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ASGSB 2004 Annual Meeting Abstracts
[94]
Xanthine Oxidase and Myoglobin Release in Post-Suspended Rats. IK Abukhalaf 1, CD Mitchell2,6, AW von Deutsch2, LE Wineski5, NA Silvestrov3 and DA von Deutsch2,3,4. 1Department of Biotechnology and Genetic Engineering, Philadelphia University, Jordan, 2NASA Space Medicine and Life Science Research Center, 3Department of Pharmacology and Toxicology, 4Clinical Research Center, 5Department of Anatomy and Neurobiology, Morehouse School of Medicine (MSM), 720 Westview Dr, SW, Atlanta, GA 30310, 6MBRS Program, MSM and Morehouse College, Atlanta, GA 30310. Objective: Xanthine oxidase (XO) released from damaged vascular endothelium could account for both the high levels of iron and oxidative stress observed during the post-suspension (PS) period. Methods: Studies were conducted using hindlimb suspended (S) and post-suspended (PS) rats. Non-suspended (NS) rats served as controls. Iron levels and XO activity were determined colorimetrically. Total glutathione was determined by HPLC. Results: In PS rats, both plasma XO activity (182.4± 32.0%, p< 0.001) at 24 hrs and mean iron content (121.2± 6.2%, p= 0.038) were significantly greater than NS controls. Plasma myoglobin levels in S rats were 35.0± 6.6% (p= 0.013) of the NS controls (100.0± 21.2%), while at 24 hrs levels were significantly greater (283.1± 74.4%, p= 0.033). With increasing plasma iron content and XO activity, GSH levels decreased over the 24 hrs of post-suspension (64.1± 5.3% of the NS control at 24 hrs). Conclusions: In PS rats, plasma XO activity, myoglobin and iron content were all significantly higher than those observed in NS controls. In contrast, plasma glutathione levels were significantly reduced in PS rats, suggesting increased levels of oxidative stress-induced by the reloading of skeletal muscles. From these studies, a better insight can be gained in developing more effective countermeasures to skeletal muscle atrophy, muscle damage, and subsequent increase in oxidative stress levels that result from skeletal muscle unloading and reloading-induced trauma. This work was supported, in part, by NASA Grant NCC9-112, NIH Grants 1R25RR17694, 5P20RR011104, and MBRS Grant 506GM08248.
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