Spontaneous skin damage and delayed wound healing in SOD1-deficient mice

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.