XANTHINE OXIDASE AND MYOGLOBIN RELEASE IN POST-SUSPENDED RATS

With prolonged exposure to a microgravity environment, astronauts experience muscle unloading and significant loss in skeletal muscle mass. Subsequently, during readaptation to Earth’s gravity astronauts (as well as animals) can experience varying degrees of muscle damage while reloading atrophied muscles. Additionally, the astronauts can suffer from post-flight symptoms of severe muscle pain, marked muscle edema, and high blood levels of muscle specific markers creatine kinase (CKmm) and myoglobin [Sayers and Clarkson, 2003]. Subsequently, excess protein loads arising from injured muscle could ultimately lead to increasing levels of oxidative damage resulting from the release of iron from heme (e.g., myoglobin and hemoglobin) and non-heme proteins [Menshikova et al, 1999; Fang et al., 2002]. However, sources of oxidative stress and subsequent damage have remained elusive. Furthermore, regions of ischemia and anoxia can cause lysis of the vascular endothelium and disruption of the sarcolemma. In damaged muscle fibers, extracellular edema, extravasated erythrocytes, macrophages and neutrophils have been observed. Studies aboard COSMOS flights revealed microhemorrhages, thrombi and segmental necrosis [Krippendorf and Riley, 1994]. In addition, exposure to radiation while in space as well as bouts of ischemia/reperfusion are undoubtedly contributing factors for increases in oxidative stress and damage occurring during readaptation. The purpose of this study was to determine whether the release of free radical generators such as xanthine oxidase (XO) could account for both the high levels of iron and oxidative stress observed during the post-suspension (PS) period.