Amplex UltraRed

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high-resolution terminology - matching measurements at high-resolution


Amplex UltraRed

Description

Amplex® UltraRed (AmR) is used as an extrinsic fluorophore for measurement of hydrogen peroxide production (ROS) by cells or mitochondrial preparations. The reaction of H2O2 and AmR is catalyzed by horseradish peroxidase to produce the red fluorescent compound resorufin (excitation wavelength 563 nm, emission 587 nm; the fluorescent product according to the supplier is called UltroxRed in the case of Amplex® UltraRed which has a similar structure to resorufin). The change of emitted fluorescence intensity is directly proportional to the concentration of H2O2 added, whereby the H2O2 is consumed.

Abbreviation: AmR

Reference: Komlódi T, Sobotka O, Gnaiger E (2021) Facts and artefacts on the oxygen dependence of hydrogen peroxide production using Amplex UltraRed. https://doi.org/10.26124/bec:2021-0004


Amplex Red or Amplex UltraRed in research articles

Citation Amplex HRP pH Limit of detection
stock final unit definition stock final
mM
µM
U/ml
U/ml
BIOTEK
10
50
pyrogallol
10
0.1
7.4
4 nM (absorption 300 nm)
Life Technologies
10
50
10
0.1
6 to 7.5
<80 nM
Towne 2004
160
0.41
7.5 to 8.5
100 nM
Zhou1997
3 ?
0.3 to 1
50 nM (10 nM optimal)
Mohanty 1997
100
10 to 100
1
18 nM
Komary 2010
1
2.5


Amplex® UltraRed in O2k-FluoRespirometry

O2k-Fluo Smart-Module and O2k-Fluo LED2-Module

In high-resolution respirometry HRR the Amplex® UltraRed method (Mohanty et al 1997) is used with the O2k-FluoRespirometer selecting the Fluorescence-Sensor Green (O2k-Series D-G: O2k-Fluo LED2-Module) and Smart Fluo-Sensor for O2k-Series H - I. Use black stoppers with black cover-slips to exclude disturbances by external light sources. The fluorescence sensors are inserted though the windows of the O2k-Chambers (Hickey et al 2012). The O2k has also been coupled to a fluorescence spectrophotometer with a light guide inserted through the black PEEK stopper (Anderson 2011).
The use of AmR in HRR to simultaneously determine respiration and H2O2 flux has been intensively tested in the Oroboros lab (see references).

Application in HRR

Amplex® UltraRed

AmR: Amplex® UltraRed from Life Technologies (former Invitrogen): A36006; 5* 1 mg commercial vials, store at -20°C.
Preparation of 10 mM stock solution (dissolved in DMSO) - see also Manual Amplex® UltraRed by Life Technologies.
Storage solution = stock solution
Prepare a 10 mM storage solution of Amplex® UltraRed reagent (AmR), which will also serve as a stock solution, by adding 340 μL of fresh, high‑quality DMSO (Sigma D8418) to one commercial vial of Amplex® UltraRed reagent (1 mg). Vortex well to dissolve. Protect AmR from light and moisture. The storage solution should then be divided into 20 µL aliquots and stored in the dark in a desiccator, protected from moisture at –20°C for future use. When stored properly, the 10 mM storage solution is stable for 6 months. We have observed that after long-term storage AmR may exert a profound inhibitory effect on cell respiration.
Note: The preparation of the 10 mM storage solution follows the procedure suggested by the manufacturer. The manufacturer states only an approximate molecular weight for the Amplex® UltraRed formulation and does not publish details how the Amplex® UltraRed formulation deviates from the substance 10-acetyl-3,7-dihydroxyphenoxazine (CAS# 119171-73-2), known as Amplex® Red.
» O2k manual titrations MiPNet09.12 O2k-Titrations
Titration into 2 mL O2k-chamber: 2 µL of 10 mM AmR stock solution, final concentration of 10 µM AmR.
AmR, similar to other chemical probes, may exert an inhibitory effect on mitochondrial and cell respiration. AmR, therefore, should be used at the lowest concentration compatible with the total H2O2 production in an experimental run, including calibrations and chemical background conversion of AmR (Makrecka-Kuka et al 2015; Komlodi et al 2018).
You may add 1 µL of the 10 mM stock solution for brief measurements to obtain a final concentration of 5 µM. Optimize the final AmR concentration according to respiration media, sample type and concentration, and experimental protocol. These determine the total AmR consumption by H2O2 production during the experiment (check by initial and final H2O2 titrations for calibration). The final concentration of AmR becomes diminished during an experiment due to AmR consumption and dilution by titrations in a SUIT protocol. Check for any potential effects of the experimental AmR concentration on respiratory activity of cells or mt-preparations, by titration of AmR after a specific respiratory state has been reached in a control experiment.

Color of AmR and the medium

Amplex UltraRed freshly dissolved should not present any color. The appearance of pink coloring may indicate that the chemical has been compromised.
During the experimental run, the product UltroxRed (or resorufin), generated from the Amplex UltraRed (or Amplex Red) plus H2O2 in the reaction catalyzed by horseradish peroxidase, accumulates in the chamber. As this chemical has a pink color, it is normal for the medium to have a pink color at the end of the experiment.

Horseradish peroxidase

Titration into into 2 mL O2k-chamber: 4 µL of HRP stock solution, final concentration 1 U/mL.
Horse radish peroxidase (Sigma-Aldrich P 8250 - 5 KU): Prepare a stock solution with 500 U HRP/mL in MiR05 or MiR05Cr; the solution can be used as storage solution at -20 °C.

Superoxide dismutase

Superoxide dismutase (SOD) is included to generate H2O2 from superoxide.
(Sigma-Aldrich S8160-15KU): We recommend to use the enzyme at 5 U/mL, the final volume to be added to the respiratory chamber has thus to be adjusted accordingly.
Experiments can be performed in the absence of SOD.

