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.
Iuchi
Yoshihito
Y
Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata 990-9585, Japan.
Roy
Dipa
D
Okada
Futoshi
F
Kibe
Noriko
N
Tsunoda
Satoshi
S
Suzuki
Saori
S
Takahashi
Motoko
M
Yokoyama
Hidekatsu
H
Yoshitake
Jun
J
Kondo
Seiji
S
Fujii
Junichi
J
D000818:Animals; D004578:Electron Spin Resonance Spectroscopy; D005143:Eyelids / Q000473:pathology; D005145:Face / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D018384:Oxidative Stress; D012871:Skin Diseases / Q000209:etiology*; D013482:Superoxide Dismutase / Q000172:deficiency*; D000072105:Superoxide Dismutase-1; D013997:Time Factors; D014945:Wound Healing
C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1