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J Appl Physiol 101: 740-744, 2006. First published May 25, 2006; doi:10.1152/japplphysiol.00144.2006
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Role of exercise intensities in oxidized low-density lipoprotein-mediated redox status of monocyte in men

Jong-Shyan Wang,1 Tan Lee,2 and Shu-Er Chow3

1Institution of Coaching Science, National College of Physical Education & Sports, Tao-Yuan; 2Department of Physiology, and 3Graduate Institute of Rehabilitation Science and Center for Gerontological Research, Chang Gung University, Tao-Yuan, Taiwan

Submitted 5 February 2006 ; accepted in final form 9 May 2006

Exercise significantly influences the progression of atherosclerosis. Oxidized LDL (ox-LDL), as a stimulator of oxidative stress, facilitates monocyte-related atherogenesis. This study investigates how exercise intensity impacts ox-LDL-mediated redox status of monocytes. Twenty-five sedentary healthy men exercised mildly, moderately, and heavily (i.e., 40, 60, and 80% maximal oxygen consumption, respectively) on a bicycle ergometer. Reactive oxygen species (ROS) production, cytosolic and mitochondrial superoxide dismutase (c-SOD and m-SOD, respectively) activities, and total and reduced-form {gamma}-glutamylcysteinyl glycine (t-GSH and r-GSH, respectively) contents in monocytes mediated by ox-LDL were measured. This experiment obtained the following findings: 1) ox-LDL increased monocyte ROS production and was accompanied by decreased c-SOD and m-SOD activities, as well as t-GSH and r-GSH contents, whereas treating monocytes with diphenyleneiodonium (DPI) (a NADPH oxidase inhibitor) or rotenone/2-thenoyltrifluoroacetone (TTFA) (mitochondrial complex I/II inhibitors) hindered ox-LDL-induced monocyte ROS production; 2) production of ROS and reduction of m-SOD activity and r-GSH content in monocyte by ox-LDL were enhanced by heavy exercise and depressed by mild and moderate exercise; and 3) heavy exercise augmented the inhibition of ox-LDL-induced monocyte ROS production by DPI and rotenone/TTFA, whereas these DPI- and rotenone/TTFA-mediated monocyte ROS productions were unchanged in response to mild and moderate exercise. We conclude that heavy exercise increases ox-LDL-induced monocyte ROS production, possibly by decreasing m-SOD activity and r-GSH content in monocytes. However, mild and moderate exercise likely protects individuals against suppression of anti-oxidative capacity of monocyte by ox-LDL.

physical activity; reactive oxygen species; SOD, GSH



Address for reprint requests and other correspondence: J.-S. Wang, Graduate Institute of Rehabilitation Science, Chang Gung Univ., 259 Wen-Hwa 1st Rd., Kwei-Shan, Tao-Yuan, 333, Taiwan (e-mail: s5692{at}mail.cgu.edu.tw)




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