Cardiac Ischemia Impairs Submaximal Mitochondrial Respiration without Dramatic Impairments of Electron Transport Chain Conductance

2014 ◽  
Vol 46 ◽  
pp. 745
Author(s):  
Sarah Kuzmiak-Glancy ◽  
Matthew W. Kay
Keyword(s):  
Electron Transport ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Cardiac Ischemia ◽  
Transport Chain

scholarly journals Age-Dependent Loss of Mitochondrial Function in Epithelial Tissue Can Be Reversed by Coenzyme Q10

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Daniel Schniertshauer ◽  
Daniel Gebhard ◽  
Jörg Bergemann
Keyword(s):  
Electron Transport ◽  
Coenzyme Q10 ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Epithelial Tissue ◽  
Atp Production ◽  
Transport Chain ◽  
Respiratory Parameters ◽  
Age Dependent ◽  
Theory Of Aging

The process of aging is characterized by the increase of age-associated disorders as well as severe diseases. Due to their role in the oxidative phosphorylation and thus the production of ATP which is crucial for many cellular processes, one reason for this could be found in the mitochondria. The accumulation of reactive oxygen species damaged mitochondrial DNA and proteins can induce mitochondrial dysfunction within the electron transport chain. According to the “mitochondrial theory of aging,” understanding the impact of harmful external influences on mitochondrial function is therefore essential for a better view on aging in general, but the measurement of mitochondrial respiration in skin cells from cell cultures cannot completely reflect the real situation in skin. Here, we describe a new method to measure the mitochondrial respiratory parameters in epithelial tissue derived from human skin biopsies using a XF24 extracellular flux analyzer to evaluate the effect of coenzyme Q10. We observed a decrease in mitochondrial respiration and ATP production with donor age corresponding to the “mitochondrial theory of aging.” For the first time ex vivo in human epidermis, we could show also a regeneration of mitochondrial respiratory parameters if the reduced form of coenzyme Q10, ubiquinol, was administered. In conclusion, an age-related decrease in mitochondrial respiration and ATP production was confirmed. Likewise, an increase in the respiratory parameters by the addition of coenzyme Q10 could also be shown. The fact that there is a significant effect of administered coenzyme Q10 on the respiratory parameters leads to the assumption that this is mainly caused by an increase in the electron transport chain. This method offers the possibility of testing age-dependent effects of various substances and their influence on the mitochondrial respiration parameters in human epithelial tissue.

Method for recovering ATP content and mitochondrial function after chemical anoxia in renal cell cultures

1994 ◽  
Vol 266 (6) ◽  
pp. C1803-C1811 ◽  
Author(s):  
R. B. Doctor ◽  
R. Bacallao ◽  
L. J. Mandel
Keyword(s):  
Electron Transport ◽  
Oxidative Metabolism ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Cultured Cells ◽  
Good Method ◽  
Complete Recovery ◽  
Specific Method ◽  
Cellular Effects ◽  
Transport Chain

Cultured renal cells provide a highly reproducible and malleable model to study cellular responses to metabolic perturbations. Nevertheless, there is currently no good method to achieve metabolic inhibition and complete recovery in cultured cells. This study describes a specific method for reversibly inhibiting both glycolytic and oxidative metabolism. Glycolysis was inhibited by removing all glycolytic substrates, and mitochondrial respiration was inhibited with rotenone, a site I inhibitor of the electron transport chain. Within 30 min, ATP values were decreased by 98%. Glycolysis was restored through the reintroduction of glucose. Oxidative metabolism was restored by the addition of heptanoate, a short odd-chain fatty acid, which supplies reducing equivalents to site II of the electron transport chain. Employing Madin-Darby canine kidney and LLC-PK1 cell lines, this protocol caused the immediate and complete recovery of mitochondrial respiration and, by 60 min, the complete recovery of cellular ATP levels. Application of this protocol should allow the investigation of the cellular effects and alterations that occur within cells recovering from sublethal energy depletion.

scholarly journals FOXM1 nuclear transcription factor translocates into mitochondria and inhibits oxidative phosphorylation

2020 ◽  
Vol 31 (13) ◽  
pp. 1411-1424
Author(s):  
Markaisa Black ◽  
Paritha Arumugam ◽  
Samriddhi Shukla ◽  
Arun Pradhan ◽  
Vladimir Ustiyan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Membrane Potential ◽  
Electron Transport ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Nuclear Transcription Factor ◽  
Transport Chain

It was found that the transcription factor FOXM1 translocates into mitochondria and inhibits mitochondrial respiration and membrane potential, directly binds to mitochondrial PTCD1, and inhibits the electron transport chain by stabilizing PTCD1.

