| Literature DB >> 20352474 |
Yoshihito Iuchi1, Dipa Roy, Futoshi Okada, Noriko Kibe, Satoshi Tsunoda, Saori Suzuki, Motoko Takahashi, Hidekatsu Yokoyama, Jun Yoshitake, Seiji Kondo, Junichi Fujii.
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.Entities:
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Year: 2010 PMID： 20352474 DOI： 10.1007/s11010-010-0449-y
Source DB: PubMed Journal: Mol Cell Biochem ISSN： 0300-8177 Impact factor: 3.396