DTPA

» See: DTPA

Calibration with H2O2

Calibration standards of H2O2: Commercial solution (Sigma-Aldrich 323381 - 25 mL hydrogen peroxide solution 3 wt.%; stabilized with acetanilide, c. 200 ppm) = 880 mM H2O2.
  1. Prepare a HCl stock solution of 10 µM HCl.
  2. H2O2 dilution 1 (1:88): add 10 µL of a commercial stock solution of 3 wt. H2O2 to 870 µL 10 µM HCl solution, to obtain a 10 mM H2O2 solution.
  3. H2O2 dilution 2 (1:250):add 4 µL of 10 mM H2O2 solution to 996 µL 10 µM HCl solution, to obtain the H2O2 stock solution of 40 µM.
The H2O2 calibration solution has to be prepared fresh every day, kept away from light exposure, and freezing should be avoided.
  • Titration into 2 mL O2k-chamber: 5 µL of the 40 µM H2O2 stock, step increase of 0.1 µM H2O2.
  • Background H2O2 calibration:
  • A set of H2O2 titrations conducted after the addition of respiration medium, (DTPA), HRP and Amplex® UltraRed to the O2k-chamber but before sample addition.
  • This step is required (1) for the calculation of chemical background fluorescence; see: MiPNet24.10 H2O2 flux analysis and How to analyze H2O2 flux in DatLab, and (2) for calculation of the sensitivity of the Amplex® UltraRed assay towards H2O2, which, therefore, serves as a quality control step. The sensitivity depends on the respiration medium and on the components of the Amplex® UltraRed assay, and in the same respiration medium, the sensitivity of the AmR assay should be in the same range. For more information: Komlodi 2018 Methods Mol Biol.
  • Background H2O2 calibration has to be performed for each individual instrumental setting (O2k, fluorescence sensor and chamber), if a new stock solution of DTPA, HRP, SOD, Amplex® UltraRed, or H2O2, is prepared, or a different respiration medium is used. As the H2O2 stock solution needs to be freshly prepared, it is recommended to perform a background H2O2 calibration before each experiment and at a minimum once per experimental day.
  • The protocol for background H2O2 calibration is provided with DatLab7.4. For further information, see: Instrumental: Browse DL-Protocols and templates
  • Afterwards we suggest to perform calibrations at the beginning (sample already present), intermittently at various respiratory states, and near the end of an experiment. These calibrations steps are recommended because over the experimental time the sensitivity decreases and chemicals can influence the sensitivity of the AmR assay towards H2O2. After the addition of the biological sample, the sensitivity usually decreases owing to the (high) antioxidant capacity of the sample. For further information, see: Komlodi 2018 Methods Mol Biol


  • Why it is necessary to perform multiple H2O2 calibrations in the Amplex® UltraRed (AmR) assay?
The sensitivity to H2O2 of the Amplex® UltraRed assay changes during the experiment, thus requires multiple calibrations. These sensitivity changes may be the function of (1) experimental time and accumulating UltroxRed (similar to resorufin), (2) changes of the optical properties due to titrations, (3) the radical scavenging capacity of the sample. Therefore, H2O2 calibrations are performed before and after sample addition, and after selected titration steps. - »Komlodi 2018 Methods Mol Biol«
The DLPs for AmR SUIT protocols already come with multiple steps of H2O2 calibrations implemented.- » SUITbrowser«
  • DatLab supports automatic H2O2 calibration by calculating the calibration parameters by linear regression and graphical display of the calibration regression.
Problem: Here is a DatLab file where I ran the H2O2 calibration protocol with 6 H2O2 titrations. I drew up 5 uL of H2O2 into the syringe for titration into each chamber individually for the first two titrations. For the remaining titrations, I drew up 10 uL of H2O2 into the syringe and added 5 uL to one chamber and the rest into the second chamber. For titrations 3 and 4 I added to chamber B first, followed by chamber A. For titrations 5 and 6 I added to chamber A first, followed by chamber B. If sensitivities are measured for each set of titrations based on the manner in which H2O2 was added to the chambers, it can be seen that the chamber which is titrated second when 10 µL of H2O2 is drawn into the syringe at one time has reduced sensitivity measurements. When fresh H2O2 is drawn up for each chamber individually, the sensitivities between chambers are much more comparable. (The numbers shown in the figures are sensitivities expressed as V/µM.)
Jennifer Norman 1.png Jennifer Norman 2.png
Answer: It is recommended to fill the syringe with H2O2 each time with 5 µL for each O2k-Chamber instead of filling up the syringe with 10 µL and titrate one chamber after the other. Based on tests of Jennifer Norman (US_CA Davis_Roshanravan B) it seems that either the syringe for H2O2 titration is not precise filling it up with the maximal volume or H2O2 might be degraded by light already in the syringe.


Experimental media for the AmR assay

Media with high antioxidant activity compete with HRP and partially consume H2O2 before it can react with AmR to form the active fluorophore UltroxRed (similar to resorufin). This was shown by comparing the resorufin-sensitivity and H2O2-sensitivity (Krumschnabel et al 2015; Komlodi et al 2018).
  • H2O2-sensitivity: the change of fluorescence signal per µM H2O2 added in calibrations with H2O2 titration in media containing HRP and AmR.
  • Resorufin-sensitivity: the change of fluorescence signal per µM resorufin added in calibrations with resorufin titration in media containing HRP and AmR.
The H2O2-sensitivity is much higher in a simple phosphate buffer compared to media with strong antioxidant capacity. In contrast, this is not the case for the resorufin-sensitivity.

H2O2 sensitivity in MiR05

We recommend running experiments in MiR05 with a sensitivity >0.5 and <3 at gain 1000 and fluorescence intensity lower than 500 . If the sensitivity is out of this range, please change the light intensity of the Fluo-sensors (in DatLab 7.4: [Oroboros O2k] \ [O2k control], click on the tab [Amperometric, Amp] and change light intensity (Amp polarization voltage [mV]). Do the calibration again by titrating H2O2 to check the sensitivity.
The sensitivity values may vary depending on the batch of medium and chemicals used.
The sensitivity value is used to calibrate the amperometric raw signal [V] to H2O2 equivalent concentration [µM]. If experiments present different sensitivities, the resulting H2O2 fluxes after calibration can still be comparable, as long as the sensitivity values are in the recommended range and the same settings are used for all experiments.

