May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Mitochondrial Superoxide and Diabetic Retinopathy
Author Affiliations & Notes
  • M. Kanwar
    Ophthalmology, Kresge Eye Institute, Detroit, Michigan
  • R. A. Kowluru
    Ophthalmology, Kresge Eye Institute, Detroit, Michigan
  • Footnotes
    Commercial Relationships M. Kanwar, None; R.A. Kowluru, None.
  • Footnotes
    Support NIH, Jvenile Diabetes research Foundation, The Thomas Foundation
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 4990. doi:
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      M. Kanwar, R. A. Kowluru; Mitochondrial Superoxide and Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4990.

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

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Purpose:: Superoxide levels are elevated in the retina in diabetes, and cytochrome c is released from the mitochondria. This study is to elucidate the mechanism involved in the oxidative damage of retinal mitochondria in diabetes, and to determine if mitochondrial superoxide dismutase (MnSOD) can provide protection.

Methods:: Effect of diabetes was investigated on superoxide and GSH levels, electron transport complexes I and III, and membrane permeability in the isolated mitochondria prepared from the retina of mice that were made diabetic. To investigate the effect of MnSOD, mitochondrial oxidative stress and electron transport complexes were determined also in the retina of mice overexpressing MnSOD (MnSOD-Tg) made diabetic with streptozotocin.

Results:: Retinal mitochondria from wild type (WT) diabetic mice had 2 fold increase in superoxide levels compared to WT-non diabetic control mice. In the same retinal mitochondria diabetes decreased GSH levels by 40% and complex III activity by about 20%, and increased the swelling by over 2 fold; however, complex I activity was not affected. Overexpression of MnSOD inhibited diabetes-induced increase in mitochondrial superoxide levels and swelling, and decrease in complex III activity, but GSH values were not statistically different in WT and MnSOD-Tg diabetic mice.

Conclusions:: Retinal mitochondria experiences increased oxidative damage in diabetes and complex III appears to be one of the major sources of increased superoxide. MnSOD provides protection from diabetes-induced abnormalities in the mitochondria, strongly implicating the role for MnSOD in the pathogenesis of retinopathy in diabetes.

Keywords: diabetic retinopathy • apoptosis/cell death • mitochondria 

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