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

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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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Acknowledgments

This work was supported, in part, by Global COE Program (F03) from the Japan Society for the Promotion of Science and by the Cosmetology Research Foundation.

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The authors have no conflict of interest to declare. The authors are responsible for generating the data and preparing the manuscript.

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Correspondence to Junichi Fujii.

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Iuchi, Y., Roy, D., Okada, F. et al. Spontaneous skin damage and delayed wound healing in SOD1-deficient mice. Mol Cell Biochem 341, 181–194 (2010). https://doi.org/10.1007/s11010-010-0449-y

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