AI Article Synopsis
- * SOD1 (-/-) mice developed facial skin issues significantly by 15 weeks, experiencing symptoms like eyelid swelling and delayed wound healing.
- * The study found that oxidative stress markers were lower in SOD1 (-/-) mice after wounding, indicating an imbalance in their skin's redox state, making it more vulnerable to damage.
Article Abstract
Superoxide dismutase 1 (SOD1) is an important antioxidative enzyme that protects skin from oxidative stress. SOD1 (-/-) mice with a genetic background of b129Sv mice showed facial skin damage after 15 weeks of age. Eyelid swelling occurred as the initial symptom and caused impairment by triggering self-scratching. The period required for wound healing in the back was markedly delayed in 20-week SOD1 (-/-) mice. Oxidative stress markers, 4-hydroxynonenal and thiobarbituric acid-reactive substances, were unexpectedly lower in SOD1 (-/-) mice at day 1 after wounding. The decay rate of electron paramagnetic resonance signal intensity of intravenously injected nitroxide radical indicated that the half-life of the signal intensity was significantly prolonged in the wounded skin of SOD1 (+/+) mice. However, while the half-life of the signal intensity in control skin was a little longer in SOD1 (-/-) mice, it did not change in wounded skin. Taken together, these data suggest that the skin of SOD1 (-/-) mice is in redox imbalance and prone to damage by wounding.
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| http://dx.doi.org/10.1007/s11010-010-0449-y | DOI Listing |
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