scholarly journals Biphasic modulation of the mitochondrial electron transport chain in myocardial ischemia and reperfusion

2012 ◽  
Vol 302 (7) ◽  
pp. H1410-H1422 ◽  
Author(s):  
Hsin-Ling Lee ◽  
Chwen-Lih Chen ◽  
Steve T. Yeh ◽  
Jay L. Zweier ◽  
Yeong-Renn Chen
Keyword(s):  
Electron Transport ◽  
Myocardial Ischemia ◽  
Electron Transport Chain ◽  
Ischemia Reperfusion ◽  
Ischemic Heart ◽  
Mitochondrial Electron Transport Chain ◽  
Immunoblotting Analysis ◽  
Myocardial Ischemia And Reperfusion ◽  
Transport Chain ◽  
Significant Difference

Mitochondrial electron transport chain (ETC) is the major source of reactive oxygen species during myocardial ischemia-reperfusion (I/R) injury. Ischemic defect and reperfusion-induced injury to ETC are critical in the disease pathogenesis of postischemic heart. The properties of ETC were investigated in an isolated heart model of global I/R. Rat hearts were subjected to ischemia for 30 min followed by reperfusion for 1 h. Studies of mitochondrial function indicated a biphasic modulation of electron transfer activity (ETA) and ETC protein expression during I/R. Analysis of ETAs in the isolated mitochondria indicated that complexes I, II, III, and IV activities were diminished after 30 min of ischemia but increased upon restoration of flow. Immunoblotting analysis and ultrastructural analysis with transmission electron microscopy further revealed marked downregulation of ETC in the ischemic heart and then upregulation of ETC upon reperfusion. No significant difference in the mRNA expression level of ETC was detected between ischemic and postischemic hearts. However, reperfusion-induced ETC biosynthesis in myocardium can be inhibited by cycloheximide, indicating the involvement of translational control. Immunoblotting analysis of tissue homogenates revealed a similar profile in peroxisome proliferator-activated receptor-γ coactivator-1α expression, suggesting its essential role as an upstream regulator in controlling ETC biosynthesis during I/R. Significant impairment caused by ischemic and postischemic injury was observed in the complexes I- III. Analysis of NADH ferricyanide reductase activity indicated that injury of flavoprotein subcomplex accounts for 50% decline of intact complex I activity from ischemic heart. Taken together, our findings provide a new insight into the molecular mechanism of I/R-induced mitochondrial dysfunction.

Mitochondrial Electron Transport Chain Defects in Acute Murine Hind Limb Ischemia/Reperfusion

2007 ◽  
Vol 14 (5 Supplement 1) ◽  
pp. S168-S168
Author(s):  
T. P. Tran ◽  
I. Frrokaj ◽  
H. Albadawi ◽  
Z. Zhu ◽  
M. Watkins ◽  
...  
Keyword(s):  
Electron Transport ◽  
Electron Transport Chain ◽  
Hind Limb ◽  
Ischemia Reperfusion ◽  
Limb Ischemia ◽  
Mitochondrial Electron Transport Chain ◽  
Hind Limb Ischemia ◽  
Transport Chain ◽  
Chain Defects

scholarly journals Elucidating Mitochondrial Electron Transport Chain Supercomplexes in the Heart During Ischemia–Reperfusion

2017 ◽  
Vol 27 (1) ◽  
pp. 57-69 ◽  
Author(s):  
Sehwan Jang ◽  
Taber S. Lewis ◽  
Corey Powers ◽  
Zaza Khuchua ◽  
Christopher P. Baines ◽  
...  
Keyword(s):  
Electron Transport ◽  
Electron Transport Chain ◽  
Ischemia Reperfusion ◽  
Mitochondrial Electron Transport Chain ◽  
Transport Chain

scholarly journals AB0031 T HELPER 17 CELLS WERE SIGNIFICANTLY DECREASED BY MITOCHONDRIAL ELECTRON TRANSPORT CHAIN COMPLEX INHIBITOR IN PATIENTS WITH RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1318.2-1318
Author(s):  
H. R. Lee ◽  
S. J. Yoo ◽  
J. Kim ◽  
I. S. Yoo ◽  
C. K. Park ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Electron Transport ◽  
Disease Activity ◽  
Th17 Cells ◽  
Electron Transport Chain ◽  
Chain Complex ◽  
Complex Iii ◽  
Mitochondrial Electron Transport Chain ◽  
Transport Chain ◽  
Healthy Control

Background:Reactive oxygen species (ROS) and T helper 17 (TH17) cells have been known to play an important role in the pathogenesis of rheumatoid arthritis (RA). However, the interrelationship between ROS and TH17 remains unclear in RAObjectives:To explore whether ROS affect TH17 cells in peripheral blood mononuclear cells (PBMC) of RA patients, we analyzed ROS expressions among T cell subsets following treatment with mitochondrial electron transport chain complex inhibitors.Methods:Blood samples were collected from 40 RA patients and 10 healthy adult volunteers. RA activity was divided according to clinical parameter DAS28. PBMC cells were obtained from the whole blood using lymphocyte separation medium density gradient centrifugation. Following PBMC was stained with Live/Dead stain dye, cells were incubated with antibodies for CD3, CD4, CD8, and CD25. After fixation and permeabilization, samples were stained with antibodies for FoxP3 and IL-17A. MitoSox were used for mitochondrial specific staining.Results:The frequency of TH17 cells was increased by 4.83 folds in moderate disease activity group (5.1>DAS28≥3.2) of RA patients compared to healthy control. Moderate RA activity patients also showed higher ratio of TH17/Treg than healthy control (3.57 folds). All RA patients had elevated expression of mitochondrial specific ROS than healthy control. When PBMC cells were treated with 2.5uM of antimycin A (mitochondrial electron transport chain complex III inhibitor) for 16 h, the frequency of TH17 cells was significantly decreased.Conclusion:The mitochondrial electron transport chain complex III inhibitor markedly downregulated the frequency of TH17 cells in moderate disease activity patients with RA. These findings provide a novel approach to regulate TH17 function in RA through mitochondrial metabolism related ROS production.References:[1]Szekanecz, Z., et al., New insights in synovial angiogenesis. Joint Bone Spine, 2010. 77(1): p. 13-9.[2]Prevoo, M.L., et al., Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum, 1995. 38(1): p. 44-8.Disclosure of Interests:None declared

scholarly journals Anticancer gold(iii)-bisphosphine complex alters the mitochondrial electron transport chain to induce in vivo tumor inhibition

2021 ◽  
Author(s):  
Jong Hyun Kim ◽  
Samuel Ofori ◽  
Sean Parkin ◽  
Hemendra Vekaria ◽  
Patrick G. Sullivan ◽  
...  
Keyword(s):  
Electron Transport ◽  
Metal Complexes ◽  
Electron Transport Chain ◽  
Chemical Diversity ◽  
Mitochondrial Electron Transport Chain ◽  
Generate Functional ◽  
Tumor Inhibition ◽  
Transport Chain

Expanding the chemical diversity of metal complexes provides a robust platform to generate functional bioactive reagents.

New inhibitors of Complex I of the mitochondrial electron transport chain with activity as pesticides

1994 ◽  
Vol 22 (1) ◽  
pp. 230-233 ◽  
Author(s):  
Robert M. Hollingworth ◽  
Kabeer I. Ahammadsahib ◽  
G. Gadelhak ◽  
J. L. McLaughlin
Keyword(s):  
Electron Transport ◽  
Complex I ◽  
Electron Transport Chain ◽  
Mitochondrial Electron Transport Chain ◽  
Transport Chain
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