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Am J Physiol Heart Circ Physiol (March 18, 2005). doi:10.1152/ajpheart.00458.2004
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Submitted on May 14, 2004
Accepted on March 13, 2005

Skeletal Muscle Reperfusion Injury is Enhanced in Extracellular Superoxide Dismutase Knockout Mouse

Jong Woong Park1, Wen-Ning Qi2, Yongting Cai2, Igor Zelko3, John Q Liu3, Long-En Chen2*, James R Urbaniak2, and Rodney J Folz3

1 Department of Orthopaedic Surgery, College of Medicine, Korea University, Seoul, Korea, Democratic People's Rep
2 Orthopaedic Microsurgery Laboratory, Department of Surgery, Duke University Medical Center, Durham, NC, USA
3 Division of Pulmonary, Allergy, and Critical Care, Departments of Medicine and Cell Biology, Duke University Medical Center, Durham, NC, USA

* To whom correspondence should be addressed. E-mail: chen0006{at}mc.duke.edu.

This study investigates the role of extracellular superoxide dismutase (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 to 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 with EC-SOD-/- mice. After 90 min reperfusion, intracellular SODs' (CuZn-SOD and Mn-SOD) mRNA levels decreased similarly in both groups. EC-SOD mRNA levels increased in WT mice while EC-SOD mRNA was undetectable , as expected, in EC-SOD-/- mice. In both groups of animals, CuZn-SOD protein levels decreased while 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 EC-SOD-/- mice. In conclusion, our data suggest that EC-SOD plays an important role in the protection of skeletal muscle I/R injury caused by excessive generation of reactive oxygen species.




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