ID 17486
本文ファイル
別タイトル
活性酸素種曝露による血管内皮細胞単層膜のアルブミン透過性 : 細胞膜カルシウムチャネルの可逆的な機能変化
著者
キーワード
Albumin permeability
Reactive oxygen intermediates
Calcium channels
Redox state
NDC
医学
抄録(英)
This study was designed to test the idea that the redox state of sulfhydryl (SH)-groups in cell-membrane Ca2+ channels plays a pivotal role in Ca2+in flux, which in turn causes an increase in albumin permeability across the cultured monolayer of porcine pulmonary artery endothelial (PPAE) cells exposed to xanthine/xanthine oxidase (X/XO). Albumin permeability as well as the concentration of intracellular Ca2+( [Ca2+]i) was increased by XKO. A Hz02 scavenger (catalase), an iron chelator (o-phenanthroline), and a hydroxyl radical scavenger (dimethyl sulfoxide) inhibited these changes provoked by XKO, in which intracellular iron-catalyzed hydroxyl radical generation was suggested to be involved. The increase in albumin permeability and [Ca2+]i continued once the PPAE cells were exposed to XKO. The [Ca2+]wi as decreased by a Ca2+ channel blocker, Ni2+, while the removal of Ni2+in creased [Ca2+]I again, suggesting the sustained Ca2+ influx through cell-membrane Ca" channels was responsible for the [Ca2+]i elevation. Ni2+f ailed to inhibit albumin permeability sustained after the removal of XKO. In contrast, SH-reducing agents (dithiothreitol and glutathione) inhibited the sustained permeability as well as Ca2+ influx. We concluded that the redox alteration of SH-groups in cell-membrane Ca2+ channels was involved in the increase in albumin permeability after exposure of the endothelial cells to oxidative stress.
内容記述
Hiroshima J. Med. Sci. Vol.49, No.1, 57-65, March, 2000 HIJM49-8
言語
英語
NII資源タイプ
学位論文
広大資料タイプ
学位論文
DCMIタイプ
text
フォーマット
application/pdf
権利情報
Copyright (c) by Author
学位記番号
甲第2110号
授与大学
広島大学(Hiroshima University)
学位名
博士(医学)
学位名の英名
Medicine
学位の種類の英名
doctoral
学位授与年月日
2000-03-07
部局名
医歯薬学総合研究科