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Difference between revisions of "Mitochondrial membrane potential"

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{{MitoPedia
{{MitoPedia
|abbr=mtMP, Δ''ψ''<sub>mt</sub>
|abbr=mtMP, Δ''ι''<sub>p<sup>+</sup></sub>, Δ<sub>el</sub>''F''<sub><u>''e''</u>p<sup>+</sup></sub> [V]
|description=The mitochondrial membrane potential, mtMP, is the electric part of the protonmotive force. mtMP is the potential difference across the inner mitochondrial (mt) membrane, Δ''ψ''<sub>mt</sub>. This suggests that the protonmotive force should be expressed in the electric unit of volt [V]. Electric force of the mitochondrial membrane potential is the electric energy change per ‘motive’ electron or per electron moved across the transmembrane potential difference, with the number of ‘motive’ electrons expressed in the unit coulomb [C].
|description=The '''mitochondrial membrane potential''' difference, mtMP or Δ''ι''<sub>p<sup>+</sup></sub> = Δ<sub>el</sub>''F''<sub><u>''e''</u>p<sup>+</sup></sub>, is the electric part of the protonmotive [[force]], Δp = Δ<sub>m</sub>''F''<sub><u>''e''</u>H<sup>+</sup></sub>.
|info=[[Mitchell 1961 Nature]]
}}
{{MitoPedia methods}}
{{MitoPedia topics}}
== High-resolution respirometry and mt-membrane potential ==


See [http://www.oroboros.at/?O2k-multisensor-manual O2k-MultiSensor Manual] for up-to-date information and discussions on the measurement of mtMP. The general manual for the OROBOROS Ion Selective Electrode system ([[ISE]] System) is in [http://www.oroboros.at/?O2k-multisensor [MiPNet15.03]]. While working with the potentiometric (pX) channel of the O2k, the general [[ESD|guidelines for avoiding damage to the oxygraph by ESD]] should be followed.
:::: Δ<sub>el</sub>''F''<sub><u>''e''</u>p<sup>+</sup></sub> = Δ<sub>m</sub>''F''<sub><u>''e''</u>H<sup>+</sup></sub> - Δ<sub>d</sub>''F''<sub><u>''e''</u>H<sup>+</sup></sub>
:::: Δ''Κ''<sub>p<sup>+</sup></sub> = Δp - Δ''”''<sub>H+</sub>·(''z''<sub>H<sup>+</sup></sub>·''F'')<sup>-1</sup>


A rudimentary protocol for measuring mitochondrial membrane potential (MiPNet14.05), its mathematical appendix and the most up-to-date spreadsheet templates, DatLab templates, and DatLab demo files, can be found [http://www.oroboros.at/?Protocols_tpp-membranepotential here].
Δ''ι''<sub>p<sup>+</sup></sub> is the potential difference across the mitochondrial inner membrane (mtIM), expressed in the electric unit of volt [V]. Electric force of the mitochondrial membrane potential is the electric energy change per ‘motive’ charge or per charge moved across the transmembrane potential difference, with the number of ‘motive’ charges expressed in the unit coulomb [C].
|info=[[Mitchell 1961 Nature]], [[Gnaiger 2020 BEC MitoPathways]]
}}
Communicated by [[Gnaiger E]] 2012-10-05, edited 2016-02-06, 2017-09-05, 2022-07-05.
:::: The chemical part of the protonmotive force, Δ<sub>d</sub>''F''<sub><u>''e''</u>H<sup>+</sup></sub> = Δ''”''<sub>H+</sub>·(''z''<sub>H<sup>+</sup></sub>·''F'')<sup>-1</sup>, stems from the difference of pH across the mt-membrane. It contains a factor that bridges the gap between the electric force [J/C] and the chemical force [J/mol]. This factor is the Faraday constant, ''F'', for conversion between electric force expressed in joules per coulomb or Volt [V=J/C] and chemical force with the unit joules per mole or Jol [Jol=J/mol],


Before measuring membrane potential via [[TPP+]] is even started, the [[TPP+ inhibitory effect]] in the studied system should be explored.How to get from the measured TPP+ concentration to the mitochondrial membrane potential: [[Calculation of mitochondrial membrane potential from measurements with a TPP electrode]]. This covers also the influence of [[Unspecific binding]].
:::::::: ''F'' = 96.4853 kJol/V = 96,485.3 C/mol


Practical difficulties in applying the method to permeabilized fibers are discussed in [[Mitochondrial_membrane_potential#Mitochondrial_membrane_potential_of_permeabilized_fibres|Mitochondrial membrane potential of permeabilized fibers]]. Some tips for [[Cleaning the TPP+ electrodes]]Some important performance parameters of the TPP electrode are summarized on this [http://www.oroboros.at/fileadmin/user_upload/MiP2010/MiP2010_Sumbalova_poster1.pdf poster]. In any way we hope you will join us for one of our [[TPP special interest group during an International Oxygraph Course]].
__TOC__
{{Technical support integrated}}
== Different methods for measurements of mt-membrane potential ==


:::: mt-Membrane potential can either be measured in the [[O2k-FluoRespirometer]] fluorometrically by using the fluorophores [[TMRM]], [[Safranin]], or [[Rhodamine 123]] or potentiometrically with the [[O2k-TPP+ ISE-Module]] electrode by using the ion reporter [[TPP+]]. All mentioned ion indicator molecules inhibit respiration, which makes it essential to test the optimum concentration.


=== Mitochondrial membrane potential and anoxia ===
== High-resolution respirometry and mt-membrane potential ==


=== Question ===
:::: The O2k-MultiSensor system provides a potentiometric and a fluorometric module for measurement of the mt-membrane potential.
::::» O2k-Manual TPP: [[MiPNet15.03 O2k-MultiSensor-ISE]]
::::» [[Tetraphenylphosphonium#O2k-technical_support |TPP: O2k-technical_support]]
::::» [[MiPNet20.13 Safranin mt-membranepotential]]
::::» [[TMRM#O2k-technical_support |TMRM: O2k-technical_support]]


Can I use anoxia as a reference state for zero (minimum) mt-membrane potential in isolated mitochondria?  I want to run experiments in series without loosing the time for washing out inhibitors or uncouplers.  The protocol includes substrates and ADP.
== Calculations ==


=== Answer ===
::::* Data analysis of [[Mitochondrial membrane potential|mitochondrial membrane potential]]  estimation using various fluorescence dyes: [[MiPNet24.09 General Template for Mt-membrane Potential Analysis]] to calculate the relative mt-membrane potential values.


Anoxia should provide a good reference value for minimum mt-membrane potential. However, you should carry out a test experiment: After reaching anoxia, add oligomycin as a test for the possibility that ATPsynthase acts as a ATPase and thus maintains a mt-membrane potential in reversed mode of operation. Then titrate uncoupler (FCCP) to collaps the mt-membrane potential under anoxia.
::::* Data analysis of [[Mitochondrial membrane potential|mitochondrial membrane potential]]  estimation with safranin using DatLab 7.4: [[MiPNet24.08 Safranin Analysis Template]] to express the mt-membrane potential values in mV.