Cardiac ischemia: Electron transport chain damages intermediary metabolism

Mitochondrion ◽  
2015 ◽  
Vol 24 ◽  
pp. S33
Author(s):  
Masood Younus ◽  
Jeremy Thompson ◽  
Ying Hu ◽  
Qun Chen ◽  
John F. Hollander ◽  
...  
Keyword(s):  
Electron Transport ◽  
Electron Transport Chain ◽  
Cardiac Ischemia ◽  
Intermediary Metabolism ◽  
Transport Chain

scholarly journals Higher Mitochondrial Respiration and Uncoupling with Reduced Electron Transport Chain Contentin Vivoin Muscle of Sedentary Versus Active Subjects

2013 ◽  
Vol 98 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Kevin E. Conley ◽  
Catherine E. Amara ◽  
Sudip Bajpeyi ◽  
Sheila R. Costford ◽  
Kori Murray ◽  
...  
Keyword(s):  
Electron Transport ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Transport Chain

Environmental toxins and Parkinson’s disease: Putative roles of impaired electron transport chain and oxidative stress

2010 ◽  
Vol 26 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Ibrahim Abdulwahid Arif ◽  
Haseeb Ahmad Khan
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Electron Transport ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Electron Flow ◽  
Oxidative Modification ◽  
Environmental Toxins ◽  
Transport Chain

Despite recent advancements in the biomedical fields, the etiology and pathogenesis of Parkinson’s disease (PD) is still poorly understood, though the crucial roles of oxidative stress and impaired mitochondrial respiration have been suggested in the development of PD. The oxidative modification of the proteins of mitochondrial electron transport chain alters their normal function leading to the state of energy crisis in neurons. Exposure of environmental chemicals such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and rotenone in mouse produces the symptoms akin to PD and therefore these neurotoxins are commonly used in experimental studies on PD. Another environmental toxin, paraquat (a commonly used herbicide) has also been implicated with the onset of PD. The neurotoxicity of these chemicals is accompanied by the blockade of electron flow from NADH dehydrogenase to coenzyme Q. The agents with the ability to improve mitochondrial respiration and ATP production have been shown to exert beneficial effects in PD patients as well as in the animal models of PD. This review summarizes the current research implicating the impairment of mitochondrial respiratory chain and the role of environmental toxins in the pathogenesis of PD.

scholarly journals Electron transport chain biogenesis activated by a JNK-insulin-Myc relay primes mitochondrial inheritance in Drosophila

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Zong-Heng Wang ◽  
Yi Liu ◽  
Vijender Chaitankar ◽  
Mehdi Pirooznia ◽  
Hong Xu
Keyword(s):  
Electron Transport ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Respiration ◽  
Electron Transport Chain ◽  
Mtdna Copy Number ◽  
Cellular Mechanisms ◽  
Dynamic Regulation ◽  
Mtdna Mutations ◽  
Transport Chain ◽  
Mtdna Replication

Oogenesis features an enormous increase in mitochondrial mass and mtDNA copy number, which are required to furnish mature eggs with an adequate supply of mitochondria and to curb the transmission of deleterious mtDNA variants. Quiescent in dividing germ cells, mtDNA replication initiates upon oocyte determination in the Drosophila ovary, which necessitates active mitochondrial respiration. However, the underlying mechanism for this dynamic regulation remains unclear. Here, we show that an feedforward insulin-Myc loop promotes mitochondrial respiration and biogenesis by boosting the expression of electron transport chain subunits and of factors essential for mtDNA replication and expression, and for the import of mitochondrial proteins. We further reveal that transient activation of JNK enhances the expression of the insulin receptor and initiates the insulin-Myc signaling loop. This signaling relay promotes mitochondrial biogenesis in the ovary, and thereby plays a role in limiting the transmission of deleterious mtDNA mutations. Our study demonstrates cellular mechanisms that couple mitochondrial biogenesis and inheritance with oocyte development.

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