Calculation of background fluorescence slope of MiR05

In the absence of sample, there is a spontaneous increase of the Ultroxred fluorescence signal over time, the extent of which depends on components of the respiration medium (Krumschnabel et al 2015). The sensitivity – the change in fluorescence per unit of H2O2 produced in or added to the chamber – depends on the medium and tends to decline over time. Both the background change in fluorescence and the change in assay sensitivity over time need to be corrected for in data analysis, for which DatLab-Analysis templates are available.
  • The Excel template is ideal for analysis of O2 and H2O2 fluxes measured in MiR05-Kit supplemented with DTPA. The background fluorescence slope of the AmR assay is dependent on the Lot number of the MiR05-Kit, therefore, in each SUIT-###_AmR folder, in the Excel templates for MiR05-Kit (supplemented with DTPA) you can find different analysis templates for each Lot number. The Excel sheets differ from each other in the correction for the background fluorescence slope. You need to use the Excel template which corresponds with the Lot# of MiR05-Kit you use. If you do not add DTPA or use homemade MiR05 instead of the MiR05-Kit, we recommend calculating the background fluorescence slope. The calculation of the background fluorescence slope is also advisable when a new batch of Amplex UltraRed is used or a newly prepared MiR05 is applied. Please follow the steps to measure and calculate background fluorescence slope:
a. Go to [Layout] menu and click into ‘O2&Amp´ and select `Standard Layouts/01 Amp Amperometric_Raw signal´.
b. Go to `Marks´ and select ‘Slope uncorrected + all info´. In the new window select `AmR slope [mV/s]´ in `Plot for Marks´.
c. Channel: `Amperometric,Amp´. Leave only this channel selected.
d. Select: `Median´.
e. Sort by: `Time´(default).
f. Then, click on [Copy to clipboard] to copy the selected values.
  • In the Amp background fluorescence slope.xlsx Excel template (see below): Click on the yellow cell A1 and paste [Ctrl+V] Amp slope from DatLab. If more than one experiment is performed, copy the Amp slope on A32, A63, A94, A126 or A158.
  • In the "Data" sheet, write the number of the FluoSensors in cells B12. If more than one sensor was tested, write the sensor number in cells B43, B74, B105, B137 or B169. The numbers can be found in the O2k control window (select in ´Oroboros O2k´ menu or press F7), ´Amperometric, Amp´ tab.
  • Equation required for the correction for the background fluorescence slope using the applied FluoSensor can be found in the figure. The values can be also found in the cells H18 and I18, H48 and I48, H79 and I79, H110 and I110, H142 and I42 or H174 and I174.
  • It is advisable to measure thebackground fluorescence slope with the same FluoSensors in the same O2k-chambers several times and then calculate the plot of the equation from more experiments. In the Excel template in the ´Summary and equation´ tab, you can copy a° and b° into the table to calculate the equation of plot.
  • In the SUIT-###_AmR analysis templates, modify the values in the equation for the background fluorescence slope (cells N66, W66, and X66).


HRP-independent background AmR flux

A study by Miwa et al 2016 (Free Radical Bio Med 90:173) suggests that the HRP-independent artificial background is related to a mitochondrially expressed carboxylesterase which converts Amplex® Red to resorufin at a high rate. The issue can be relatively easily solved by adding a protease inhibitor to various mitochondrial preparations as described here.
For further information see the Discussion page.

AmR assay dilution

How to minimize dilution of the AmR assay upon sample addition
To minimize the dilution of the AmR assay either:
1.) Decrease the titration volume of the sample by using a more concentrated sample solution
2.) Titrate additionally the components of the AmR assay together with the sample
3.) After AmR background calibration, empty and wash the chamber, then add buffer and sample and start titrating the components of the AmR assay into the closed O2k-chamber.
In either case 2 or 3, use media and chemicals from the same batch.
Of note, performing H2O2 calibration directly after sample addition allows for calculating the sensitivity to correct the fluorescence signal for sample dilution.

Artefacts

Liver homogenate

Liver homogenate cannot be used with the Amplex® UltraRed assay. - See:Tissue homogenate

Injection artefact

Injection of chemicals (e.g. substrates, uncouplers, inhibitors, H2O2) can cause artefacts as observed in the figure:
Injection artefact AmR.png
The marks should always be set on the stable signal avoiding the artefacts area.
Injection artefact AmR marks.png

NADH and reduced glutathione

Votyakova TV, Reynolds IJ (2014 Arch Biochem Biophys 431:138-44) showed that NADH and reduced glutathione are able to react with AmR in the presence of O2 and HRP and create a background in the absence of mitochondria. If the mitochondria remain intact, this above-mentioned reaction is negligible. If you add SOD (superoxide dismutase), you can avoid this side-effect of the AmR assay.

Substances incompatible with the Amplex® UltraRed assay

The following substances/ classes of substances are strictly incompatible with the Amplex® Red method for theoretical reasons:
  • Strongly redox-active substances, e.g. cytochrome c, TMPD/Ascorbate
  • Catalase and other substances consuming or scavenging H2O2. The effect of substances in the medium that slowly consume H2O2 is taken into account by the calibration procedure. However, such substances decrease the sensitivity of the method. Note that catalase can be a valuable tool for checking artefacts. See:Avoiding artefacts.
The effect of other substances should be checked by experiments without biological sample, including comparing the sensitivity (result of calibration) before and after injecting the substances.
In preliminary experiments Oroboros Instruments evaluated small amounts (as typically used in SUIT protocols) of the following substances as compatible with the method:
DMSO, ethanol, malate, glutamate, pyruvate (a strong scavanger of H2O2), succinate, (ADP + Mg2+), (ATP + Mg2+), rotenone, FCCP, CCCP, oligomycin, antimycin A, malonate, myxothiazol

Avoiding artefacts

The Amplex® method is based on the H2O2 dependent oxidation of AmR to UltroxRed by HRP. Under unfavorable conditions AmR may be oxidized even in the absence of H2O2. At a small rate such an oxidation occurs in the presence of HRP even without any sample present. The magnitude of this background signal ("drift") depends, among other things, on the light intensity used and can therefore be minimized by using the suggested or lower light intensity. Components of the sample may however induce a far higher, non H2O2 related rate of AmR oxidation. Therefore, especially when applying the method on new types of samples the method should be checked for artifacts. A few approaches are listed here:
Sequential addition of HRP and AmR: This method is particular easy to implement if AmR and HRP have to be added to the chamber already containing the sample anyway: First, inject Amplex® Red and wait a few minutes for flux stabilization. The Amp slope has to stay near zero. Then add HRP. The Amp slope should increase and correspond to the H2O2 production. If a significant Amp slope is detected before the addition of HRP this increase in fluorescence is not caused by H2O2 production. The experiment can be continued as usual after this test. If the sample is injected routinely into the chamber already containing AmR and HRP the method can not be applied. In this case, it is suggested to change this sequence at least for one experiment.
Addition of catalase: After a H2O2 flux (production) is established, a high dose (e.g. 10 µL of a 280,000 U/mL stock solution) of catalase is injected. Catalase competes with HRP for the available H2O2. Then the apparent H2O2 flux (the Amp slope) should be reduced to near zero as a control for distinguishing an unspecific chemical background slope from H2O2 dependent Amplex® UltraRed oxidation.
Note: The experiment cannot be continued afterwards for measurement of hydrogen peroxide production, whereas respiration can be recorded onwards.

Oxygen range

The H2O2 production of mitochondria is oxygen dependent Komlodi 2021 BEC AmR-O2. The oxygen concentration can be controlled in the O2k-chamber while running the AmR assay. We recommend running the assay at low O2 concentration, e.g., between 60 and 30 µM O2. If this is not possible, it is advisable to run all assays in the same [O2] range, and take marks for different conditions under a similar [O2] to minimize variability.

Nitrogen or hydrogen injection

  • To decrease the oxygen concentration in the O2k-chamber using nitrogen or hydrogen see Setting the oxygen concentration.
  • Check Oxia for fast and safe production of hydrogen (and oxygen).