Careful: Ethanol as a carrier for oligomycin and FCCP exerts a chemical side effect on the TPP+ signal, which has to be evaluated in a separate control experiment and subtracted from the experimental trace.
:::::* The calculation used to calculate the mt-membrane potential values are provided here complying with Oroboros transparency policy, see the following page: [[Safranin]]


:::::* for detailed explanation, see [[MiPNet24.11 mtMP calculation]]
== Excel analysis templates ==
:::* More advanced Excel analysis templates for the respective SUIT protocols to calculate the relative mt-membrane potential values are available on this page.
::::* The calculations used in the excel analysis template are provided complying with Oroboros transparency policy: [https://wiki.oroboros.at/index.php/Flux_/_Slope]


::::*''Last update 2021-09-06'': Chemical background correction was implemented into the Excel analysis templates.
::::* For [[SUIT-006 Fluo mt D034]] protocol, see template: [[File:SUIT-006 Fluo mt D034 general.xlsx]] and a demo [[File:SUIT-006 Fluo mt D034 general demo.xlsx]]
::::* For [[SUIT-020 Fluo mt D033]] protocol, see template: [[File:SUIT-020 Fluo mt D033 general.xlsx]] and a demo [[File:SUIT-020 Fluo mt D033 general demo.xlsx]]
::::* For [[SUIT-021 Fluo mt D036]] protocol, see template: [[File:SUIT-021 Fluo mt D036 general.xlsx]] and a demo [[File:SUIT-021 Fluo mt D036 general demo.xlsx]]


== Mitochondrial membrane potential of permeabilized fibres ==
:::* Manual:[[MiPNet24.09 General Template for Mt-membrane Potential Analysis]]
== [[SUITbrowser]] question: Mitochondrial membrane potential ==
:::: Several [[SUIT]] protocols are focused on the measurement of mt-membrane potential by potentiometric and fluorometric techniques.
:::: Use the [https://suitbrowser.oroboros.at/ SUITbrowser] to find the best protocol to answer this and other research questions.


Is it possible to measure [[mitochondrial membrane potential]] of permeabilized fibres? Yes.
The examples in the Membrane Potential protocol [http://www.oroboros.at/index.php?id=protocosl_tpp-membranepotential [MiPNet14.05]] are with permeabilized cells not permeabilized fibers. In the meantime, we have also worked with isolated mitochondria - as expected this proofed to be easier than the permeabilized cells. Indeed that is the reason we started with permeabilized cells: Early experiments showed it doable but since its more difficult than isolated mitos all performance results obtained should be transferable to (or even be better with) isolated mitos. But what about [[Permeabilized muscle fibre|permeabilized muscle fibers]]?


[[Image:O2k-Publications.jpg|left|150px|link=http://www.bioblast.at/index.php/O2k-Publications:  Topics|O2k-Publications in the MiPMap]]


'''''Sort in ascending/descending order by a click on one of the small symbols in squares below'''''.
Default sorting: chronological. Empty fields appear first in ascending order.
{{#ask:[[Category:Publications]] [[Instrument and method::Oxygraph-2k]] [[Topic::mt-Membrane potential]]
|?Was published in year=Year
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}}


=== General ===
== Keywords: Force and membrane potential ==
We and several of our customers are currently extending the use of the [[TPP]] electrode for measuring mitochondrial membrane potential to permeabilized fibers. Fist results show:
{{Keywords: Force and membrane potential}}
 
{{MitoPedia concepts
Yes, its possible!
|mitopedia concept=Respiratory state, Recommended, Ergodynamics
 
}}
Before this development started, there were basic two considerations:
{{MitoPedia methods
 
|mitopedia method=Respirometry, Fluorometry
a.) we have not found any reference that describes this to have been done. So one could see it as a totally new, presumable difficult technique, that needs a lot of methods development.
}}
 
{{MitoPedia topics
b.) on the other hand, one can argue: what’s really the difference between permeabilized cultured cells and permeabilized fibers. Maybe a bit more of non mitochondrial cell material, but otherwise?
|mitopedia topic=EAGLE
 
}}
 
{{Labeling
The first step definitely is to guess the required sample amount. From experiments with isolated mitos or permeabilized cells one can see what concentration of mitos is necessary to obtain noticeable differences in the TPP concentration. This will have to be converted (e.g. via the respiratory rate) to a amount of sample necessary for permeabilized fibers. Maybe even more sample is necessary to compensate for more "outside binding" in permeabilized fibers. Even with permeabilized cells higher sample amounts are required, as compared with standard high resolution respiratory measurements. Then there have to be some modifications in the protocol, especially how the sample is introduced. It is important that the total amount of TPP in the chamber is known at all times. It follows that the sample may not be preconditioned outside of the chamber to TPP, and even a rough estimation of the sample volume will be necessary.
|additional=MitoPedia:NextGen-O2k
If we go now totally into the realm of speculation: Might there be any specific reasons why the method just does not work with permeabilized fibers even after method development?
}}
One could postulate that rather big junks of very hydrophobic material (fat) might "hover" up all the TPP. However, due to the far higher TPP concentration inside the mitochochondria as compared to the outside concentration (because of the membrane potential) external "unspecific binding" is usually nearly negligible for permeabilized cells......
 
 
 
=== Introduction of the Sample ===
 
 
The established was to measure mitochondrial membrane potential for isolated mitochondria (and permeabilized cells) is to calibrate the TPP electrode by adding TPP in several steps to the indented measuring chamber. With the final calibration step the planned starting TPP concentration is reached. Then the sample is injected into the "calibrated" chamber. Therefore, unlike in the application of other potentiometric methods (pH, Ca2+,..) the "calibration" does in fact serve TWO different purposes:
1.) calibration of the sensor (of course)
2.) establishing the total amount of TPP present in the chamber. This amount has to be a precisely known for the calculation of delta Psi from the measured [TPP]
 
==== Problems ====
Introduction of the sample is a key problem in extending the TPP+ method for measuring mitochondrial membrane potential for two different reasons:
 
A.) Disturbance of the calibration itself: That is after the necessary handling steps the calibration parameters determined during the calibration run are no longer correct (due to geometry changes, ...)
 
B.) Changing the total amount of TPP preset in the chamber: If solution is lost or additional liquid has to be added during the introduction of the sample the information about the total amount of TPP+ may easily get lost:
Even for permeabilized cells, this was a major issue and was solved by injection a quite concentrated sample solution as fast as possible into the chamber: A fast injection ensured that the replacement of TPP containing medium in the chamber by the medium containing sample but no TPP+ can be treated as a simple process, not involving:
1.) any mixing of the solutions before the displacement is complete
2.) any uptake of TPP by the sample before the displacement is complete. Therefore the introduction could be treated as a simple dilution of a solution with a known TPP conc. with a solution containing no TPP. (see also Note 1)
 
All methods to introduce a sample have to consider both problems.
 
