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1 Pulmonary, Critical Care Medicine & Sleep Medicine, The Ohio State University, Columbus, OH, USA
* To whom correspondence should be addressed. E-mail: clanton.1{at}osu.edu.
Many tissues produce reactive oxygen species (ROS) during reoxygenation following hypoxia or ischemia; however, whether ROS are formed during hypoxia is controversial. The hypothesis was tested that ROS are generated in skeletal muscle during exposure to acute hypoxia, prior to reoxygenation. Isolated rat diaphragm strips were loaded with dihydrofluorescein-DA (Hfluor-DA), a probe that is oxidized to fluorescein (Fluor) by intracellular ROS. Changes in the fluorescence due to Fluor, NADH and FAD were measured using a tissue fluorometer. The system had a detection limit of 1 µM H2O2 applied to the muscle superfusate. When the superfusion buffer was changed rapidly from 95% O2 to 0%, 5%, 21% or 40% O2, transient elevations in the Fluor were observed that were proportional to the rise in NADH fluorescence and inversely proportional to level of O2 exposure. This signal could be completely inhibited with 40 µM ebselen, a glutathione peroxidase mimic. Following the brief hypoxia exposure (10 min), or exposure to brief periods of H2O2, the fluorescence signal returned to baseline. Furthermore, tissues loaded with oxidized form of the probe (Fluor-DA) showed a similar pattern of response that could be inhibited with ebselen. These results suggest that Fluor and Hfluor exist in a partially reversible redox state within the tissue. When Hfluor-loaded tissues were contracted with low-frequency twitches, Fluor emission and NADH emission were significantly elevated, in a way that resembled the hypoxia-induced signal. We conclude that in the transition to low intracellular PO2, a burst of intracellular ROS is formed that may have functional implications regarding skeletal muscle O2 sensing systems and responses to acute metabolic stress.
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