Permeabilized fibers

Why are permeabilized muscle fibers (pfi) a poor sample type for studying reactive oxygen species (ROS) production?
In experiments with pfi, high oxygen concentrations are needed to avoid oxygen limitation. However, the high oxygen pressures used may artificially increase ROS, including H2O2 production, making pfi a less optimal model for ROS production studies. See: Oxygen dependence of pfi

Experimental SOP

H2O2 flux analysis and mark setting

Excel analysis templates

  • Excel templates are provided for analysis of the H2O2 measurements. It can be found in the upper menu in DatLab in Protocols/SUIT: Browse DL-Protocols and templates and then select your protocol (e.g. SUIT-009/SUIT-009_AmR/SUIT-009_AmR_ce-pce_D019).
  • The calculations used in the excel analysis template are provided complying with Oroboros transparency policy: [1]
  • The excel analysis templates are updated for the respective SUIT protocol. The latest versions are available here (last update 2021-09-20):

SUIT protocols

Technical support

Set marks to calibrate the fluorescence signal using Amplex® UltraRed assay

To calibrate the fluorescence signal in molar units [µM], set the marks on the black plot.
» MiPNet20.14 AmplexRed H2O2-production
» Amp calibration - DatLab

Set marks to analyse H2O2 flux

» MiPNet20.14 AmplexRed H2O2-production
» Smoothing
» H2O2 flux analysis video

Data analysis with the Excel template

» MiPNet24.10 H2O2 flux analysis
» H2O2 analysis
» H2O2 flux analysis video

Defective fluorescence module

Exchange of filters in the fluorescence sensors

» Exchanging filter set of the Smart Fluo-Sensors

How to connect the Smart Fluo-Sensors to the O2k?