==== Possible methods ====
1.)The obvious method: '''opening the chambers''' and placing the permeabilized fiber in the chamber:
From very few and insufficient trials at Oroboros it would seem that problem I.) (loss of calibration information) is maybe less severe than initially thought or is at least less significant that problem B.). This could be checked by practicing the opening and closing the chamber with the introduction of any biological material. Typical opening and closing the camber will result in loss of liquid, necessitate the introduction of new liquid. To circumvent Problem B (change of TPP+ conc.) even in such a blind trial it would be necessary to replace all liquid lost with medium containing exactly the TPP concentration established din the chamber before opening it. However Problem B might proof crucial: After introducing permeabilized fibers they immediately start to take up TPP. Opening and closing the chamber typically requires quite a lot of “bubble fighting” and placing liquid on top of the stopper. While (pre-warmed) medium containing exactly the initial TPP+ conc. after calibration can be used for this operations, the concentration in the chamber will already be different bat this time due to TPP uptake. The problem will be the more significant the longer this operations continue and the more liquid is moved around.
 
 
2.)Introduction of the sample via '''a dedicated large additional port''': Such a port would have to be closed during operation and calibration by a plug completely filling the bore (a plug e.g. only filling the top part of the stopper would create a huge unstirred zone inside the stopper, incompatible with high resolution respirometry). The construction of such a stopper that ensures a tight fit might pose some technical problems but is probable doable. Operation could work in the following way:
* End of calibration run, top of stopper is dry
* Plug for “sample port” is removed: since top of stopper is dry no additional liquid gets into the chamber
* Sample is introduced using ?very special forceps?,  ?a biopsy needle ?,  ?a steel wire? (volume of sample introduced should be known or very small)
* To enable bubble free closing: A very small volume (just as much as necessary) volume of pre warmed medium is immediately filed into the chamber via the “sample” port and the sample port is immediately closed with the plug. A small volume will be extruded from the chamber via the injection port. Because the sample already started to take up TPP+, the concentration of the volume extruded will not be exactly known (the volume will ideally be the sample volume + the volume added before closing the port).  The volume should be kept as small as possible to minimize the error.
This method requires a special stopper and plug, the handling procedure for introducing the sample has to be very special because the diameter  of the “sample port” necessarily has to be quite small (there is just not too much space left) and introduced new problems regarding the design and closing procedure of the fitting plug. The advantage is that it is not necessary to move the electrodes.
 
3.)Using the '''existing ports''' for an approach similar to the one discussed under point two. Depending on the method found to insert the sample into the chamber, either the '''reference electrode''' or the '''TPP electrode''' would be removed from the stopper (try top). The further process would be as described above.  The closing of the bore (with the electrode) is already a quite established process. If it is possible to use the port of the reference electrode, a very small (or considering the sample volume: no) additional solution (pre-warmed containing the initial TPP concentration as a first order approximation) can be used.
Advantage: No modification of stopper required, same development of “introduction skills” necessary as for method 2. Same advantages / disadvantages in regard to “Problem B” as for Method 2
Disadvantage: possible disturbance of the calibration by moving one electrode. At least for removing and re-inserting the reference electrode this problem seems (from limited experience) to be quite small. This can be easily tested. Removal and reinsertion of electrodes should be done with stirrers switched off.
 
 
4.)Using a '''partially homogenized sample''', injecting it: probable not doable with current (and possible) permeabilization protocols.
 
5.)'''Preferred Method:''' Introduction of the sample via the '''titration port''': Requires obviously the most sophisticated tool for getting the sample in, but only minimal distortion.
 
 
==== Evaluation and solution by the Neufer Group at East Carolina University ====
 
The group of [[US NC Greenville Neufer PD|Darrell Neufer at East Carolina University, Greenville, NC, USA]], evaluated two of the discussed approaches and presented a solution. For their full contribution see the Discussion page. In summary
* the port for the reference electrode is used to introduce the sample
* the sample is split into several parts
* if necessary, the sample pieces are introduced into the chamber using a standard Hamilton syringe and the reference electrode itself
* other methods for sample insertion were tested and rejected
 
'''Until full integration of their method into this page see the contribution of the Neufer group on the [[Talk:Mitochondrial_membrane_potential|Discussion page]] for a detailed description.'''
 
 
 
 
==== Method used by the OROBOROS O2k-Team ====
The method described above was further refined by the OROBOROS O2k-Team in Innsbruck using a glass Pasteur pipette to introduce the sample into the chamber via the port for the reference electrode. For full details see the [[Talk:Mitochondrial_membrane_potential|Discussion page]].
 
 
=== Performing the measurement ===
 
==== Reoxygenation and high oxygen ====
 
The method recommended by Oroboros Instruments to do a re-oxygenation in the presence of additional electrodes is to inject H2O2 into a medium containing catalase, avoiding any mechanical disturbances, see the protocol for the MiR06 medium [http://www.oroboros.at/index.php?id=protocols_miro6 MiPNet14.13]. However, if the presence of catalase in the medium is not desired or the necessary increase in oxygen concentration is larger than recommended for the MiR06 approach ( ΔcO2 ≀200 ÎŒmol/l) the method decribed by the Neufer group ion the discussion section seems to be an alternative.
 
Because the H2O2 method is limited to a delta cO2 of 200 ”mol/l the initial high oxygen concentration should be achieved with the gas opahse method before the statr of the experiment. The O2 level can then be maintained by H2O2 injections without opening the chamber.
 
==== Slowness of TPP uptake /release ====
TPP uptake and release seems generally to be slower for permeabilzed fibers than for isolated mitochondria or permeabilized cells. However, the extend of this effect was reported to be very different by different groups. It is not yet clear what causes extremely slow uptake/ release in some cases but not in others.
 
 
=== Calculation of the membrane potential ===
 
For issues regarding the actual calculation of the mitochondrial membrane potential, see [[Calculation of mitochondrial membrane potential from measurements with a TPP electrode]], where also the complications to the calculation introduced by the presence of non mitochondrial material is discussed.
 
A specific issue of permeabilized fibres (in contrast to isolated mitos, permeabilized cells, or homogenate) is that the sample is not distributed homogeneously. Any injections during the experiment will dilute the TPP concentration but will not dilute the sample. Therefore, all quantities depending on the amount of sample (Pcell, Pmt, Vmt(absolut)) have to be set to a fixed value (= the starting value) when using the OROBOROS calculation spreadsheets.
 
=== See also ===
[[Mitochondrial membrane potential]]
 
[[ISE]]
 
[[MiPNet14.14 PermeabilizedFibrePreparation]]
 
[[Pesta 2012 Methods Mol Biol]]
 
 
{{#set:Technical service=pX signal}}

Revision as of 20:37, 10 July 2022


high-resolution terminology - matching measurements at high-resolution


Mitochondrial membrane potential

Description

The mitochondrial membrane potential difference, mtMP or Διp+ = ΔelFep+, is the electric part of the protonmotive force, Δp = ΔmFeH+.

