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1 Dept. of Internal Med. and Physiology, Ohio State University, Columbus, Ohio, United States
* To whom correspondence should be addressed. E-mail: thomas.clanton{at}osumc.edu.
The existence of hypoxia-induced reactive oxygen species (ROS) production remains controversial. However, numerous observations with a variety of methods and in many cells and tissue types are supportive of this idea. Skeletal muscle appears to behave much like heart in that in the early stages of hypoxia there is a transient elevation in ROS, whereas in chronic exposure to very severe hypoxia there is evidence of ongoing oxidative stress. Important remaining questions which are addressed in this review include: Are there levels of PO2 in skeletal muscle, typical of physiologic or mildly pathophysiologic conditions, which are low enough to induce significant ROS production? Does the ROS associated with muscle contractile activity reflect imbalances in oxygen uptake and demand that drive the cell to a more reduced state? What are the possible molecular mechanisms by which ROS may be elevated in hypoxic skeletal muscle? Is the production of ROS in hypoxia of physiological significance, both with respect to cell signaling pathways promoting cell function and with respect to damaging effects of long term exposure? Discussion of these and other topics leads to general conclusions that hypoxia-induced ROS may be a normal physiologic response to imbalance in oxygen supply and demand or environmental stress and may play a yet undefined role in normal response mechanisms to these stimuli. However, in chronic and extreme hypoxic exposure, muscle may fail to maintain a normal redox homeostasis, resulting in cell injury or dysfunction.
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