| Project/Area Number |
12470082
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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 |
Hygiene
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| Research Institution | The University of Tokyo |
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Principal Investigator |
WATANBE Chiho Graduate School of Medicins, Associate Professor, 大学院・医学系研究科, 助教授 (70220902)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHINAGA Jun Graduate School of Frontier Sciences, Associate Professor, 大学院・新領域創成科学研究科, 助教授 (70222396)
ENOMOTO Shuichi RIKEN, Institute of Physical & Chemical Research, Senior Researcher, 加速器基盤研究部, 先任研究員 (10271553)
SATOH Hiroshi Tohoku Univ., Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (40125571)
中澤 港 東京大学, 大学院・医学系研究科, 助手 (40251227)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥13,400,000 (Direct Cost: ¥13,400,000)
Fiscal Year 2002: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2001: ¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2000: ¥5,400,000 (Direct Cost: ¥5,400,000)
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| Keywords | Inorganic arsenic / delayed effects / prenatal exposure / Selenium / selenium deficiency / behavioral effects / neurotransmitters / ヒ素 / 周産期曝露 / グルタチオンペルオキシダーゼ / チオレドキシンレダクターゼ / モリス迷路 / 学習機能 / 砒素 / マルチトレーサー / 発達毒性 / 神経毒性 / 行動毒性 |
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| Research Abstract |
Contamination of groundwater with naturally-derived inorganic arsenic has been reported from various counties in the world, pausing serious threat to more than 50 millions of people. Although the health effects of chronic arsenic exposure has been extensively investigated, its potential effects on developing organisms have scarcely been examined so far. Since developing organism are often more sensitive to environmental threat than the adults, the present study focused on the possible effects of prenatal exposure to inorganic arsenic on fetus and offspring.
i) Effect of maternal arsenic exposure on selenium and selenoenzymes in fetus. C57BL/6J mice were exposed to arsenite at doses that would not overt toxicity between GD7-16. On GD17, mice were dissected, and tissue levels of selenium, arsenic and selenoenzymes were determined. Effect of dietary-induced selenium deficiency was also evaluated. It was found that selenium deficiency facilitated the accumulation of arsenic both in motemal and fetal tissues up to 1.5 fold compared to control (Se sufficient) group. Also, arsenic exposure affected the tissue levels of selenium and selenoenzyme activities. Among the observed effects, activity of the thioredoxine reductase (TRxR) in the fetal liver was enhanced and suppressed in Se sufficient and deficient status, respectively ; such modification by Se status was not observed in maternal tissues. These results suggested that the toxicity of arsenic may be enhanced under Se deficiency and that fetus is more sensitive to the change of Se status than adults. li) The behavior of offspring bom to dam mice exposed to arsenic during gestation was examined. At the doses that was not overtly toxic, development of some motor functions were retarded and the open-field behavior at 8wk of age was altered by the arsenic exposure, indicating that prenatal arsenic exposure could result in altered behavior, which was accompanied by some changes in brain monoamines.
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