| Project/Area Number |
06680509
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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 |
環境影響評価(含放射線生物学)
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| Research Institution | The University of Tokushima |
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Principal Investigator |
TOMIYOSHI Fukiyo Faculty of Integarted Arts and Sciences, The University of Tokushima, Professor, 総合科学部, 教授 (20035819)
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| Co-Investigator(Kenkyū-buntansha) |
OYAMA Yasuo Faculty of Integrated Arts and Sciences, The University of Tokushima, Professor, 総合科学部, 教授 (80214229)
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| Project Period (FY) |
1994 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1995: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Organometal / Intracellular Ca / Cell viability / 神経毒性 / 膜イオン透過性 / 蛍光プローブ / fluo-3 / ethidium / フローサイトメーター / レーザー共焦点顕微鏡 / 細胞内カルシウムイオン / 蛍光化学 |
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| Research Abstract |
The effects of tri-n-butyltin on the cell viability and the intracellular Ca2+ concentration ([Ca2+]i) were examined by a flow cytometer and a confocal laser-microscope in rat cerebellar neurons using a combination of two fluorescent dyes, fluo-3 for monitoring changes in intracellular Ca concentration and ethidium for estimating cell viability to reveal the contribution of tri-n-butyltin-induced increase in the [Ca2+]i to its cytotoxicity. Tri-n-butyltin decreased the cell viability in an association with increased [Ca2+]i at concentrations of 0.3 microM or greater. Decreasing or increasing the extracellular Ca2+ concentration ([Ca2+]o) decreased or increased the cell viability, respectively. However, cell viability in the presence of ionomycin which increased [Ca2+]i more profoundly than tri-n-butyltin was higher than that in presence of tri-n-butyltin. Tri-n-butyltin also decreased the cell viability under nominally [Ca2+]o-free condition although the [Ca2+]i increase by tri-n-butyltin was still lower than the control [Ca2+]i under normal [Ca2+]o (2mM). Therefore, it is unlikely that neuronal death induced by tri-n-butyltin in entirely dependent on the tri-n-butyltin-induced increase in [Ca2+]i.
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