scholarly journals Reappraisal of the e.p.r. signals in (post)-ischaemic cardiac tissue

1989 ◽  
Vol 264 (3) ◽  
pp. 687-694 ◽  
Author(s):  
A M van der Kraaij ◽  
J F Koster ◽  
W R Hagen
Keyword(s):  
Electron Transfer ◽  
Free Radicals ◽  
Reperfusion Injury ◽  
Respiratory Chain ◽  
Cardiac Tissue ◽  
Direct Detection ◽  
Mitochondrial Respiratory Chain ◽  
Isolated Rat Heart ◽  
Oxygen Derived Free Radicals ◽  
Rat Hearts

The present study was designed to measure directly, using e.p.r. spectroscopy, oxygen-derived free radicals in (post)-ischaemic or (post)-anoxic rat hearts. Rat hearts were rapidly freeze-clamped at 77 K under normoxic, anoxic, ischaemic or reperfusion conditions. The samples were measured at three different temperatures (13, 77 and 115 K) and at several microwave power levels, and were compared with isolated rat heart mitochondria. Samples were prepared both by grinding and as tissue cuts. The two preparation techniques gave identical e.p.r. results, which excludes the occurrence of grinding artifacts. No free radical signals linked to reperfusion injury were detected. Several electron transfer centres known in the mitochondrial respiratory chain were measured. The signals previously assigned to post-ischaemic reperfusion injury were found to originate from electron transfer centres of the respiratory chain, predominantly the iron-sulphur cluster S-1 in succinate dehydrogenase. The differences in signal intensity between normoxic, ischaemic and reperfused hearts were found to result from the different redox stages of these centres under the various conditions tested. These findings do not necessarily imply that oxygen-derived free radicals are not formed in cardiac tissue during (post)-ischaemic reperfusion. The constitutive background of paramagnetism from the respiratory chain, however, seriously hampers the direct detection of comparatively low concentrations of free radicals in cardiac tissue. It is therefore expedient to focus future experiments in this field on the use of spin-trapping agents.

Nanosized non-proteinaceous complexes III and IV mimicking electron transfer of mitochondrial respiratory chain

2021 ◽  
Author(s):  
Iago A. Modenez ◽  
Lucyano J.A. Macedo ◽  
Antonio F.A.A. Melo ◽  
Andressa R. Pereira ◽  
Osvaldo N. Oliveira Jr ◽  
...  
Keyword(s):  
Electron Transfer ◽  
Respiratory Chain ◽  
Mitochondrial Respiratory Chain ◽  
Mitochondrial Respiratory

In vivo measurement of oxygen-derived free radicals during reperfusion injury

Microsurgery ◽  
2002 ◽  
Vol 22 (3) ◽  
pp. 108-113 ◽  
Author(s):  
Rolf Büttemeyer ◽  
Andreas W. Philipp ◽  
Julian W. Mall ◽  
Bixia Ge ◽  
Frieder W. Scheller ◽  
...  
Keyword(s):  
Free Radicals ◽  
Reperfusion Injury ◽  
In Vivo Measurement ◽  
Oxygen Derived Free Radicals

scholarly journals Five decades of research on mitochondrial NADH-quinone oxidoreductase (complex I)

2018 ◽  
Vol 399 (11) ◽  
pp. 1249-1264 ◽  
Author(s):  
Tomoko Ohnishi ◽  
S. Tsuyoshi Ohnishi ◽  
John C. Salerno
Keyword(s):  
Electron Transfer ◽  
Respiratory Chain ◽  
Complex I ◽  
Proton Translocation ◽  
Atp Synthesis ◽  
Mitochondrial Respiratory Chain ◽  
Proton Pumping ◽  
Entry Site ◽  
Quinone Oxidoreductase ◽  
Terminal Electron Acceptor

