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Updated: Jul 14, 2026
En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
Published on: February 25, 2016
Effect of aging, MnSOD deficiency, and genetic background on endothelial function: evidence for MnSOD
Kathryn A Brown1, Sean P Didion, Jon J Andresen
1Departments of Pharmacology, Cardiovascular Center, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA 52242, USA.
Objective:
The goal of this study was to compare vascular function, superoxide levels, and MnSOD protein expression in young (4 to 7 months) and old (22 to 24 months) MnSOD+/+ and MnSOD-deficient (MnSOD+/-) mice.
Methods And Results:
Relaxation of aorta in vitro to the endothelium-dependent dilator acetylcholine (ACh) was similar in young MnSOD+/+ (n=9) and young MnSOD+/- (n=6) mice. This response was impaired in old MnSOD+/+ (n=8) mice and old MnSOD+/- mice (n=14), with dysfunction being greater in old MnSOD-deficient mice (eg, 100 micromol/L ACh produced 77+/-3% [mean+/-SE], 77+/-3%, 70+/-4%, and 57+/-4% relaxation in young MnSOD+/+, young MnSOD+/-, old MnSOD+/+, and old MnSOD+/- mice, respectively). The endothelial dysfunction was similar in mice on both C57BL/6 and CD-1 genetic backgrounds. In contrast to ACh, responses to the endothelium-independent dilator sodium nitroprusside were enhanced in old MnSOD+/+ and MnSOD+/- mice compared with both groups of young mice (P<0.05). Superoxide levels, as measured using lucigenin-enhanced chemiluminescence, were increased more than 2-fold in old MnSOD+/- mice compared with old MnSOD+/+ and young mice (P<0.05).
Conclusions:
These data provide the first direct evidence that MnSOD haploinsufficiency results in increased vascular oxidative stress and endothelial dysfunction with aging.
Insights
Manganese superoxide dismutase (MnSOD) deficiency leads to increased vascular oxidative stress and endothelial dysfunction in aging mice. This study shows MnSOD haploinsufficiency exacerbates age-related vascular problems.
Area of Science:
- Cardiovascular Biology
- Oxidative Stress Research
- Aging Studies
Background:
- Manganese superoxide dismutase (MnSOD) is a key antioxidant enzyme.
- Aging is associated with increased oxidative stress and vascular dysfunction.
- The role of MnSOD in age-related vascular changes requires further elucidation.
Purpose of the Study:
- To compare vascular function, superoxide levels, and MnSOD protein expression.
- To investigate the impact of MnSOD deficiency on vascular health during aging.
- To assess differences between young and old mice with varying MnSOD levels.
Main Methods:
- Vascular function assessed via in vitro aortic relaxation to acetylcholine (endothelium-dependent) and sodium nitroprusside (endothelium-independent).
- Superoxide levels measured using lucigenin-enhanced chemiluminescence.
- Comparisons made between young (4-7 months) and old (22-24 months) MnSOD+/+ and MnSOD+/- mice.
Main Results:
- Endothelium-dependent relaxation was impaired in old mice of both genotypes, more so in MnSOD+/- mice.
- Endothelium-independent relaxation was enhanced in old mice compared to young mice.
- Superoxide levels were significantly increased in old MnSOD+/- mice.
Conclusions:
- MnSOD haploinsufficiency causes increased vascular oxidative stress.
- MnSOD deficiency contributes to endothelial dysfunction with aging.
- These findings highlight MnSOD's critical role in mitigating age-related vascular decline.
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