ΔelFep+ = ΔmFeH+ - ΔdFeH+
Διp+ = Δp - Δ”H+·(zH+·F)-1

Διp+ is the potential difference across the mitochondrial inner membrane (mtIM), expressed in the electric unit of volt [V]. Electric force of the mitochondrial membrane potential is the electric energy change per ‘motive’ charge or per charge moved across the transmembrane potential difference, with the number of ‘motive’ charges expressed in the unit coulomb [C].

Abbreviation: mtMP, Διp+, ΔelFep+ [V]

Reference: Mitchell 1961 Nature, Gnaiger 2020 BEC MitoPathways 

Communicated by Gnaiger E 2012-10-05, edited 2016-02-06, 2017-09-05, 2022-07-05.
The chemical part of the protonmotive force, ΔdFeH+ = Δ”H+·(zH+·F)-1, stems from the difference of pH across the mt-membrane. It contains a factor that bridges the gap between the electric force [J/C] and the chemical force [J/mol]. This factor is the Faraday constant, F, for conversion between electric force expressed in joules per coulomb or Volt [V=J/C] and chemical force with the unit joules per mole or Jol [Jol=J/mol],
F = 96.4853 kJol/V = 96,485.3 C/mol
Template NextGen-O2k.jpg


MitoPedia O2k and high-resolution respirometry: O2k-Open Support 


Different methods for measurements of mt-membrane potential

mt-Membrane potential can either be measured in the O2k-FluoRespirometer fluorometrically by using the fluorophores TMRM, Safranin, or Rhodamine 123 or potentiometrically with the O2k-TPP+ ISE-Module electrode by using the ion reporter TPP+. All mentioned ion indicator molecules inhibit respiration, which makes it essential to test the optimum concentration.

High-resolution respirometry and mt-membrane potential

The O2k-MultiSensor system provides a potentiometric and a fluorometric module for measurement of the mt-membrane potential.
» O2k-Manual TPP: MiPNet15.03 O2k-MultiSensor-ISE
» TPP: O2k-technical_support
» MiPNet20.13 Safranin mt-membranepotential
» TMRM: O2k-technical_support

Calculations

  • The calculation used to calculate the mt-membrane potential values are provided here complying with Oroboros transparency policy, see the following page: Safranin

Excel analysis templates

  • More advanced Excel analysis templates for the respective SUIT protocols to calculate the relative mt-membrane potential values are available on this page.
  • The calculations used in the excel analysis template are provided complying with Oroboros transparency policy: [1]

SUITbrowser question: Mitochondrial membrane potential

Several SUIT protocols are focused on the measurement of mt-membrane potential by potentiometric and fluorometric techniques.
Use the SUITbrowser to find the best protocol to answer this and other research questions.