AbstractNADH-quinone oxidoreductase (complex I) is the largest and most complicated enzyme complex of the mitochondrial respiratory chain. It is the entry site into the respiratory chain for most of the reducing equivalents generated during metabolism, coupling electron transfer from NADH to quinone to proton translocation, which in turn drives ATP synthesis. Dysfunction of complex I is associated with neurodegenerative diseases such as Parkinson’s and Alzheimer’s, and it is proposed to be involved in aging. Complex I has one non-covalently bound FMN, eight to 10 iron-sulfur clusters, and protein-associated quinone molecules as electron transport components. Electron paramagnetic resonance (EPR) has previously been the most informative technique, especially in membranein situanalysis. The structure of complex 1 has now been resolved from a number of species, but the mechanisms by which electron transfer is coupled to transmembrane proton pumping remains unresolved. Ubiquinone-10, the terminal electron acceptor of complex I, is detectable by EPR in its one electron reduced, semiquinone (SQ) state. In the aerobic steady state of respiration the semi-ubiquinone anion has been observed and studied in detail. Two distinct protein-associated fast and slow relaxing, SQ signals have been resolved which were designated SQNfand SQNs. This review covers a five decade personal journey through the field leading to a focus on the unresolved questions of the role of the SQ radicals and their possible part in proton pumping.

scholarly journals Oxygen Sensing and HIF-1 Activation Does Not Require an Active Mitochondrial Respiratory Chain Electron-transfer Pathway

2001 ◽  
Vol 276 (25) ◽  
pp. 21995-21998 ◽  
Author(s):  
Vickram Srinivas ◽  
Irene Leshchinsky ◽  
Nianli Sang ◽  
Michael P. King ◽  
Alex Minchenko ◽  
...  
Keyword(s):  
Electron Transfer ◽  
Respiratory Chain ◽  
Oxygen Sensing ◽  
Mitochondrial Respiratory Chain ◽  
Electron Transfer Pathway ◽  
Mitochondrial Respiratory

Preconditioning potential of purmorphamine: a hedgehog activator against ischaemic reperfusion injury in ovariectomised rat heart

Perfusion ◽  
2017 ◽  
Vol 33 (3) ◽  
pp. 209-218 ◽  
Author(s):  
Shweta Sharma ◽  
Avileen Kaur ◽  
Saurabh Sharma
Keyword(s):  
Myocardial Infarction ◽  
Reperfusion Injury ◽  
Rat Heart ◽  
Cardiac Tissue ◽  
Isolated Rat Heart ◽  
Control Group ◽  
Surgical Removal ◽  
Triphenyltetrazolium Chloride ◽  
Tnf Α ◽  
Pharmacological Preconditioning

Objective: The present study was been designed to investigate the role and pharmacological potential of hedgehog in oestrogen-deficient rat heart. Methods: Oestrogen deficiency was produced in female Wistar rats by the surgical removal of both ovaries and these animals were used four weeks later. Isolated rat heart was subjected to 30 min ischaemia followed by 120 min of reperfusion (I/R). The heart was subjected to pharmacological preconditioning with the hedgehog agonist purmorphamine (1μM) and GDC-0449, a hedgehog antagonist, in the last episode of reperfusion before I/R. Myocardial infarction was assessed in terms of the increase in lactate dehydrogenase (LDH), creatinine kinase-MB (CK-MB), myeloperoxidase (MPO) level and infarct size (triphenyltetrazolium chloride staining). Immunohistochemistry analysis was done for the assessment of tumour necrosis factor (TNF)-α level in cardiac tissue. eNOS expression was estimated by rt-PCR. Results: Pharmacological preconditioning with purmorphamine significantly attenuated I/R-induced myocardial infarction, TNF-α, MPO level and release of LDH and CK-MB compared to the I/R control group. However, GDC-0449 prevented the ameliorative preconditioning effect of estradiol. Conclusion: It may be concluded that the hedgehog agonist purmorphamine prevents the ovariectomised heart from ischaemic reperfusion injury.

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