Mitochondrial complex I in the post-ischemic heart: reperfusion-mediated oxidative injury and protein cysteine sulfonation.

Title

Mitochondrial complex I in the post-ischemic heart: reperfusion-mediated oxidative injury and protein cysteine sulfonation.

Creator

Kang Patrick T; Chen Chwen-Lih; Lin Paul; Zhang Liwen; Zweier Jay L; Chen Yeong-Renn

Publisher

Journal of molecular and cellular cardiology

Date

2018
2018-08

Description

A serious consequence of ischemia-reperfusion injury (I/R) is oxidative damage leading to mitochondrial dysfunction. Such I/R-induced mitochondrial dysfunction is observed as impaired state 3 respiration and overproduction of O2(-). The cascading ROS can propagate cysteine oxidation on mitochondrial complex I and add insult to injury. Herein we employed LC-MS/MS to identify protein sulfonation of complex I in mitochondria from the infarct region of rat hearts subjected to

Subject

Complex I; Mitochondrial dysfunction; Myocardial ischemia and reperfusion; Protein cysteine sulfonation; Protein structure

Rights

Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).

Pages

190–204

Volume

121

Citation

Kang Patrick T; Chen Chwen-Lih; Lin Paul; Zhang Liwen; Zweier Jay L; Chen Yeong-Renn, “Mitochondrial complex I in the post-ischemic heart: reperfusion-mediated oxidative injury and protein cysteine sulfonation.,” NEOMED Bibliography Database, accessed August 2, 2021, https://neomed.omeka.net/items/show/3825.

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