| Project/Area Number |
13460139
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Applied veterinary science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
DOI Kunio The University of Tokyo, Graduate School of Agricultural and Life Sciences, Professor, 大学院・農学生命科学研究科, 教授 (70155612)
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| Co-Investigator(Kenkyū-buntansha) |
OZAKI Hiroshi The University of Tokyo, Graduate School of Agricultural and Life Sciences, Professor, 大学院・農学生命科学研究科, 教授 (30134505)
NISHIHARA Masugi The University of Tokyo, Graduate School of Agricultural and Life Sciences, Professor, 大学院・農学生命科学研究科, 教授 (90145673)
ONO Ken-ichiro The University of Tokyo, Graduate School of Agricultural and Life Sciences, Professor, 大学院・農学生命科学研究科, 教授 (50111480)
KUWAHARA Masaki The University Tokyo, Graduate School of Agricultural and Life Science, Associate Professor, 大学院・農学生命科学研究科, 助教授 (30205273)
NAKAYAMA Hiroyuki The University of Tokyo, Graduate School of Agricultural and Life Sciences, Associate Professor, 大学院・農学生命科学研究科, 助教授 (40155891)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥15,000,000 (Direct Cost: ¥15,000,000)
Fiscal Year 2003: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2002: ¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 2001: ¥6,500,000 (Direct Cost: ¥6,500,000)
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| Keywords | apoptosis / cell cycle arrest / fetal brain / chemicals / mechanisms / ENU / A ra-C / 5AzC / NMDA / fetotoxicity / placental toxicity / ethylnitrosourea / 5-azacytidine / apotosis / Ethylnitrosourea / ラット胎仔中枢神経 / ラット胎盤 / アポトーシス / 細胞周期停止 / rpL4 / mistosis |
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| Research Abstract |
Mechanisms of chemical-induced fetal brain toxicity were studies using the combination of 6 chemicals and mice or rats. As a result, apoptosis and cell cycle arrest were generally observed in neural epithelial cells. However, the site and sequence of apoptosis and the phase of cell cycle arrest were different among chemicals. In addition, except for T-2 toxin, apoptosis and cell cycle arrest occurred through p53-dependent pass way. In the case of T-2 toxin, apoptosis was induced by oxidative stress and subsequent mitochondrial damage. Furthermore, in the cases of ENU, Ara-C and T-2 toxin, apoptosis and cell cycle arrest were induced also in placenta through the same pass way in the fetal brain.
These results are considered to be very useful for further investigation of the mechanisms of fetotoxicity.
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