| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2013-05-29 |
| タイトル |
|
|
タイトル |
REMARKABLE INCREASE OF CYTOCHROME C OXIDASE SUBUNIT I AFTER GLOBAL CEREBRAL ISCHEMIA |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
global cerebral ischemia |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
cytochrome c oxidase |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
immunohistochemistry |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
western blot |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 作成者 |
Takahashi, Yusuke
Sugawara, Taku
Miyazaki, Toshio
Hideaki, Itoh
Mizoi, Kazuo
|
| 内容記述 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Cerebral ischemia is known to produce excessive reactive oxygen species (ROS) in mitochondria, and these radicals initiate radical chain reactions, causing cellular macromolecule damage and also promote mitochondrial apoptosis pathway, ultimately leading to cell death. However, little is known about the mitochondrial functional change after ischemia. We studied expression of cytochrome c oxidase (COX), a terminal, rate-limiting enzyme of the respiratory chain to generate ATP, after global cerebral ischemia in rats. Immunofluorescent staining and Western blot were performed to investigate the spatial and temporal changes in two important COX subunits, mitochondria- encoded COX subunit I (COX I) and nucleus-encoded COX subunit IV (COX IV). In normal condition, these subunits have to be precisely regulated in a 1 : 1 stoichiometry to assemble functional COX holoenzyme. In this study, a massive increase in COX I, which is disproportionate to COX IV was observed at 1 and 6 h after lethal ischemia, preceding delayed neuronal death. In contrast to lethal ischemia, mild sublethal ischemia did not elicit obvious alteration in COX I and IV. This aberrant increase in COX I may be an early sign of delayed neuronal death or may predict later electron transport chain dysfunction to generate ATP. |
|
言語 |
en |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 書誌情報 |
ja : 秋田医学
巻 39,
号 2,
p. 53-59,
発行日 2013-02-28
|
| 収録物識別子 |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
03866106 |
| 収録物識別子 |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AN00009294 |
| 出版者 |
|
|
出版者 |
秋田医学会 |
|
言語 |
ja |
akitai39(53).pdf (1.7 MB)
