To clarify the role of iron in oxidative stress in skeletal muscle atrophied by immobilization, we investigated the effect of deferoxamine--an iron-chelating agent. Deferoxamine, iron-saturated deferoxamine and double-distilled water (control) were administered subcutaneously from the 4th day after immobilization via osmotic pumps to male Wistar rats (14 weeks old), one ankle joint of which was immobilized in the extended position. After 12 days' immobilization, soleus--typical slow red muscles were collected from both hind limbs and their levels of thiobarbituric acid-reactive substance (TBARS) and glutathione were measured. Deferoxamine suppressed the increase of TBARS and glutathione disulfide in atrophied muscle while iron-saturated deferoxamine did not, which strongly suggests that the iron-chelating action of deferoxamine suppressed the increased oxidative stress. This means that iron plays a very important role in increasing oxidative stress in atrophied muscle. In addition, deferoxamine decreased the degree of atrophy, an effect thought to be mediated by the suppression of oxidative stress.
Single ankle joints of male Wistar rats (15-week-old) were immobilized in the extended position for 7 days and remobilized for 5 days after the immobilization period. Atrophic and contralateral soleus, typical slow red muscles, were collected and their levels of thiobarbituric acid-reactive substance (TBARS) and glutathione were measured. Five-day remobilization did not increase muscle weight significantly. However, there were significant increases in TBARS and oxidized glutathione in the recovering muscle, which strongly suggested that enhanced oxidative stress occurred during the recovery from disuse muscle atrophy. Vitamin E injection accelerated the recovery from atrophy, thus showing that oxidative stress slowed it down.
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