Ischemia-reperfusion injury in rat skeletal muscle is attenuated by zinc aspartate

Background. Oxygen-derived free radical-induced cell injury has been suggested to have a pivotal role in the etiology of ischemia-reperfusion injury. Thus, several lines of evidence indicate that antioxidant agents may be useful therapeutics in this condition. In this regard, the effect of zinc aspartate on ischemia-reperfusion injury was investigated in skeletal muscle. Materials and methods. Tourniquet ischemia-reperfusion injury method was applied to Sprague-Dawley rats. Experimental groups were as follows: 1) sham control, 2) rats received zinc aspartate, 3) rats received hind limb tourniquet operation (left side), and 4) rats received hind limb tourniquet operation and zinc aspartate. Viability of muscle was evaluated by triphenyltetrazolium chloride dye method by using a spectrophotometer. Malondialdehyde, superoxide dismutase, catalase, glutathione, and glutathione peroxidase were measured in muscle, heart, lung, and blood via a spectrophotometer. Results. The viabilities of ischemic limbs, percentage of the contralateral control muscle, in group 1, 2,3, and 4 were 114 +/- 12%, 87% +/- 5%, 20% +/- 2%, and 95 +/- 10%, respectively. In muscle, increased malondialdehyde and decreased superoxide dismutase, catalase, and glutathione levels in group 3 were normalized by zinc aspartate in both left and right limbs. While malondialdehyde levels in heart and blood increased in group 3, the levels of superoxide dismutase, catalase, glutathione, and glutathione peroxidase were lower in group 3 than those in group 1. All these alterations were prevented by zinc aspartate. Malondialdehyde level of lung in group 3 was significantly higher than group 1 and 2. However, this augmentation was halted by zinc aspartate. The decrease in superoxide dismutase levels in group 3 was statistically reversed by the administration of zinc aspartate. Conclusion. Zinc aspartate seems to be an effective treatment option against ischemia-reperfusion injury. (c) 2007 Elsevier Inc. All rights reserved.