» Smart Fluo-Sensor assembly

References

O2k-Demo experiments

O2k-Publications: H2O2

O2k-Publications in the MiPMap
Click to expand or collaps
List of publications: Amplex UltraRed - >>>>>>> - Click on [Expand] or [Collapse] - >>>>>>>
 YearReferenceOrganismTissue;cellStressDiseases
Li 2024 Sci Rep2024Li J, Zhang S, Li C, Zhang X, Shan Y, Zhang Z, Bo H, Zhang Y (2024) Endurance exercise-induced histone methylation modification involved in skeletal muscle fiber type transition and mitochondrial biogenesis. Sci Rep 14:21154. https://doi.org/10.1038/s41598-024-72088-6RatSkeletal muscle
Coulson 2024 J Exp Biol2024Coulson SZ, Guglielmo CG, Staples JF (2024) Migration increases mitochondrial oxidative capacity without increasing reactive oxygen species emission in a songbird. J Exp Biol 227:jeb246849. https://doi.org/10.1242/jeb.246849BirdsSkeletal muscle
Al-Sabri 2024 Sci Rep2024Al-Sabri MH, Ammar N, Korzh S, Alsehli AM, Hosseini K, Fredriksson R, Mwinyi J, Williams MJ, Boukhatmi H, Schiöth HB (2024) Fluvastatin-induced myofibrillar damage is associated with elevated ROS, and impaired fatty acid oxidation, and is preceded by mitochondrial morphological changes. https://doi.org/10.1038/s41598-024-53446-wDrosophilaSkeletal muscle
Cefis 2024 Acta Physiol (Oxf)2024Cefis M, Dargegen M, Marcangeli V, Taherkhani S, Dulac M, Leduc-Gaudet JP, Mayaki D, Hussain SNA, Gouspillou G (2024) MFN2 overexpression in skeletal muscles of young and old mice causes a mild hypertrophy without altering mitochondrial respiration and H2O2 emission. Acta Physiol (Oxf) [Epub ahead of print]. https://doi.org/10.1111/apha.14119MouseSkeletal muscleAging;senescence
Sorby-Adams 2024 Redox Biol2024Sorby-Adams A, Prime TA, Miljkovic JL, Prag HA, Krieg T, Murphy MP (2024) A model of mitochondrial superoxide production during ischaemia-reperfusion injury for therapeutic development and mechanistic understanding. Redox Biol 72:103161. https://doi.org/10.1016/j.redox.2024.103161RatHeartIschemia-reperfusion
Oxidative stress;RONS
Noerregaard 2024 J Physiol2024Noerregaard LB, Hansen CC, Wickham KA, Moeller S, Olsen K, Ehlers T, Bangsbo J, Hellsten Y (2024) Exercise training alters skeletal muscle microvascular endothelial cell properties in recent postmenopausal females. J Physiol [Epub ahead of print]. https://doi.org/10.1113/jp286269HumanSkeletal muscle
Endothelial;epithelial;mesothelial cell
Dulac 2024 J Physiol2024Dulac M, Hajj-Boutros G, Sonjak V, Faust A, Hussain SNA, Chevalier S, Dionne IJ, Morais JA, Gouspillou G (2024) A multimodal exercise countermeasure prevents the negative impact of head-down tilt bed rest on muscle volume and mitochondrial health in older adults. J Physiol [Epub ahead of print]. https://doi.org/10.1113/jp285897HumanSkeletal muscleAging;senescence
Holwerda 2024 J Cachexia Sarcopenia Muscle2024Holwerda AM, Dirks ML, Barbeau PA, Goessens J, Gijsen A, van Loon LJC, Holloway GP (2024) Mitochondrial bioenergetics are not associated with myofibrillar protein synthesis rates. J Cachexia Sarcopenia Muscle [Epub ahead of print]. https://doi.org/10.1002/jcsm.13532Human
Mouse
Skeletal muscle
Dominguez-Lopez 2023 Neuropharmacology2023Dominguez-Lopez S, Ahn B, Sataranatarajan K, Ranjit R, Premkumar P, Van Remmen H, Beckstead MJ (2023) Long-term methamphetamine self-administration increases mesolimbic mitochondrial oxygen consumption and decreases striatal glutathione. https://doi.org/10.1016/j.neuropharm.2023.109436MouseNervous system
Batterson 2023 Physiol Rep2023Batterson PM, McGowan EM, Borowik AK, Kinter MT, Miller BF, Newsom SA, Robinson MM (2023) High-fat diet increases electron transfer flavoprotein synthesis and lipid respiration in skeletal muscle during exercise training in female mice. https://doi.org/10.14814/phy2.15840MouseSkeletal muscle
Gautam 2023 Neurobiol Dis2023Gautam M, Genç B, Helmold B, Ahrens A, Kuka J, Makrecka-Kuka M, Günay A, Koçak N, Aguilar-Wickings IR, Keefe D, Zheng G, Swaminathan S, Redmon M, Zariwala HA, Özdinler PH (2023) SBT-272 improves TDP-43 pathology in ALS upper motor neurons by modulating mitochondrial integrity, motility, and function. https://doi.org/10.1016/j.nbd.2023.106022RatHeart
Nervous system
Neurodegenerative
Leduc-Gaudet 2023 Nat Commun2023Leduc-Gaudet JP, Franco-Romero A, Cefis M, Moamer A, Broering FE, Milan G, Sartori R, Chaffer TJ, Dulac M, Marcangeli V, Mayaki D, Huck L, Shams A, Morais JA, Duchesne E, Lochmuller H, Sandri M, Hussain SNA, Gouspillou G (2023) MYTHO is a novel regulator of skeletal muscle autophagy and integrity. https://doi.org/10.1038/s41467-023-36817-1MouseSkeletal muscle
Salmon 2023 Geroscience2023Salmón P, Millet C, Selman C, Monaghan P, Dawson NJ (2023) Tissue-specific reductions in mitochondrial efficiency and increased ROS release rates during ageing in zebra finches, Taeniopygia guttata. https://doi.org/10.1007/s11357-022-00624-1BirdsSkeletal muscle
Liver
Oxidative stress;RONSAging;senescence
Devaux 2023 J Comp Physiol B2023Devaux JBL, Hedges CP, Birch N, Herbert N, Renshaw GMC, Hickey AJR (2023) Electron transfer and ROS production in brain mitochondria of intertidal and subtidal triplefin fish (Tripterygiidae). https://doi.org/10.1007/s00360-023-01495-4FishesNervous systemOxidative stress;RONS
Czyzowska 2023 Redox Biol2023Czyżowska A, Brown J, Xu H, Sataranatarajan K, Kinter M, Tyrell VJ, O'Donnell VB, Van Remmen H (2023) Elevated phospholipid hydroperoxide glutathione peroxidase (GPX4) expression modulates oxylipin formation and inhibits age-related skeletal muscle atrophy and weakness. https://doi.org/10.1016/j.redox.2023.102761MouseSkeletal muscleAging;senescence
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.00565.2022MouseFatOxidative stress;RONSObesity
Fletcher 2023 Transl Res2023Fletcher E, Miserlis D, Sorokolet K, Wilburn D, Bradley C, Papoutsi E, Wilkinson T, Ring A, Ferrer L, Haynatzki G, Smith RS, Bohannon WT, Koutakis P (2023) Diet-induced obesity augments ischemic myopathy and functional decline in a murine model of peripheral artery disease. https://doi.org/10.1016/j.trsl.2023.05.002MouseSkeletal muscleMyopathy
Obesity
Steffen 2023 J Exp Biol2023Steffen JBM, Sokolov EP, Bock C, Sokolova IM (2023) Combined effects of salinity and intermittent hypoxia on mitochondrial capacity and reactive oxygen species efflux in the Pacific oyster, Crassostrea gigas. https://doi.org/10.1242/jeb.246164MolluscsLung;gillOxidative stress;RONS