O2k-Publications in the MiPMap
Sort in ascending/descending order by a click on one of the small symbols in squares below.
Default sorting: chronological. Empty fields appear first in ascending order.
 YearReferenceOrganismTissue;cell
Ravasz 2024 Sci Rep2024Ravasz D, Bui D, Nazarian S, Pallag G, Karnok N, Roberts J, Marzullo BP, Tennant DA, Greenwood B, Kitayev A, Hill C, KomlĂłdi T, Doerrier C, Cunatova K, Fernandez-Vizarra E, Gnaiger E, Kiebish Michael A, Raska A, Kolev K, Czumbel B, Narain NR, Seyfried TN, Chinopoulos C (2024) Residual Complex I activity and amphidirectional Complex II operation support glutamate catabolism through mtSLP in anoxia. Sci Rep 14:1729. https://doi.org/10.1038/s41598-024-51365-4MouseHeart
Liver
Donnelly 2024 Redox Biol2024Donnelly C, KomlĂłdi T, Cecatto C, Cardoso LHD, Compagnion A-C, Matera A, Tavernari D, Campiche O, Paolicelli RC, Zanou N, Kayser B, Gnaiger E, Place N (2024) Functional hypoxia reduces mitochondrial calcium uptake. Redox Biol 71:103037. https://doi.org/10.1016/j.redox.2024.103037Human
Mouse		Heart
Skeletal muscle
Dabrowska 2023 Int J Mol Sci2023Dabrowska A, Zajac M, Bednarczyk P, Lukasiak A (2023) Effect of quercetin on mitoBKCa channel and mitochondrial function in human bronchial epithelial cells exposed to particulate matter. Int J Mol Sci 24:638. https://doi.org/10.3390/ijms24010638HumanLung;gill
Endothelial;epithelial;mesothelial cell
Som 2023 Am J Physiol Cell Physiol2023Som R, Fink BD, Yu L, Sivitz WI (2023) Oxaloacetate regulates complex II respiration in brown fat: dependence on UCP1 expression. Am J Physiol Cell Physiol 324:C1236-48. doi: 10.1152/ajpcell.00565.2022MouseFat
Krause 2023 J Transl Med2023Krause J, Nickel A, Madsen A, Aitken-Buck HM, Stoter AMS, Schrapers J, Ojeda F, Geiger K, Kern M, Kohlhaas M, Bertero E, Hofmockel P, HĂŒbner F, Assum I, Heinig M, MĂŒller C, Hansen A, Krause T, Park DD, Just S, AĂŻssi D, Börnigen D, Lindner D, Friedrich N, Alhussini K, Bening C, Schnabel RB, Karakas M, Iacoviello L, Salomaa V, Linneberg A, Tunstall-Pedoe H, Kuulasmaa K, Kirchhof P, Blankenberg S, Christ T, Eschenhagen T, Lamberts RR, Maack C, Stenzig J, Zeller T (2023) An arrhythmogenic metabolite in atrial fibrillation. https://doi.org/10.1186/s12967-023-04420-zHumanHeart
Donnelly 2023 MitoFit2023Donnelly C, Komlódi T, Cecatto C, Cardoso LHD, Compagnion AC, Matera A, Tavernari D, Zanou N, Kayser B, Gnaiger E, Place N (2023) Functional hypoxia reduces mitochondrial calcium uptake. MitoFit Preprints 2023.2. https://doi.org/10.26124/mitofit:2023-0002 — 2024-11-17 published in Redox Biol.Human
Mouse		Skeletal muscle
Heart
Nervous system
Other cell lines
Tomar 2022 Biochim Biophys Acta Bioenerg2022Tomar N, Zhang X, Kandel SM, Sadri S, Yang C, Liang M, Audi SH, Cowley AW Jr, Dash RK (2022) Substrate-dependent differential regulation of mitochondrial bioenergetics in the heart and kidney cortex and outer medulla. https://doi.org/10.1016/j.bbabio.2021.148518RatHeart
Kidney
Ceja-Galicia 2022 Antioxidants (Basel)2022Ceja-Galicia ZA, GarcĂ­a-Arroyo FE, Aparicio-Trejo OE, El-Hafidi M, Gonzaga-SĂĄnchez G, LeĂłn-Contreras JC, HernĂĄndez-Pando R, Guevara-Cruz M, Tovar AR, Rojas-Morales P, Aranda-Rivera AK, SĂĄnchez-Lozada LG, Tapia E, Pedraza-Chaverri J (2022) Therapeutic effect of curcumin on 5/6Nx hypertriglyceridemia: association with the improvement of renal mitochondrial ÎČ-oxidation and lipid metabolism in kidney and liver. https://doi.org/10.3390/antiox11112195RatKidney
Fink 2022 FASEB Bioadv2022Fink BD, Rauckhorst AJ, Taylor EB, Yu L, Sivitz WI (2022) Membrane potential-dependent regulation of mitochondrial complex II by oxaloacetate in interscapular brown adipose tissue. FASEB Bioadv 4:197-210. https://doi.org/10.1096/fba.2021-00137Fat
Komlodi 2022 BEC2022Komlódi T, Tretter L (2022) The protonmotive force – not merely membrane potential. Bioenerg Commun 2022.16. https://doi.org/10.26124/bec:2022-0016
Bouitbir 2022 Int J Mol Sci2022Bouitbir J, Panajatovic MV, KrĂ€henbĂŒhl S (2022) Mitochondrial toxicity associated with imatinib and sorafenib in isolated rat heart fibers and the cardiomyoblast H9c2 cell line. Int J Mol Sci 23:2282. https://doi.org/10.3390/ijms23042282RatHeart
Pallag 2022 Int J Mol Sci2022Pallag G, Nazarian S, Ravasz D, Bui D, KomlĂłdi T, Doerrier C, Gnaiger E, Seyfried TN, Chinopoulos C (2022) Proline oxidation supports mitochondrial ATP production when Complex I is inhibited. https://doi.org/10.3390/ijms23095111MouseLiver
Kidney
Fink 2021 Pharmacol Res Perspect2021Fink BD, Yu L, Coppey L, Obrosov A, Shevalye H, Kerns RJ, Yorek MA, Sivitz WI (2021) Effect of mitoquinone on liver metabolism and steatosis in obese and diabetic rats. Pharmacol Res Perspect 9:e00701.RatLiver
Schmidt 2021 J Biol Chem2021Schmidt CA, Fisher-Wellman KH, Neufer PD (2021) From OCR and ECAR to energy: perspectives on the design and interpretation of bioenergetics studies. J Biol Chem 207:101140. https://doi.org/10.1016/j.jbc.2021.101140
Jasz 2021 J Cell Mol Med2021JĂĄsz DK, SzilĂĄgyi ÁL, Tuboly E, BarĂĄth B, MĂĄrton AR, Varga P, Varga G, Érces D, MohĂĄcsi Á, SzabĂł A, BozĂł R, Gömöri K, Görbe A, Boros M, Hartmann P (2021) Reduction in hypoxia-reoxygenation-induced myocardial mitochondrial damage with exogenous methane. https://doi.org/10.1111/jcmm.16498RatHeart
Juhaszova 2021 Function (Oxf)2021Juhaszova M, Kobrinsky E, Zorov DB, Nuss HB, Yaniv Y, Fishbein KW, de Cabo R, Montoliu L, Gabelli SB, Aon MA, Cortassa S, Sollott SJ (2021) ATP synthase K+- and H+-fluxes drive ATP synthesis and enable mitochondrial K+-"uniporter" function: I. Characterization of ion fluxes. Function (Oxf) 3(2):zqab065. doi: 10.1093/function/zqab065
MiPNet24.08 Safranin Analysis Template2020-05-13
O2k-Protocols
Excel template for safranin data analysis.
MiPNet25.14 TPP Analysis Template2020-##-##
O2k-Protocols
Excel template for TPP data analysis.
Dolezelova 2020 PLoS Biol2020DoleĆŸelovĂĄ E, KunzovĂĄ M, Dejung M, Levin M, Panicucci B, Regnault C, Janzen CJ, Barrett MP, Butter F, ZĂ­kovĂĄ A (2020) Cell-based and multi-omics profiling reveals dynamic metabolic repurposing of mitochondria to drive developmental progression of Trypanosoma brucei. PLoS Biol 18:e3000741.Protists
Oellermann 2020 Sci Rep2020Oellermann M, Hickey AJR, Fitzgibbon QP, Smith G (2020) Thermal sensitivity links to cellular cardiac decline in three spiny lobsters. Sci Rep 10:202.CrustaceansHeart
Smith 2020 J Biol Chem2020Smith CD, Schmidt CA, Lin CT, Fisher-Wellman KH, Neufer PD (2020) Flux through mitochondrial redox circuits linked to nicotinamide nucleotide transhydrogenase generates counterbalance changes in energy expenditure. J Biol Chem 295:16207-16.MouseSkeletal muscle
Cecatto 2020 Mitochondrion2020Cecatto C, Amaral AU, Wajner A, Wajner SM, Castilho RF, Wajner M (2020) Disturbance of mitochondrial functions associated with permeability transition pore opening induced by cis-5-tetradecenoic and myristic acids in liver of adolescent rats. Mitochondrion 50:1-13.RatLiver
Other cell lines
Hassan 2020 MitoFit Preprint Arch2020Hassan Hazirah, Gnaiger Erich, Zakaria Fazaine, Makpol Suzana, Abdul Karim Norwahidah (2020) Alterations in mitochondrial respiratory capacity and membrane potential: a link between mitochondrial dysregulation and autism. https://doi.org/10.26124/mitofit:200003Human
Cecatto 2020 Toxicol In Vitro2020Cecatto C, Amaral AU, Roginski AC, Castilho RF, Wajner M (2020) Impairment of mitochondrial bioenergetics and permeability transition induction caused by major long-chain fatty acids accumulating in VLCAD deficiency in skeletal muscle as potential pathomechanisms of myopathy. Toxicol In Vitro 62:104665.RatSkeletal muscle
Charles 2020 Nanomedicine (Lond)2020Charles C, Cohen-Erez I, Kazaoka B, Melnikov O, Stein DE, Sensenig R, Rapaport H, Orynbayeva Z (2020) Mitochondrial responses to organelle-specific drug delivering nanoparticles composed of polypeptide and peptide complexes. Nanomedicine (Lond) 15:2917-32.HumanEndothelial;epithelial;mesothelial cell
