In vivo studies on the toxic effects of microcystins on mitochondrial electron transport chain and ion regulation in liver and heart of rabbit

2008 ◽  
Vol 148 (3) ◽  
pp. 204-210 ◽  
Author(s):  
Yanyan Zhao ◽  
Ping Xie ◽  
Rong Tang ◽  
Xuezhen Zhang ◽  
Li Li ◽  
...  
Keyword(s):  
Electron Transport ◽  
Electron Transport Chain ◽  
Toxic Effects ◽  
In Vivo Studies ◽  
Mitochondrial Electron Transport Chain ◽  
Ion Regulation ◽  
Transport Chain

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.

Decrease in cytochrome c oxidase reserve capacity diminishes robustness of Drosophila melanogaster and shortens lifespan

2014 ◽  
Vol 459 (1) ◽  
pp. 127-135 ◽  
Author(s):  
Vladimir Klichko ◽  
Barbara H. Sohal ◽  
Svetlana N. Radyuk ◽  
William C. Orr ◽  
Rajindar S. Sohal
Keyword(s):  
Drosophila Melanogaster ◽  
Electron Transport ◽  
Cytochrome C ◽  
Structure Function ◽  
Cytochrome C Oxidase ◽  
Electron Transport Chain ◽  
Reserve Capacity ◽  
Mitochondrial Electron Transport Chain ◽  
Transport Chain

The suppression of cytochrome c oxidase function exerts deleterious rather than benign effects on fitness and survival. The structure/function of cytochrome c oxidase, a mitochondrial electron-transport chain oxidoreductase, can be re-engineered in vivo.

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

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

Palmitate increases superoxide production through mitochondrial electron transport chain and NADPH oxidase activity in skeletal muscle cells

2008 ◽  
Vol 216 (3) ◽  
pp. 796-804 ◽  
Author(s):  
Rafael Herling Lambertucci ◽  
Sandro Massao Hirabara ◽  
Leonardo dos Reis Silveira ◽  
Adriana Cristina Levada‐Pires ◽  
Rui Curi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electron Transport ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Electron Transport Chain ◽  
Muscle Cells ◽  
Superoxide Production ◽  
Mitochondrial Electron Transport Chain ◽  
Nadph Oxidase Activity ◽  
Transport Chain
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