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Laouafa 2019 Acta Physiol (Oxf)2019Laouafa S, Roussel D, Marcouiller F, Soliz J, Gozal D, Bairam A, Joseph V (2019) Roles of oestradiol receptor alpha and beta against hypertension and brain mitochondrial dysfunction under intermittent hypoxia in female rats. Acta Physiol (Oxf) 226:e13255.RatNervous systemHypoxia
Monteiro 2019 J Bioenerg Biomembr2019Monteiro J, Assis-de-Lemos G, de-Souza-Ferreira E, Marques AM, Neves GA, Silveira MS, Galina A (2019) Energization by multiple substrates and calcium challenge reveal dysfunctions in brain mitochondria in a model related to acute psychosis. J Bioenerg Biomembr 52:1-15.MouseNervous systemOxidative stress;RONSOther
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Lefranc 2019 Hypertension2019Lefranc C, Friederich-Persson M, Braud L, Palacios-Ramirez R, Karlsson S, Boujardine N, Motterlini R, Jaisser F, Nguyen Dinh Cat A (2019) MR (mineralocorticoid receptor) induces adipose tissue senescence and mitochondrial dysfunction leading to vascular dysfunction in obesity. Hypertension 73:458-68.MouseFatAging;senescence
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Holsgrove 2019 Thesis2019Holsgrove A (2019) The effect of temperature on cardiac energetics in the rainbow trout, Onchorhynchus mykiss. Phd Thesis 166.FishesHeart
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Halling 2019 Am J Physiol Endocrinol Metab2019Halling JF, Jessen H, Nøhr-Meldgaard J, Thiellesen Buch B, Masselkhi Christensen N, Gudiksen A, Ringholm S, Neufer PD, Prats C, Pilegaard H (2019) PGC-1α regulates mitochondrial properties beyond biogenesis with aging and exercise training. Am J Physiol Endocrinol Metab 317:E513-E525.MouseSkeletal muscleAging;senescence
Szibor 2019 Biochim Biophys Acta Bioenerg2019Szibor Marten, Gainutdinov Timur, Fernandez-Vizarra Erika, Dufour Eric, Gizatullina Zemfira, Debska-Vielhaber Grazyna, Heidler Juliana, Wittig Ilka, Viscomi Carlo, Gellerich Frank Norbert, Moore Anthony L (2019) Bioenergetic consequences from xenotopic expression of a tunicate AOX in mouse mitochondria: switch from RET and ROS to FET. Biochim Biophys Acta Bioenerg 1861:148137.MouseHeart
McBride 2019 Arch Biochem Biophys2019McBride S, Wei-LaPierre L, McMurray F, MacFarlane M, Qiu X, Patten DA, Dirksen RT, Harper ME (2019) Skeletal muscle mitoflashes, pH, and the role of uncoupling protein-3. Arch Biochem Biophys 663:239-48.MouseSkeletal muscleOxidative stress;RONS
Ahn 2019 J Cachexia Sarcopenia Muscle2019Ahn B, Ranjit R, Premkumar P, Pharaoh G, Piekarz KM, Matsuzaki S, Claflin DR, Riddle K, Judge J, Bhaskaran S, Satara Natarajan K, Barboza E, Wronowski B, Kinter M, Humphries KM, Griffin TM, Freeman WM, Richardson A, Brooks SV, Van Remmen H (2019) Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fiber branching. J Cachexia Sarcopenia Muscle 10:411-28.MouseSkeletal muscleOxidative stress;RONS
Shirakawa 2019 Sci Rep2019Shirakawa R, Yokota T, Nakajima T, Takada S, Yamane M, Furihata T, Maekawa S, Nambu H, Katayama T, Fukushima A, Saito A, Ishimori N, Dela F, Kinugawa S, Anzai T (2019) Mitochondrial reactive oxygen species generation in blood cells is associated with disease severity and exercise intolerance in heart failure patients. Sci Rep 9:14709.HumanBlood cellsOxidative stress;RONSCardiovascular
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Cannon 2019 J Appl Physiol (1985)2019Cannon DT, Rodewohl L, Adams V, Breen EC, Bowen TS (2019) Skeletal myofiber VEGF deficiency leads to mitochondrial, structural and contractile alterations in mouse diaphragm. J Appl Physiol (1985) 127:1360-69.MouseSkeletal muscle
Bundgaard 2019 Sci Rep2019Bundgaard A, James AM, Gruszczyk AV, Martin J, Murphy MP, Fago A (2019) Metabolic adaptations during extreme anoxia in the turtle heart and their implications for ischemia-reperfusion injury. Sci Rep 9:2850.Mouse
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Cooper 2019 Exp Physiol2019Cooper MA, McCoin C, Pei D, Thyfault JP, Koestler D, Wright DE (2019) Reduced mitochondrial reactive oxygen species production in peripheral nerves of mice fed a ketogenic diet. Exp Physiol 103:1206-12.MouseNervous system
Stepanova 2019 Antioxid Redox Signal2019Stepanova Anna, Sosunov S, Niatsetskaya Z, Konrad Csaba, Starkov AA, Manfredi G, Wittig I, Ten V, Galkin A (2019) Redox-dependent loss of flavin by mitochondrial complex I in brain ischemia/reperfusion injury. Antioxid Redox Signal 31:608-22.MouseNervous systemIschemia-reperfusion
Isei 2019 Free Radic Biol Med2019Isei MO, Kamunde C (2019) Effects of copper and temperature on heart mitochondrial hydrogen peroxide production. Free Radic Biol Med 147:114-28.FishesHeartOxidative stress;RONS
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McMurray 2019 FASEB J2019McMurray F, MacFarlane M, Kim K, Patten DA, Wei-LaPierre L, Fullerton MD, Harper ME (2019) Maternal diet-induced obesity alters muscle mitochondrial function in offspring without changing insulin sensitivity. FASEB J 33:13515-26.MouseSkeletal muscleOxidative stress;RONSDiabetes
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Burney 2018 Thesis2018Burney E (2018) Characterization of mitochondrial metabolism in L6 rat myoblasts. Bachelor's Thesis p50.RatOther cell lines
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Aparicio-Trejo 2018 Free Radic Biol Med2018Aparicio-Trejo OE, Reyes-Fermín LM, Briones-Herrera A, Tapia E, León-Contreras JC, Hernández-Pando R, Sánchez-Lozada LG, Pedraza-Chaverri J (2018) Protective effects of N-acetyl-cysteine in mitochondria bioenergetics, oxidative stress, dynamics and S-glutathionylation alterations in acute kidney damage induced by folic acid. Free Radic Biol Med 130:379-96.RatKidneyOxidative stress;RONSOther
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Dawson 2018 Acta Physiol (Oxf)2018Dawson NJ, Lyons SA, Henry DA, Scott GR (2018) Effects of chronic hypoxia on diaphragm function in deer mice native to high altitude. Acta Physiol (Oxf) 223:e13030.Other mammalsSkeletal muscleHypoxia
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Lopez-Manzano 2017 Chem Res Toxicol2017Lopez-Manzano E, Cronican AA, Frawley KL, Peterson J, Pearce LL (2017) Cyanide scavenging by a cobalt Schiff-base macrocycle: a cost-effective alternative to corrinoids. Chem Res Toxicol 29:1011-9.
Briston 2017 Sci Rep2017Briston T, Roberts M, Lewis S, Powney B, M Staddon J, Szabadkai G, Duchen MR (2017) Mitochondrial permeability transition pore: sensitivity to opening and mechanistic dependence on substrate availability. Sci Rep 7:10492.RatLiverPermeability transition