Aparicio-Trejo 2020 Free Radic Biol Med2020Aparicio-Trejo OE, Avila-Rojas SH, Tapia E, Rojas-Morales P, LeĂłn-Contreras JC, MartĂ­nez-Klimova E, HernĂĄndez-Pando R, SĂĄnchez-Lozada LG, Pedraza-Chaverri J (2020) Chronic impairment of mitochondrial bioenergetics and ÎČ-oxidation promotes experimental AKI-to-CKD transition induced by folic acid. Free Radic Biol Med 154:18-32.RatKidney
Gnaiger 2020 BEC MitoPathways2020Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002Human
Mouse		Heart
Skeletal muscle
Fibroblast
Lozano 2020 Part Fibre Toxicol2020Lozano O, Silva-Platas C, Chapoy-Villanueva H, PĂ©rez BE, Lees JG, Ramachandra CJA, Contreras-Torres FF, LĂĄzaro-Alfaro A, Luna-Figueroa E, Bernal-RamĂ­rez J, Gordillo-Galeano A, Benitez A, Oropeza-AlmazĂĄn Y, Castillo EC, Koh PL, Hausenloy DJ, Lim SY, GarcĂ­a-Rivas G (2020) Amorphous SiO2 nanoparticles promote cardiac dysfunction via the opening of the mitochondrial permeability transition pore in rat heart and human cardiomyocytes. Part Fibre Toxicol 17:15.Rat
Human		Heart
Wang 2020 J Mol Med (Berl)2020Wang SY, Zhu Siyu, Wu Jian, Zhang Maomao, Xu Yousheng, Xu Wei, Cui Jinjin, Yu Bo, Cao Wei, Liu Jingjin (2020) Exercise enhances cardiac function by improving mitochondrial dysfunction and maintaining energy homoeostasis in the development of diabetic cardiomyopathy. J Mol Med (Berl) 98:245-61.MouseHeart
Shuvo 2019 J Bioenerg Biomembr2019Shuvo SR, Wiens LM, Subramaniam S, Treberg JR, Court DA (2019) Increased reactive oxygen species production and maintenance of membrane potential in VDAC-less Neurospora crassa mitochondria. J Bioenerg Biomembr 51:341-54.Fungi
Spinazzi 2019 Proc Natl Acad Sci U S A2019Spinazzi M, Radaelli E, Horré K, Arranz AM, Gounko NV, Agostinis P, Maia TM, Impens F, Morais VA, Lopez-Lluch G, Serneels L, Navas P, De Strooper B (2019) PARL deficiency in mouse causes Complex III defects, coenzyme Q depletion, and Leigh-like syndrome. Proc Natl Acad Sci U S A 116:277-86. 10.1073/pnas.1811938116MouseNervous system
Lau 2019 Comp Biochem Physiol B Biochem Mol Biol2019Lau GY, Milsom WK, Richards JG, Pamenter ME (2019) Heart mitochondria from naked mole-rats (Heterocephalus glaber) are more coupled, but similarly susceptible to anoxia-reoxygenation stress than in laboratory mice (Mus musculus). Comp Biochem Physiol B Biochem Mol Biol 240:110375.Mouse
Other mammals		Heart
Devaux 2019 Front Physiol2019Devaux JBL, Hedges CP, Birch N, Herbert N, Renshaw GMC, Hickey AJR (2019) Acidosis maintains the function of brain mitochondria in hypoxia-tolerant triplefin fish: a strategy to survive acute hypoxic exposure? Front Physiol 9:1941.FishesNervous system
Esselun 2019 Oxid Med Cell Longev2019Esselun C, Bruns B, Hagl S, Grewal R, Eckert GP (2019) Differential effects of silibinin A on mitochondrial function in neuronal PC12 and HepG2 liver cells. Oxid Med Cell Longev 2019:1652609.Human
Rat		Nervous system
Liver
Rojas-Morales 2019 Free Radic Biol Med2019Rojas-Morales P, León-Contreras JC, Aparicio-Trejo OE, Reyes- Ocampo JG, Medina-Campos ON, Jiménez-Osorio AS, Gonzålez-Reyes S, Marquina- Castillo B, Hernåndez-Pando R, Barrera-Oviedo D, Sånchez-Lozada LG, Pedraza-Chaverri J, Tapia E (2019) Fasting reduces oxidative stress, mitochondrial dysfunction and fibrosis induced by renal ischemia-reperfusion injury. Free Radic Biol Med 135:60-67.RatKidney
Dilberger 2019 Oxid Med Cell Longev2019Dilberger B, Baumanns S, Schmitt F, Schmiedl T, Hardt M, Wenzel U, Eckert GP (2019) Mitochondrial oxidative stress impairs energy metabolism and reduces stress resistance and longevity of C. elegans. Oxid Med Cell Longev 2019:6840540.Caenorhabditis elegans
Malyala 2019 PLoS Comput Biol2019Malyala S, Zhang Y, Strubbe JO, Bazil JN (2019) Calcium phosphate precipitation inhibits mitochondrial energy metabolism. PLoS Comput Biol 15:e1006719.Guinea pigHeart
Fink 2019 FASEB J2019Fink BD, Yu L, Sivitz WI (2019) Modulation of complex II-energized respiration in muscle, heart, and brown adipose mitochondria by oxaloacetate and complex I electron flow. FASEB J 33:11696-705.MouseHeart
Skeletal muscle
Fat
Menezes-Filho 2018 Biochim Biophys Acta Bioenerg2018Menezes-Filho SL, Amigo I, Luévano-Martínez LA, Kowaltowski AJ (2018) Fasting promotes functional changes in liver mitochondria. Biochim Biophys Acta Bioenerg 1860:129-35.MouseLiver
Cecatto 2018 FEBS J2018Cecatto C, Amaral AU, da Silva JC, Wajner A, Schimit MOV, da Silva LHR, Wajner SM, Zanatta A, Castilho RF, Wajner M (2018) Metabolite accumulation in VLCAD deficiency markedly disrupts mitochondrial bioenergetics and Ca2+ homeostasis in the heart. FEBS J 285:1437-55.RatHeart
Other cell lines
McLaughlin 2018 Biochem Biophys Res Commun2018McLaughlin KL, McClung JM, Fisher-Wellman KH (2018) Bioenergetic consequences of compromised mitochondrial DNA repair in the mouse heart. Biochem Biophys Res Commun 504:742-48.MouseHeart
Komlodi 2018 J Bioenerg Biomembr2018KomlĂłdi T, Geibl FF, Sassani M, Ambrus A, Tretter L (2018) Membrane potential and delta pH dependency of reverse electron transport-associated hydrogen peroxide production in brain and heart mitochondria. J Bioenerg Biomembr 50:355-365Guinea pigHeart
Nervous system
Smirnova 2018 Sci Rep2018Smirnova IA, Ädelroth P, Brzezinski P (2018) Extraction and liposome reconstitution of membrane proteins with their native lipids without the use of detergents. Sci Rep 8:14950.
Hayward 2018 Thesis2018Hayward L (2018) The effect of anoxia on mitochondrial function in a hibernator (Ictidomys tridecemlineatus). Master's Thesis 57.Other mammalsLiver
Fisher-Wellman 2018 Cell Rep2018Fisher-Wellman KH, Davidson MT, Narowski TM, Lin CT, Koves TR, Muoio DM (2018) Mitochondrial diagnostics: A multiplexed assay platform for comprehensive assessment of mitochondrial energy fluxes. Cell Rep 24:3593-606.MouseHeart
Skeletal muscle
De Carvalho 2017 Toxicol Research2017de Carvalho NR, Rodrigues NR, Macedo GE, Boligon AA, de Campos MM, Posser T, Cunha FAB, Coutinho HD, Klamt F, Bristot IJ, Merritt TJS, Franco JL (2017) Eugenia uniflora leaves essential oil promotes mitochondrial dysfunction in Drosophila melanogaster through the inhibition of oxidative phosphorylation. Toxicol Research 6:526-34 .Drosophila
Nogueira 2017 Free Radic Biol Med2017Nogueira NP, Saraiva FMS, Oliveira MP, Mendonca APM, Inacio JDF, Almeida-Amaral EE, Menna-Barreto RF, Laranja GAT, Lopes Torres EJ, Oliveira MF, Paes MC (2017) Heme modulates Trypanosoma cruzi bioenergetics inducing mitochondrial ROS production. Free Radic Biol Med 108:183-91.Protists
Castellano-Gonzalez 2016 Oncotarget2016Castellano-GonzĂĄlez G, Pichaud N, Ballard JW, Bessede A, Marcal H, Guillemin GJ (2016) Epigallocatechin-3-gallate induces oxidative phosphorylation by activating cytochrome c oxidase in human cultured neurons and astrocytes. Oncotarget 7:7426-40HumanNervous system
Moon 2016 J Biol Chem2016Moon SH, Mancuso DJ, Sims HF, Liu X, Nguyen AL, Yang K, Guan S, Dilthey BG, Jenkins CM, Weinheimer CJ, Kovacs A, Abendschein D, Gross RW (2016) Cardiac myocyte-specific knock-out of calcium-independent phospholipase A2Îł (iPLA2Îł) decreases oxidized fatty acids during ischemia/reperfusion and reduces infarct size. J Biol Chem 291:19687-700.MouseHeart
Kucera 2015 Oxid Med Cell Longev2015Kucera O, Mezera V, Moravcova A, Endlicher R, Lotkova H, Drahota Z, Cervinkova Z (2015) In vitro toxicity of epigallocatechin gallate in rat liver mitochondria and hepatocytes. Oxid Med Cell Longev 2015:476180.RatLiver
Casanova 2014 Biochim Biophys Acta2014Casanova E, Baselga-Escudero L, Ribas-Latre A, Arola-Arnal A, Bladé C, Arola L, Salvadó MJ (2014) Epigallocatechin gallate counteracts oxidative stress in docosahexaenoxic acid-treated myocytes. Biochim Biophys Acta 1837:783-91.RatSkeletal muscle
Other cell lines
Kukat 2014 PLoS Genet2014Kukat A, Dogan SA, Edgar D, Mourier A, Jacoby C, Maiti P, Mauer J, Becker C, Senft K, Wibom R, Kudin AP, Hultenby K, Flögel U, Rosenkranz S, Ricquier D, Kunz WS, Trifunovic A (2014) Loss of UCP2 attenuates mitochondrial dysfunction without altering ROS production and uncoupling activity. https://doi.org/10.1371/journal.pgen.1004385MouseHeart
