Abstract
Exposure to acute hypoxia may stimulate an increase in intracellular reactive oxygen species (ROS) formation leading to subsequent muscular injuries. Hypoxic preconditioning (HPC), which involves cycles of brief exposure to low and normal oxygen, may alleviate this ROS induced damage. However, the mechanism of HPC has not been fully elucidated. In this study, we hypothesized that HPC can mitigate intramuscular ROS in mouse skeletal muscle during hypoxia. Mouse diaphragm was isolated and loaded with dihydrofluorescein (a fluorescent probe) in order to detect ROS production in real time via confocal microscopy during a hypoxic period. Diaphragm strips were either non-treated (n = 5), treated with HPC (5 cycles; n = 5), or subject to antioxidant treatment (ebselen; n = 4), followed by a 30 min hypoxic exposure (PO2 = 5 Torr). Data were analyzed using a multi-way ANOVA, and expressed as means ± SE. In the control, intracellular ROS levels increased after 20 min of hypoxia, and this increase continued until the end of the 30 min hypoxic exposure. However, there was no substantial ROS formation in muscles treated with either HPC or the antioxidant, ebselen. Our data suggest that HPC suppresses intracellular ROS generation in respiratory skeletal muscle subjected to a hypoxic condition. Thus, we speculate that HPC can be used as a potential drug-free treatment to prevent oxidative injuries in respiratory muscle during hypoxia. Supported by OU General Fund G110, and Research Excellence Fund of Biomedical Research, OSU-HRS Fund 013000.
Published Version
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