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Skeletal muscle reperfusion injury is enhanced in extracellular superoxide dismutase knockout mouse

¹Department of Orthopaedic Surgery, College of Medicine, Korea University, Seoul, Korea; and ²Division of Pulmonary, Allergy, and Critical Care, Departments of Medicine and Cell Biology, and ³Orthopaedic Microsurgery Laboratory, Department of Surgery, Duke University Medical Center, Durham, North Carolina

Submitted 14 May 2004 ; accepted in final form 13 March 2005

This study investigates the role of extracellular SOD (EC-SOD), the major extracellular antioxidant enzyme, in skeletal muscle ischemia and reperfusion (I/R) injury. Pedicled cremaster muscle flaps from homozygous EC-SOD knockout (EC-SOD^–/–) and wild-type (WT) mice were subjected to 4.5-h ischemia and 90-min reperfusion followed by functional and molecular analyses. Our results revealed that EC-SOD^–/– mice showed significantly profound I/R injury compared with WT littermates. In particular, there was a delayed and incomplete recovery of arterial spasm and blood flow during reperfusion, and more severe acute inflammatory reaction and muscle damage were noted in EC-SOD^–/– mice. After 90-min reperfusion, intracellular SOD [copper- and zinc-containing SOD (CuZn-SOD) and manganese-containing (Mn-SOD)] mRNA levels decreased similarly in both groups. EC-SOD mRNA levels increased in WT mice, whereas EC-SOD mRNA was undetectable, as expected, in EC-SOD^–/– mice. In both groups of animals, CuZn-SOD protein levels decreased and Mn-SOD protein levels remained unchanged. EC-SOD protein levels decreased in WT mice. Histological analysis showed diffuse edema and inflammation around muscle fibers, which was more pronounced in EC-SOD^–/– mice. In conclusion, our data suggest that EC-SOD plays an important role in the protection from skeletal muscle I/R injury caused by excessive generation of reactive oxygen species.

reactive oxygen species; vessel diameter; blood flow

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