Pham 2014 Am J Physiol2014Pham T, Loiselle D, Power A, Hickey AJ (2014) Mitochondrial inefficiencies and anoxic ATP hydrolysis capacities in diabetic rat heart. Am J Physiol 307:C499–507.RatHeart
Gnaiger 2014 MitoPathways2014
O2k-Protocols
Gnaiger E (2014) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 4th ed. Mitochondr Physiol Network 19.12. Oroboros MiPNet Publications, Innsbruck:80 pp. — see 5th edition: Gnaiger 2020 BEC MitoPathways.		Human
Mouse		Heart
Skeletal muscle
Fibroblast
Glaser 2014 Thesis2014Glaser V (2014) Efeitos da hiperglicemia cronica e seus metabolitos, metilglioxal e produtos terminais de glicacao, na fisiologia e dinamica mitochondrial no sistema nervoso central. PhD Thesis 1-117.RatNervous system
Other cell lines
Duicu 2013 Can J Physiol Pharmacol2013Duicu OM, Mirica SN, Gheorgheosu DE, Privistirescu AI, Fira-Mladinescu O, Muntean DM (2013) Ageing-induced decrease in cardiac mitochondrial function in healthy rats. Can J Physiol Pharmacol 91:593-600.RatHeart
Dos Santos 2013 J Bioenerg Biomembr2013dos Santos RS, Peçanha FL, da-Silva WS (2013) Functional characterization of an uncoupling protein in goldfish white skeletal muscle. J Bioenerg Biomembr 45:243-51.FishesSkeletal muscle
Volejnikova 2013 FEMS Yeast Res2013VolejnĂ­kovĂĄ A, HlouskovĂĄ J, Sigler K, PichovĂĄ A (2013) Vital mitochondrial functions show profound changes during yeast culture ageing. FEMS Yeast Res 13:7-15.Saccharomyces cerevisiae
Fungi
Sarti 2013 Int J Mol Sci2013Sarti P, Magnifico MC, Altieri F, Mastronicola D, Arese M (2013) New evidence for cross talk between melatonin and mitochondria mediated by a circadian-compatible interaction with nitric oxide. Int J Mol Sci 14:11259-76.HumanOther cell lines
Felser 2013 Toxicol Sci2013Felser A, Blum K, Lindinger PW, Bouitbir J, Kraehenbuehl S (2013) Mechanisms of hepatocellular toxicity associated with dronedarone - a comparison to amiodarone. Toxicol Sci 131:480-90.Human
Rat		Liver
Krako 2013 J Alzheimers Dis2013Krako N, Magnifico MC, Arese M, Meli G, Forte E, Lecci A, Manca A, Giuffrù A, Mastronicola D, Sarti P, Cattaneo A (2013) Characterization of mitochondrial dysfunction in the 7PA2 cell model of Alzheimer’s disease. J Alzheimers Dis 37:747-58.CHO
Bustamante 2012 Alcohol2012Bustamante J, Karadayian AG, Lores-Arnaiz S, Cutrera RA (2012) Alterations of motor performance and brain cortex mitochondrial function during ethanol hangover. Alcohol 46:473-9.MouseNervous system
Kumari 2012 PLoS One2012Kumari S, Mehta SL, Li PA (2012) Glutamate induces mitochondrial dynamic imbalance and autophagy activation: preventive effects of selenium. PLoS One 7:e39382.MouseNervous system
Other cell lines
Selivanov 2012 PLoS Comput Biol2012Selivanov VA, Cascante M, Friedman M, Schumaker MF, Trucco M, Votyakova TV (2012) Multistationary and oscillatory modes of free radicals generation by the mitochondrial respiratory chain revealed by a bifurcation analysis. PLoS Comput Biol 8(9):e1002700. doi: 10.1371/journal.pcbi.1002700.RatNervous system
Albertini 2012 Aging (Albany NY)2012Albertini E, KozieƂ R, Duerr A, Neuhaus M, Jansen-Duerr P (2012) Cystathionine beta synthase modulates senescence of human endothelial cells. Aging (Albany NY) 4:664-73.HumanEndothelial;epithelial;mesothelial cell
HUVEC
Leuner 2012 Mol Neurobiol2012Leuner K, Schulz K, SchĂŒtt T, Pantel J, Prvulovic D, Rhein V, Savaskan E, Czech C, Eckert A, MĂŒller WE (2012) Peripheral mitochondrial dysfunction in Alzheimer's disease: focus on lymphocytes. Mol Neurobiol 46:194-204.HumanBlood cells
Lymphocyte
Brown 2012 Am J Physiol Regul Integr Comp Physiol2012Brown JC, Chung DJ, Belgrave KR, Staples JF (2012) Mitochondrial metabolic suppression and reactive oxygen species production in liver and skeletal muscle of hibernating thirteen-lined ground squirrels. Am J Physiol Regul Integr Comp Physiol 302:R15-28.Other mammalsSkeletal muscle
Liver
Selivanov 2011 PLoS Comput Biol2011Selivanov VA, Votyakova TV, Pivtoraiko VN, Zeak J, Sukhomlin T, Trucco M, Roca J, Cascante M (2011) Reactive oxygen species production by forward and reverse electron fluxes in the mitochondrial respiratory chain. PLoS Comput Biol 7(3):e1001115. doi: 10.1371/journal.pcbi.1001115.RatNervous system
Chinopoulos 2011 Methods Mol Biol2011Chinopoulos C, Zhang SF, Thomas B, Ten V, Starkov AA (2011) Isolation and functional assessment of mitochondria from small amounts of mouse brain tissue. Methods Mol Biol 793:311-24.RatNervous system
Brown 2011 Am J Physiol Regul Integr Comp Physiol2011Brown JC, Chung DJ, Belgrave KR, Staples JF (2011) Mitochondrial metabolic suppression and reactive oxygen species production in liver and skeletal muscle of hibernating thirteen-lined ground squirrels. Am J Physiol Regul Integr Comp Physiol 302:15-28.Other mammalsSkeletal muscle
Liver
Sommer 2010 Eur Respir J2010Sommer N, Pak O, Schörner S, Derfuss T, Krug A, Gnaiger E, Ghofrani HA, Schermuly RT, Huckstorf C, Seeger W, Grimminger F, Weissmann N (2010) Mitochondrial cytochrome redox states and respiration in acute pulmonary oxygen sensing. https://doi.org/10.1183/09031936.00013809HumanLung;gill
Endothelial;epithelial;mesothelial cell
Dikov 2010 Exp Gerontol2010Dikov D, Aulbach A, Muster B, Dröse S, Jendrach M, Bereiter-Hahn J (2010) Do UCP2 and mild uncoupling improve longevity? Exp Gerontol 45:586-95.HeLa
Fibroblast
HUVEC
Stankova 2010 Toxicol In Vitro2010Staƈková P, Kučera O, Lotková H, Rouơar T, Endlicher R, Cervinková Z (2010) The toxic effect of thioacetamide on rat liver in vitro. Toxicol In Vitro 24:2097-2103.Liver
Xie 2010 Acta Biochim Pol2010Xie X, Chowdhury SR, Sangle G, Shen GX (2010) Impact of diabetes-associated lipoproteins on oxygen consumption and mitochondrial enzymes in porcine aortic endothelial cells. Acta Biochim Pol 57:393-8.PigEndothelial;epithelial;mesothelial cell
Ziabreva 2010 Glia2010Ziabreva I, Campbell G, Rist J, Zambonin J, Rorbach J, Wydro MM, Lassmann H, Franklin RJ, Mahad D (2010) Injury and differentiation following inhibition of mitochondrial respiratory chain Complex IV in rat oligodendrocytes. Glia 58:1827-37.RatNervous system
Wrzosek 2009 Eur J Pharmacol2009Wrzosek A, Lukasiak A, Gwozdz P, Malinska D, Kozlovski VI, Szewczyk A, Chlopicki S, Dolowy K (2009) Large-conductance K+ channel opener CGS7184 as a regulator of endothelial cell function. Eur J Pharmacol 602:105-11.Pig
Rat		Heart
Endothelial;epithelial;mesothelial cell
Menna-Barreto 2009 Free Radic Biol Med2009Menna-Barreto RF, Goncalves RL, Costa EM, Silva RS, Pinto AV, Oliveira MF, de Castro SL (2009) The effects on Trypanosoma cruzi of novel synthetic naphthoquinones are mediated by mitochondrial dysfunction. Free Radic Biol Med 47:644-53.Protists
Soller 2007 Mol Pharmacol2007Soller M, Dröse S, Brandt U, BrĂŒne B, von Knethen A (2007) Mechanism of Thiazolidinedione-dependent cell death in Jurkat T cells. Mol Pharmacol 71:1535-44.Heart
Other cell lines
Labajova 2006 Anal Biochem2006Labajova A, Vojtiskova A, Krivakova P, Kofranek J, Drahota Z, Houstek J (2006) Evaluation of mitochondrial membrane potential using a computerized device with a tetraphenylphosphonium-selective electrode. Anal Biochem 353:37-42.RatLiver
Huetter 2004 Biochem J2004HĂŒtter E, Renner K, Pfister G, Stöckl P, Jansen-DĂŒrr P, Gnaiger E (2004) Senescence-associated changes in respiration and oxidative phosphorylation in primary human fibroblasts. https://doi.org/10.1042/BJ20040095HumanFibroblast
Schoenfeld 2004 Biochem J2004Schönfeld P, Kahlert S, Reiser G (2004) In brain mitochondria the branched-chain fatty acid phytanic acid impairs energy transduction and sensitizes for permeability transition. Biochem J 383:121–28.Nervous system
Pecina 2003 Biochim Biophys Acta2003Pecina P, Capkova M, Chowdhury SK, Drahota Z, Dubot A, Vojtiskova A, Hansikova H, Houstekova H, Zeman J, Godinot C, Houstek J (2003) Functional alteration of cytochrome c oxidase by SURF1 mutations in Leigh syndrome. Biochim Biophys Acta 1639:53-63.HumanEndothelial;epithelial;mesothelial cell
Fibroblast
Gregori 2002 Methods Cell Sci2002Grégori G, Denis M, LefÚvre D, Beker B (2002) A flow cytometric approach to assess phytoplankton respiration. Methods Cell Sci 24: 99-106.Plants
Eubacteria

