Acute Exercise Induced Mitochondrial H2O2 Production in Mouse Skeletal Muscle: Association with p66Shc and FOXO3a Signaling and Antioxidant Enzymes. (22nd March 2015)

• Record Type: Journal Article
• Authors: Wang, Ping; Li, Chun Guang; Qi, Zhengtang; Cui, Di; Ding, Shuzhe
• Other Names: Zhang Y. Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2015(2015)
• Publication Date: 2015-03-22
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2015/536456
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : Exercise induced skeletal muscle phenotype change involves a complex interplay between signaling pathways and downstream regulators. This study aims to investigate the effect of acute exercise on mitochondrial H2 O2 production and its association withp 66Shc, FOXO3a, and antioxidant enzymes. Male ICR/CD-1 mice were subjected to an acute exercise. Muscle tissues (gastrocnemius and quadriceps femoris) were taken after exercise to measure mitochondrial H2 O2 content, expression ofp 66Shc and FOXO3a, and the activity of antioxidant enzymes. The results showed that acute exercise significantly increased mitochondrial H2 O2 content and expressions ofp 66Shc and FOXO3a in a time-dependent manner, with a linear correlation between the increase in H2 O2 content andp 66Shc or FOXO3a expression. The activity of mitochondrial catalase was slightly reduced in the 90 min exercise group, but it was significantly higher in groups with 120 and 150 min exercise compared to that of 90 min exercise group. The activity of SOD was not significantly affected. The results indicate that acute exercise increases mitochondrial H2 O2 production in the skeletal muscle, which is associated with the upregulation ofp 66Shc and FOXO3a. The association ofp 66Shc and FOXO3a signaling with exercise induced H2 O2 generation may play a role in regulating cellular oxidative stress during acute exercise.