Research on a new oxygen radicals-eliminating system induced by aerobic physical exercise
| Project/Area Number |
16500429
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Sports science
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| Research Institution | Kobe Gakuin University |
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Principal Investigator |
OKAMOTO Tadashi Kobe Gakuin University, The Faculty of Pharmaceutical Sciences, Professor, 薬学部, 教授 (80194398)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Takayuki Kobe Gakuin University, The Faculty of Pharmaceutical Sciences, Lecturer, 薬学部, 講師 (40216726)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | coenzyme Q / ubiquinone / aerobic physical exercise / oxygen radicals / reduced form of coenzyme Q / ubiquinol / コエンザイムQ10 / ユビキノン-10 / 還元型コエンザイムQ10 / ユビキノール-10 / 活性酸素 / 疲労 / レドックスサイクル / コエンザイムQ_<10> / 抗酸化作用 / NADPH-コエンザイムQ還元酵素 / 筋疲労 |
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| Research Abstract |
In this research, we studied a role of the NAD(P)H-coenzyme Q reductase in a cellular redox cycle of coenzyme Q as a new oxygen radicals-eliminating system.
The effects of simvastatin (statin), an inhibitor of 3-hydroxy-3-methylglutaryl CoA reductase, on oxidative stress resistance and the NAD(P)H-coenzyme Q reductase activity were investigated. Oral administration of statin suppressed the biosynthesis of coenzyme Q, which shares the same biosynthesis pathway as cholesterol up to farnesyl pyrophosphate, thus compromising the physiological function of reduced coenzyme Q, which possesses antioxidant activity. When statin was administered to mice, the levels of oxidized and reduced coenzyme Qs in serum, liver, and heart, decreased significantly when compared with those of control. Statin also reduced not only the activity of NAD(P)H-coenzyme Q reductase but also the resistance of heart and liver mitochondria to lipid peroxidation induced by Fe^<2+>-ascorbate. However, these undesirable eff
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ects induced by statin were alleviated by coadministering coenzyme Q10 with simvastatin to mice. These observations suggested that cytosolic NAD(P)H-coenzyme Q reductase is responsible for cellular coenzyme Q redox cycle as an endogenous antioxidant.
On the other hand, we also studied the relationship between an aerobic physical exercise and coenzyme Q redox cycle. As an aerobic exercise, swimming was selected in this study. Swimming exercises were performed with a weight corresponding to 3% body weight attached the tail of a rat. In response to the swimming performance, serum levels of lactate and LDH release increased in rats. The content ratio of the reduced form of coenzyme Q to the total coenzyme Q was significantly lower than that of non-exercise group. Furthermore, oral administration of coenzyme Q10 to rats significantly enhanced the endurance performance time and cytosolic NAD(P)H-coenzyme Q reductase. These results suggested that NAD(P)H-coenzyme Q reductase play a beneficial role in the elimination of swimming exercise-derived oxygen radicals. Less
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Report
(4 results)
Research Products
(17 results)