Trewin 2017 PLOS ONE2017Trewin AJ, Levinger I, Parker L, Shaw CS, Serpiello FR, Anderson MJ, McConell GK, Hare DL, Stepto NK (2017) Acute exercise alters skeletal muscle mitochondrial respiration and H2O2 emission in response to hyperinsulinemic-euglycemic clamp in middle-aged obese men. PLOS ONE 12:e0188421.HumanSkeletal muscleOxidative stress;RONSObesity
Jang 2017 Biol Open2017Jang DH, Seeger SC, Grady ME, Shofer FC, Eckmann DM (2017) Mitochondrial dynamics and respiration within cells with increased open pore cytoskeletal meshes. Biol Open 6:1831-9.HumanEndothelial;epithelial;mesothelial cell
Fibroblast
Oxidative stress;RONSCancer
Stepanova 2017 J Cereb Blood Flow Metab2017Stepanova A, Kahl A, Konrad C, Ten V, Starkov AS, Galkin A (2017) Reverse electron transfer results in a loss of flavin from mitochondrial complex I: Potential mechanism for brain ischemia-reperfusion injury. J Cereb Blood Flow Metab 37:3649-58.MouseNervous systemIschemia-reperfusion
Koning 2017 J Cereb Blood Flow Metab2017Koning G, Leverin AL, Nair S, Schwendimann L, Ek J, Carlsson Y, Gressens P, Thornton C, Wang X, Mallard C, Hagberg H (2017) Magnesium induces preconditioning of the neonatal brain via profound mitochondrial protection. J Cereb Blood Flow Metab 39:1038-55.RatIschemia-reperfusion
Hypoxia
Khalifa 2017 Physiol Rep2017Khalifa AR, Abdel-Rahman EA, Mahmoud AM, Ali MH, Noureldin M, Saber SH, Mohsen M, Ali SS (2017) Sex-specific differences in mitochondria biogenesis, morphology, respiratory function, and ROS homeostasis in young mouse heart and brain. Physiol Rep 5. pii: e13125.MouseHeart
Nervous system
Aging;senescence
Cardiovascular
Other
Cardoso 2017 Biochim Biophys Acta2017Cardoso GMF, Pletsch JT, Parmeggiani B, Grings M, Glanzel NM, Bobermin LD, Amaral AU, Wajner M, Leipnitz G (2017) Bioenergetics dysfunction, mitochondrial permeability transition pore opening and lipid peroxidation induced by hydrogen sulfide as relevant pathomechanisms underlying the neurological dysfunction characteristic of ethylmalonic encephalopathy. Biochim Biophys Acta 1863:2192-2201.RatNervous systemPermeability transitionOther
Lau 2017 Dissertation2017Lau G (2017) Adaptive variation of mitochondrial function in response to oxygen variability in intertidal sculpins (Cottidae, Actinopterygii). Dissertation p148.FishesNervous systemHypoxia
Sharaf 2017 Aquat Toxicol2017Sharaf MS, Stevens D, Kamunde C (2017) Zinc and calcium alter the relationship between mitochondrial respiration, ROS and membrane potential in rainbow trout (Oncorhynchus mykiss) liver mitochondria. Aquat Toxicol 189:170-83.FishesLiver
Goedecke 2017 JMIR Res Protoc2017Goedecke JH, Mendham AE, Clamp L, Nono Nankam PA, Fortuin-de Smidt MC, Phiri L, Micklesfield LK, Keswell D, Woudberg NJ, Lecour S, Alhamud A, Kaba M, Lutomia FM, van Jaarsveld PJ, de Villiers A, Kahn SE, Chorell E, Hauksson J, Olsson T (2017) An exercise intervention to unravel the mechanisms underlying insulin resistance in a cohort of black South African women: Protocol for a randomized controlled trial. JMIR Res Protoc 03/10/2017:9098.HumanSkeletal muscle
Fat
Diabetes
Obesity
Power 2016 Am J Physiol Heart Circ Physiol2016Power AS, Pham T, Loiselle DS, Crossman DH, Ward ML, Hickey AJ (2016) Impaired ADP channeling to mitochondria and elevated reactive oxygen species in hypertensive hearts. https://doi.org/10.1152/ajpheart.00050.2016RatHeartCardiovascular
Abdel-Rahman 2016 Oxid Med Cell Longev2016Abdel-Rahman EA, Mokhtar A, Aaliya A, Radwan Y, Yasseen B, Al-Okda A, Atwa A, Elhanafy E, Habashy M, Ali SS (2016) Resolving contributions of oxygen-consuming and ROS-generating enzymes at the synapse. Oxid Med Cell Longev p19.MouseNervous systemOxidative stress;RONS
Du 2016 J Exp Biol2016Du SN, Mahalingam S, Borowiec BG, Scott GR (2016) Mitochondrial physiology and reactive oxygen species production are altered by hypoxia acclimation in killifish (Fundulus heteroclitus). J Exp Biol 219:1130-8.FishesLiverOxidative stress;RONS
Gorbacheva 2016 International Symposium Mitochondrial Motility2016Gorbacheva OS, Strutynskyi RB, Khmil NV, Belosludtseva NV, Murzaeva SV, Korobeynikova MO, Alilova GA, Lezhnev EI, Mironova GD (2016) Study of the influence of flocalin on the energy and ion exchanges in rat liver mitochondria. International Symposium Mitochondrial Motility 73-7.RatLiverCardiovascular
Bouitbir 2016 Antioxid Redox Signal2016Bouitbir J, Singh F, Charles AL, Schlagowski AI, Bonifacio A, Echaniz-Laguna A, Geny B, Krähenbühl S, Zoll J (2016) Statins trigger mitochondrial ROS-induced apoptosis in glycolytic skeletal muscle. Antioxid Redox Signal 24:84-98.RatSkeletal muscle
Other cell lines
Oxidative stress;RONSCardiovascular
Myopathy
Mezera 2016 Oxid Med Cell Longev2016Mezera V, Endlicher R, Kucera O, Sobotka O, Drahota Z, Cervinkova Z (2016) Effects of epigallocatechin gallate on tert-butyl hydroperoxide-induced mitochondrial dysfunction in rat liver mitochondria and hepatocytes. Oxid Med Cell Longev 7573131:8pp.RatLiver
Timpani 2016 Neurotherapeutics2016Timpani CA, Trewin AJ, Stojanovska V, Robinson A, Goodman CA, Nurgali K, Betik AC, Stepto N, Hayes A, McConell GK, Rybalka E (2016) Attempting to compensate for reduced neuronal nitric oxide synthase protein with nitrate supplementation cannot overcome metabolic dysfunction but rather has detrimental effects in Dystrophin-deficient mdx muscle. Neurotherapeutics 14:429-46.MouseSkeletal muscleOther
Schiffer 2016 Am J Physiol Cell Physiol2016Schiffer TA, Peleli M, Sundqvist ML, Ekblom B, Lundberg JO, Weitzberg E, Larsen FJ (2016) Control of human energy expenditure by cytochrome c oxidase subunit IV-2. Am J Physiol Cell Physiol 311:C452-61.HumanSkeletal muscle
HEK
Oxidative stress;RONS
Hypoxia
Larsen 2016 FASEB J2016Larsen FJ, Schiffer TA, Ørtenblad N, Zinner C, Morales-Alamo D, Willis SJ, Calbet JA, Holmberg HC, Boushel R (2016) High-intensity sprint training inhibits mitochondrial respiration through aconitase inactivation. FASEB J 30:417-27.HumanSkeletal muscleOxidative stress;RONS
Karlsson 2016 Shock2016Karlsson M, Hara N, Morata S, Sjövall F, Kilbaugh T, Hansson MJ, Uchino H, Elmér E (2016) Diverse and tissue-specific mitochondrial respiratory response in a mouse model of sepsis-induced multiple organ failure. Shock 45:404-10.MouseNervous system
Liver
Oxidative stress;RONSSepsis
Liepinsh 2016 Biochem J2016Liepinsh E, Makrecka-Kuka M, Volska K, Kuka J, Makarova E, Antone U, Sevostjanovs E, Vilskersts R, Strods A, Tars K, Dambrova M (2016) Long-chain acylcarnitines determine ischaemia/reperfusion-induced damage in heart mitochondria. Biochem J 473:1191-202.RatHeartIschemia-reperfusion
