| Budget Amount *help |
¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Superoxide dismutases (SODs) are antioxidant proteins converting superoxide to hydrogen peroxide. In vertebrate cells, SOD1 is present in the cytoplasm, with small levels found in the nucleus and mitochondrial intermembrane space. SOD2 is present in the mitochondrial matrix. We conditionally disrupted the SOD1 or SOD2 gene in DT40 cells and found that depletion of SOD1 caused lethality, while depletion of SOD2 led to growth retardation. The lethality in SOD1-depleted cells was rescued by ascorbic acid. We demonstrated that ascorbic acid off set growth defects observed in SOD2-depleted cells and lowered mitochondrial superoxide to physiological levels in both SOD1- or SOD2-depleted cells. Depletion of SOD1 or SOD2 resulted in the accumulation of intracellular oxidative stress. This oxidative stress was reduced by ascorbic acid. Our study suggests that ascorbic acid can be applied as an antioxidant that mimics the functions of cytoplasmic and mitochondrial SODs.
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