『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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種別 (必須): 学術論文 (審査論文) [継承]
言語 (必須): 英語 [継承]
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審査 (推奨): Peer Review [継承]
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組織 (推奨): 1.徳島大学.総合科学部.自然システム学科.生命科学講座 (〜2009年3月31日) [継承]
著者 (必須): 1. (英) Horimoto Kanna (日) (読)
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2. (英) Nishimura Yumiko (日) (読)
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3. (英) Oyama Tomohiro (日) (読)
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4. (英) Onoda Kyoko (日) (読)
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5. (英) Matsui Hiroko (日) (読)
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6. (英) Oyama Toshihisa (日) (読)
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7.金丸 芳 ([徳島大学.大学院社会産業理工学研究部.生物資源産業学域.食料科学系.食料科学分野]/[徳島大学.生物資源産業学部.生物資源産業学科.食料科学講座])
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8.増田 俊哉
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9.小山 保夫
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題名 (必須): (英) Reciprocal effects of glucose on the process of cell death induced by calcium ionophore or H2O2 in rat lymphocytes  (日)    [継承]
副題 (任意):
要約 (任意): (英) We have examined the effects of glucose at high concentrations on the process of cell death induced by excessive increase in intracellular Ca2+ concentration ([Ca2+]i) or oxidative stress in rat lymphocytes. The cell death elicited by the excessive increase in [Ca2+]i seemed to be induced by an activation of Ca2+-dependent K+ channels because the inhibitors for Ca2+-dependent K+ channels attenuated the decrease in cell viability. Glucose at 30-50 mM augmented the decrease in cell viability by the excessive increase in [Ca2+]i. It was not specific for glucose because it was the case for sucrose or NaCl, suggesting an involvement of increased osmolarity in adverse action of glucose. On the contrary, glucose protected the cells suffering from oxidative stress induced by H2O2, one of reactive oxygen species. It was also the case for fructose or sucrose, but not for NaCl. The process of cell death induced by H2O2 started, being independent from the presence of glucose. Glucose delayed the process of cell death induced by H2O2. Sucrose and fructose also protected the cells against oxidative stress. The reactivity of sucrose to reactive oxygen species is lower than those of glucose and fructose. The order in the reactivity cannot explain the protective action of glucose. Glucose at high concentrations exerts reciprocal actions on the process of cell death induced by the oxidative stress and excessive increase in [Ca2+]i.  (日)    [継承]
キーワード (推奨): 1. (英) Animals (日) (読) [継承]
2. (英) Calcimycin (日) (読) [継承]
3. (英) Calcium (日) (読) [継承]
4. (英) Cell Death (日) (読) [継承]
5. (英) Cell Survival (日) (読) [継承]
6. (英) Charybdotoxin (日) (読) [継承]
7. (英) Clotrimazole (日) (読) [継承]
8. (英) Dose-Response Relationship, Drug (日) (読) [継承]
9. (英) Flow Cytometry (日) (読) [継承]
10. (英) Glucose (日) (読) [継承]
11. (英) Hydrogen Peroxide (日) (読) [継承]
12. (英) Ionophores (日) (読) [継承]
13. (英) Male (日) (読) [継承]
14. (英) Osmolar Concentration (日) (読) [継承]
15. (英) Oxidative Stress (日) (読) [継承]
16. (英) Rats (日) (読) [継承]
17. (英) Rats, Wistar (日) (読) [継承]
18. (英) T-Lymphocytes (日) (読) [継承]
発行所 (推奨): Elsevier Science [継承]
誌名 (必須): Toxicology ([Elsevier Science])
(pISSN: 0300-483X, eISSN: 1879-3185)

ISSN (任意): 0300-483X
ISSN: 0300-483X (pISSN: 0300-483X, eISSN: 1879-3185)
Title: Toxicology
Title(ISO): Toxicology
Publisher: Elsevier BV
 (NLM Catalog  (Scopus  (CrossRef (Scopus information is found. [need login])
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都市 (任意): アムステルダム (Amsterdam/[オランダ王国]) [継承]
年月日 (必須): 西暦 2006年 9月 31日 (平成 18年 9月 31日) [継承]
URL (任意):
DOI (任意): 10.1016/j.tox.2006.05.004    (→Scopusで検索) [継承]
PMID (任意): 16784802    (→Scopusで検索) [継承]
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備考 (任意): 1.(英) Article.Affiliation: Laboratories of Cell Signaling and Bioorganochemistry, Faculty of Integrated Arts and Sciences, The University of Tokushima, Tokushima 770-8502, Japan.  (日)    [継承]
2.(英) Article.PublicationTypeList.PublicationType: Journal Article  (日)    [継承]

標準的な表示

和文冊子 ● Kanna Horimoto, Yumiko Nishimura, Tomohiro Oyama, Kyoko Onoda, Hiroko Matsui, Toshihisa Oyama, Kaori Kanemaru, Toshiya Masuda and Yasuo Oyama : Reciprocal effects of glucose on the process of cell death induced by calcium ionophore or H2O2 in rat lymphocytes, Toxicology, Vol.225, No.2-3, 97-108, 2006.
欧文冊子 ● Kanna Horimoto, Yumiko Nishimura, Tomohiro Oyama, Kyoko Onoda, Hiroko Matsui, Toshihisa Oyama, Kaori Kanemaru, Toshiya Masuda and Yasuo Oyama : Reciprocal effects of glucose on the process of cell death induced by calcium ionophore or H2O2 in rat lymphocytes, Toxicology, Vol.225, No.2-3, 97-108, 2006.

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