Baeder 2016 Int J Dent2016Baeder AC, Napa K, Richardson ST, Taylor OJ, Andersen SG, Wilcox SH, Winden DR, Reynolds PR, Bikman BT (2016) Oral gingival cell cigarette smoke exposure induces muscle cell metabolic disruption. Int J Dent 2016:2763160.MouseSkeletal muscle
Alleman 2016 Am J Physiol Heart Circ Physiol2016Alleman RJ, Tsang AM, Ryan TE, Patteson DJ, McClung JM, Spangenburg EE, Shaikh SR, Neufer PD, Brown DA (2016) Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics. Am J Physiol Heart Circ Physiol 310:H1360-70.RatHeartIschemia-reperfusionCardiovascular
Kluckova 2015 Cell Death Dis2015Kluckova K, Sticha M, Cerny J, Mracek T, Dong L, Drahota Z, Gottlieb E, Neuzil J, Rohlena J (2015) Ubiquinone-binding site mutagenesis reveals the role of mitochondrial complex II in cell death initiation. Cell Death Dis 6:e1749.Other mammalsLung;gill
Other cell lines
Fibroblast
Cell death
Oxidative stress;RONS
Makrecka-Kuka 2015 Biomolecules2015Makrecka-Kuka M, Krumschnabel G, Gnaiger E (2015) High-resolution respirometry for simultaneous measurement of oxygen and hydrogen peroxide fluxes in permeabilized cells, tissue homogenate and isolated mitochondria. https://doi.org/10.3390/biom5031319Human
Mouse
Heart
Nervous system
HEK
Oxidative stress;RONS
Ferrera 2015 J Thorac Cardiovasc Surg2015Ferrera R, Benhabbouche S, Da Silva CC, Alam MR, Ovize M (2015) Delayed low pressure at reperfusion: A new approach for cardioprotection. J Thorac Cardiovasc Surg 150:1641-8.RatHeartIschemia-reperfusion
Permeability transition
Petrus 2015 Can J Physiol Pharmacol2015Petruş A, Duicu OM, Sturza A, Noveanu L, Kiss L, Dănilă M, Baczkó I, Muntean DM, Jost N (2015) Modulation of mitochondrial respiratory function and ROS production by novel benzopyran analogues. Can J Physiol Pharmacol 93:811-8.RatHeartIschemia-reperfusion
Krumschnabel 2015 Methods Mol Biol2015Krumschnabel G, Fontana-Ayoub M, Sumbalova Z, Heidler J, Gauper K, Fasching M, Gnaiger E (2015) Simultaneous high-resolution measurement of mitochondrial respiration and hydrogen peroxide production. Methods Mol Biol 1264:245-61. https://doi.org/10.1007/978-1-4939-2257-4_22MouseNervous systemOxidative stress;RONS
Beaudoin 2014 J Physiol2014Beaudoin MS, Perry CC, Arkell A, Chabowski A, Simpson JA, Wright DC, Holloway GP (2014) In the ZDF rat, impairments in mitochondrial palmitoyl-CoA respiratory kinetics that precede the development of diabetic cardiomyopathy are prevented by resveratrol supplementation. J Physiol 592:2519-33.RatHeartDiabetes
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.RatHeartIschemia-reperfusion
Oxidative stress;RONS
Mitochondrial disease
Diabetes
Myopathy
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.1004385MouseHeartOxidative stress;RONS
Hunter 2014 PhD Thesis2014Hunter FW (2014) Old target; new paradigm: Determinants of sensitivity to hypoxia-directed anticancer prodrugs. PhD Thesis:1-353.Other mammalsCHOCancer
Tretter 2014 Free Radic Biol Med2014Tretter L, Horvath G, Hölgyesi A, Essek F, Adam-Vizi V (2014) Enhanced hydrogen peroxide generation accompanies the beneficial bioenergetic effects of methylene blue in isolated brain mitochondria. Free Radic Biol Med 77:317-30.Guinea pigNervous system
Iftikar 2014 Thesis University of Auckland2014Iftikar FI (2014) Testing the role of heart mitochondrial stability and function in heart failure of ectotherms exposed to heat stress. Thesis University of Auckland:167pp.FishesHeartOxidative stress;RONS
Temperature
Soltysinska 2014 PLoS One2014Soltysinska E, Bentzen BH, Barthmes M, Hattel H, Thrush AB, Harper ME, Qvortrup K, Larsen FJ, Schiffer TA, Losa-Reyna J, Straubinger J, Kniess A, Thomsen MB, Brüggemann A, Fenske S, Biel M, Ruth P, Wahl-Schott C, Boushel RC, Olesen SP, Lukowski R (2014) KCNMA1 encoded cardiac BK channels afford protection against ischemia-reperfusion injury. PLoS One 9:e103402.MouseHeart
Skeletal muscle
Ischemia-reperfusion
Oxidative stress;RONS
Hara 2013 Eur J Anaesthesiol2013Hara N, Karlsson M, Sjövall F, Hansson Magnus J, Elmér E, Uchino H (2013) Early brain mitochondrial dysfunction in a mouse model of sepsis: 7AP4‐9. Eur J Anaesthesiol 30,112-112.MouseNervous systemOxidative stress;RONSSepsis
Jelenik 2013 Eur Heart J2013Jelenik T, Floegel U, Phielix E, Kaul K, Nowotny P, Partke HP, Schrader J, Roden M, Szendroedi S (2013) Non-alcoholic fatty liver disease and insulin resistance are associated with increased cardiac oxidative stress in mice. Eur Heart J 34:P5045.MouseHeartOxidative stress;RONS
Reilly 2013 J Exp Biol2013Reilly BD, Hickey AJ, Cramp RL, Franklin CE (2013) Decreased hydrogen peroxide production and mitochondrial respiration in skeletal muscle but not cardiac muscle of the green-striped burrowing frog, a natural model of muscle disuse. J Exp Biol 217:1087-93.AmphibiansHeart
Skeletal muscle
Oxidative stress;RONS
Iftikar 2013 PLoS One2013Iftikar FI, Hickey AJ (2013) Do mitochondria limit hot fish hearts? Understanding the role of mitochondrial function with heat stress in Notolabrus celidotus. PLoS One 8:e64120.FishesHeartOxidative stress;RONS
Tretter 2012 Free Radic Biol Med2012Tretter Laszlo, Adam-Vizi Vera (2012) High Ca2+ load promotes hydrogen peroxide generation via activation of α-glycerophosphate dehydrogenase in brain mitochondria. Free Radic Biol Med 53:2119-30.Guinea pigNervous systemOxidative stress;RONS
Affourtit 2012 Methods Mol Biol2012Affourtit C, Quinlan CL, Brand MD (2012) Measurement of proton leak and electron leak in isolated mitochondria. Methods Mol Biol 810:165-82.RatSkeletal muscleOxidative stress;RONS
Hickey 2012 J Comp Physiol B2012Hickey AJ, Renshaw GM, Speers-Roesch B, Richards JG, Wang Y, Farrell AP, Brauner CJ (2012) A radical approach to beating hypoxia: depressed free radical release from heart fibers of the hypoxia-tolerant epaulette shark (Hemiscyllum ocellatum). J Comp Physiol B 182:91-100.FishesHeartIschemia-reperfusion
Oxidative stress;RONS
Hunter 2012 Biochem Pharmacol2012Hunter FW, Wang J, Patel R, Hsu HL, Hickey AJ, Hay MP, Wilson WR (2012) Homologous recombination repair-dependent cytotoxicity of the benzotriazine di-N-oxide CEN-209: Comparison with other hypoxia-activated prodrugs. Biochem Pharmacol 83:574–85.CHOOxidative stress;RONS
Tretter 2007 J Neurochem2007Tretter L, Adam-Vizi V (2007) Uncoupling is without an effect on the production of reactive oxygen species by in situ synaptic mitochondria. J Neurochem 103:1864-71.Other mammalsNervous systemOxidative stress;RONS




Keywords: H2O2


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