Keywords: Force and membrane potential


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Fundamental relationships
» Force
» Affinity
» Flux
» Advancement
» Advancement per volume
» Stoichiometric number
mt-Membrane potential and protonmotive force
» Protonmotive force
» Mitochondrial membrane potential
» Chemical potential
» Faraday constant
» Format
» Uncoupler
O2k-Potentiometry
» O2k-Catalogue: O2k-TPP+ ISE-Module
» O2k-Manual: MiPNet15.03 O2k-MultiSensor-ISE
» TPP - O2k-Procedures: Tetraphenylphosphonium
» Specifications: MiPNet15.08 TPP electrode
» Poster
» Unspecific binding of TPP+
» TPP+ inhibitory effect
O2k-Fluorometry
» O2k-Catalogue: O2k-FluoRespirometer
» O2k-Manual: MiPNet22.11 O2k-FluoRespirometer manual
» Safranin - O2k-Procedures: MiPNet20.13 Safranin mt-membranepotential / Safranin
» TMRM - O2k-Procedures: TMRM
O2k-Publications
» O2k-Publications: mt-Membrane potential
» O2k-Publications: Coupling efficiency;uncoupling


MitoPedia concepts: Respiratory state, Recommended, Ergodynamics 


MitoPedia methods: Respirometry, Fluorometry 


MitoPedia topics: EAGLE 


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