Open AccessUncoupling of the Electron Transport Chain Compromises Mitochondrial Oxidative Phosphorylation and Exacerbates Stroke Outcomes
Author(s) -
Kimberly Grasmick,
Heng Hu,
Emily Hone,
Imran Farooqi,
Stephanie L. Rellick,
James W. Simpkins,
Xuefang Ren
Publication year - 2018
Publication title -
journal of neuroinfectious diseases
Language(s) - English
Resource type - Journals
eISSN - 2314-7334
pISSN - 2314-7326
DOI - 10.4172/2314-7326.1000283
Subject(s) - oxidative phosphorylation , stroke (engine) , bioenergetics , mitochondrion , electron transport chain , respiratory chain , medicine , tetrazolium chloride , chemistry , ischemia , biology , pharmacology , biochemistry , mechanical engineering , engineering
Mitochondrial dysfunction is known to be implicated in stroke, but the complex mechanisms of stroke have led to few stroke therapies. The present study to disrupted mitochondrial oxidative phosphorylation through a known electron transport chain (ETC) uncoupler, Carbonyl cyanide-4 (trifluoromethoxy) phenylhydrazone (FCCP). Analyzing the resulting neurological deficits as well as infarct volume could help determine the role of mitochondria in stroke outcome and determine whether uncoupling the ETC could potentially be a strategy for new stroke therapies. The objective of this study was to determine the effects of uncoupling electron flow on mitochondrial oxidative phosphorylation and stroke infarction.