PMID- 20072911
OWN - NLM
STAT- MEDLINE
DCOM- 20100405
LR  - 20131121
IS  - 1940-6029 (Electronic)
IS  - 1064-3745 (Linking)
VI  - 594
DP  - 2010
TI  - Electron paramagnetic resonance oximetry and redoximetry.
PG  - 85-105
LID - 10.1007/978-1-60761-411-1_6 [doi]
AB  - Reactive oxygen/nitrogen species (ROS/RNS) have been increasingly recognized as 
      important mediators and play a number of critical roles in cell injury, 
      metabolism, disease pathology, diagnosis, and clinical treatment. Electron 
      paramagnetic resonance (EPR) spectroscopy enables the spectral information at 
      certain spatial position, and, from the observed line-width and signal intensity, 
      the localized tissue oxygenation, and tissue redox status can be determined. We 
      applied in vivo EPR oximetry and redoximetry technique and implemented its 
      physiological/pathophysiological applications, along with the use of 
      biocompatible lithium pthalocyanine (liPc) and nitroxide redox sensitive probes, 
      on in vivo tissue oxygenation and redox profile of the ischemic and reperfused 
      heart in living animals. We have observed that the hypoxia during myocardial 
      ischemia limited mitochondrial respiration and caused a shift of tissue redox 
      status to a more reduced state. ROS/RNS generated at the beginning of reperfusion 
      not only caused a shift of redox status to a more oxidized state which may 
      contribute to the postischemic myocardial injury, but also a marked suppression 
      of in vivo tissue O(2) consumption in the postischemic heart through modulation 
      of mitochondrial respiration based on alterations in enzyme activity and mRNA 
      expression of NADH dehydrogenase (NADH-DH) and cytochrome c oxidase (CcO). In 
      addition, ischemic preconditioning was found to be able to markedly attenuate 
      postischemic myocardial hyperoxygenation with less ROS/RNS generation and 
      preservation of mitochondrial O(2) metabolism, due to conserved NADH-DH and CcO 
      activities. These studies have demonstrated that EPR oximetry and redoximetry 
      techniques have advanced to a stage that enables in-depth insight in the process 
      of ischemia reperfusion injury.
FAU - He, Guanglong
AU  - He G
AD  - The Center for Biomedical EPR Spectroscopy and Imaging, Davis Heart and Lung 
      Research Institute and Division of Cardiovascular Medicine, Department of 
      Internal Medicine, The Ohio State University College of Medicine, Columbus, OH, 
      USA. Guanglong.He@osumc.edu
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Methods Mol Biol
JT  - Methods in molecular biology (Clifton, N.J.)
JID - 9214969
RN  - 0 (Free Radicals)
RN  - 3604-79-3 (3-nitrotyrosine)
RN  - 42HK56048U (Tyrosine)
RN  - EC 1.6.99.3 (NADH Dehydrogenase)
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
RN  - GAN16C9B8O (Glutathione)
RN  - ULW86O013H (Glutathione Disulfide)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Chromatography, High Pressure Liquid
MH  - Electron Spin Resonance Spectroscopy/*methods
MH  - Electron Transport Complex IV/metabolism
MH  - Free Radicals/metabolism
MH  - Glutathione/metabolism
MH  - Glutathione Disulfide/metabolism
MH  - Immunohistochemistry
MH  - Ischemic Preconditioning
MH  - Male
MH  - Mice
MH  - NADH Dehydrogenase/metabolism
MH  - Oxidation-Reduction
MH  - Oximetry/*methods
MH  - Tyrosine/analogs & derivatives/metabolism
EDAT- 2010/01/15 06:00
MHDA- 2010/04/07 06:00
CRDT- 2010/01/15 06:00
PHST- 2010/01/15 06:00 [entrez]
PHST- 2010/01/15 06:00 [pubmed]
PHST- 2010/04/07 06:00 [medline]
AID - 10.1007/978-1-60761-411-1_6 [doi]
PST - ppublish
SO  - Methods Mol Biol. 2010;594:85-105. doi: 10.1007/978-1-60761-411-1_6.