120
Number of pages10
JournalFree Radical Biology and Medicine
Volume24
Issue number1
DOIs
StatePublished - Jan 1 1998

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Keywords

  • Diabetes
  • Endothelial dysfunction
  • NADH oxidase
  • Oxidative injury
  • Retinopathy
  • Vascular leakage

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

Cite this

Ellis, E. A., Grant, M. B., Murray, F. T., Wachowski, M. B., Guberski, D. L., Kubilis, P. S., & Lutty, G. A. (1998). Increased nadh oxidase activity in the retina of the BBZ/WOR diabetic rat. Free Radical Biology and Medicine, 24(1), 111-120. https://doi.org/10.1016/S0891-5849(97)00202-5