| Autor: |
Strobel, Natalie A., Matsumoto, Aya, Peake, Jonathan M., Marsh, Susan A., Peternelj, Tina‐Tinkara, Briskey, David, Fassett, Robert G., Coombes, Jeff S., Wadley, Glenn D. |
| Předmět: |
|
| Zdroj: |
Physiological Reports; Dec2014, Vol. 2 Issue 12, pn/a-N.PAG, 10p |
| Abstrakt: |
We investigated the relationship between markers of mitochondrial biogenesis, cell signaling, and antioxidant enzymes by depleting skeletal muscle glutathione with diethyl maleate (DEM) which resulted in a demonstrable increase in oxidative stress during exercise. Animals were divided into six groups: (1) sedentary control rats; (2) sedentary rats + DEM; (3) exercise control rats euthanized immediately after exercise; (4) exercise rats + DEM; (5) exercise control rats euthanized 4 h after exercise; and (6) exercise rats + DEM euthanized 4 h after exercise. Exercising animals ran on the treadmill at a 10% gradient at 20 m/min for the first 30 min. The speed was then increased every 10 min by 1.6 m/min until exhaustion. There was a reduction in total glutathione in the skeletal muscle of DEM treated animals compared to the control animals ( P < 0.05). Within the control group, total glutathione was higher in the sedentary group compared to after exercise ( P < 0.05). DEM treatment also significantly increased oxidative stress, as measured by increased plasma F2-isoprostanes ( P < 0.05). Exercising animals given DEM showed a significantly greater increase in peroxisome proliferator activated receptor γ coactivator-1 α (PGC-1 α) mRNA compared to the control animals that were exercised ( P < 0.05). This study provides novel evidence that by lowering the endogenous antioxidant glutathione in skeletal muscle and inducing oxidative stress through exercise, PGC-1 α gene expression was augmented. These findings further highlight the important role of exercise induced oxidative stress in the regulation of mitochondrial biogenesis. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
