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Overexpression of mitochondrial superoxide dismutase in mice protects the retina from diabetes-induced oxidative stress
Abstract
The retina experiences mitochondrial dysfunction in diabetes, superoxide levels are elevated, and mitochondrial superoxide dismutase (MnSOD) activity is decreased. Inhibition of superoxide accumulation in diabetes prevents mitochondrial dysfunction, apoptosis of retinal capillary cells, and the development of retinal histopathology. The purpose of this study is to examine the effect of overexpression of MnSOD on oxidative stress, DNA damage, and nitrative stress in the retina of diabetic mice. After 7 weeks of diabetes in MnSOD overexpressing (hemizygous) mice (MnSOD-Tg) and in their age-matched nontransgenic mice, parameters of oxidative stress and nitrative stress were measured in the retina. Overexpression of MnSOD prevented diabetes-induced decreases in retinal GSH levels and the total antioxidant capacity. In the same retina, MnSOD overexpression also inhibited diabetes-induced increases in the levels of 8-OHdG and nitrotyrosine. This suggests that MnSOD could be implicated in the pathogenesis of retinopathy by protecting the retina from increased oxidative damage experienced in diabetic conditions. Thus, understanding how changes in mitochondrial function result in the development of diabetic retinopathy could help identify SOD mimics to inhibit its development.
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“In another report, this group showed that MnSOD overexpression in transgenic mice inhibited oxidative damage to the retina, manifest as 8-OHdG and nitrotyrosine (173).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [173]
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Metadata
- Authors
- Kowluru, R. A., Kowluru, V., Xiong, Y., & Ho, Y.-S.
- Affiliations
- Wayne State University (US)
- University of Michigan (US)
- Corresponding author
- Kowluru, Renu A.
- ORCID
- Xiong, Ye
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2006-10
- Volume
- 41
- Issue
- 8
- Pages
- 1191-1196
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W2002675245
- Cited by
- 233
- References
- 43
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 3 · 2023: 7 · 2022: 5 · 2021: 13 · 2020: 9 · 2019: 11 · 2018: 7 · 2017: 13 · 2016: 16 · 2015: 14 · 2014: 13 · 2013: 14 · 2012: 16
- FWCI
- 12.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p30es006639-15)
- National Institute of Environmental Health Sciences (P30-ES006639)
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
- Keywords
- mitochondrial superoxide dismutase, diabetic retinopathy, oxidative stress, nitrative stress, mitochondrial dysfunction, DNA damage, 8-hydroxy-2'-deoxyguanosine, nitrotyrosine, glutathione, antioxidant capacity, superoxide dismutase mimetic
- MeSH terms
- Animals, Diabetes Mellitus, Experimental, Diabetic Retinopathy, Female, Humans, Male, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Retina, Superoxide Dismutase, Gene Expression, Oxidative Stress, Mice
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