Study of failure in mitosis and meiosis caused by oxidative stress using oocytes from SOD1 deficient mice
| Project/Area Number |
21580342
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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 |
Applied animal science
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| Research Institution | Yamagata University |
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Principal Investigator |
KIMURA Naoko 山形大学, 農学部, 教授 (70361277)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 卵母細胞 / 受精卵 / 酸化ストレス / SOD1 / 発生障害 / 細胞周期 / 老化 / 卵子 / 卵成熟 / 卵巣機能 / 卵子・受精卵 / 酸化的発生障害 / SOD1欠損 |
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| Research Abstract |
This study was conducted to elucidate the molecular mechanism of early developmental arrest in in vitro-produced embryos and oocyte aging, using superoxide dismutase 1-deficient (SOD1KO) mice. We found total 2-cell arrest of embryos from SOD1-deficient mice oocytes in culture under atmospheric oxygen conditions. Since the mitochondrial function of ATP production via oxidative phosphorylation was almost normal in the embryos, the mechanism of cell cycle regulation might be a target of elevated ROS. Also, the oxidative stress caused by a SOD1 deficiency during oocyte maturation causes the failure of pronucleus formation after fertilization. This impairment seems to be irrelevant to the abnormality of egg activation events, CGs exocytosis and CaMKγ activation, implying an injury to the cell cycle regulation of the meiosis II exit. Thus, investigation of oocytes/embryos from SOD1KO mice would provide a useful clue to an understanding of the mechanisms involved in early developmental arrest in in vitro-produced embryos and oocyte aging.
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Report
(4 results)
Research Products
(45 results)
