Evidence map›Paper›PMID 25416361›Full record

ArticleMethods in enzymology2014

Use of potentiometric fluorophores in the measurement of mitochondrial reactive oxygen species.

Brian M Polster, David G Nicholls, Shealinna X Ge, Brian A Roelofs

Open access · greenAbstract read
In one paragraph

Article in Methods in enzymology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
27.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Measurement of Mitochondrial ROS Formation.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
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  10. Golgi-IP, a tool for multimodal analysis of Golgi molecular content.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Mitochondrial responses to intracellular CaJournal of neurophysiology · 2023
    Article
  12. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Brian M PolsterDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, Maryland, USA; Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA. Electronic address: bpolster@anes.umm.edu.
David G NichollsDepartment of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Lund University Diabetes Centre, CRC, Malmö, Sweden; Buck Institute for Research on Aging, Novato, California, USA.
Shealinna X GeDepartment of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research (STAR), University of Maryland School of Medicine, Baltimore, Maryland, USA.
Brian A RoelofsDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Center for Biomedical Engineering and Technology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
University of Maryland, Baltimore · USBuck Institute for Research on Aging · US

Funding

Novel Mechanisms of Microglial Neurotoxicity at Physiological OxygenR01NS085165 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI POLSTER, BRIAN M · 2013 to 2017
$1.7M
NINDS NIH HHS R01 NS085165
6 · The paper itself

Abstract

Mitochondrial reactive oxygen species (ROS) are implicated in signal transduction, inflammation, neurodegenerative disorders, and normal aging. Net ROS release by isolated brain mitochondria derived from a mixture of neurons and glia is readily quantified using fluorescent dyes. Measuring intracellular ROS in intact neurons or glia and assigning the origin to mitochondria are far more difficult. In recent years, the proton-motive force crucial to mitochondrial function has been exploited to target a variety of compounds to the highly negative mitochondrial matrix using the lipophilic triphenylphosphonium cation (TPP(+)) as a "delivery" conjugate. Among these, MitoSOX Red, also called mito-hydroethidine or mito-dihydroethidium, is prevalently used for mitochondrial ROS estimation. Although the TPP(+) moiety of MitoSOX enables the manyfold accumulation of ROS-sensitive hydroethidine in the mitochondrial matrix, the membrane potential sensitivity conferred by TPP(+) creates a daunting set of challenges not often considered in the application of this dye. This chapter provides recommendations and cautionary notes on the use of potentiometric fluorescent indicators for the approximation of mitochondrial ROS in live neurons, with principles that can be extrapolated to nonneuronal cell types. It is concluded that mitochondrial membrane potential changes render accurate estimation of mitochondrial ROS using MitoSOX difficult to impossible. Consequently, knowledge of mitochondrial membrane potential is essential to the application of potentiometric fluorophores for the measurement of intramitochondrial ROS.

Indexed as

AnimalsEthidiumFluorescenceFluorescent DyesMembrane Potential, MitochondrialMitochondriaNeuronsPhenanthridinesPotentiometryRatsReactive Oxygen Species5-(6'-triphenylphosphoniumhexyl)-5,6-dihydro-6-phenyl-3,8-phenanthridinediamminedihydroethidiumEthidiumFluorescent DyeshydroethidinePhenanthridinesReactive Oxygen SpeciesDihydroethidiumHydroethidineMembrane potentialMitoSOXRespirationROSSeahorseSuperoxideTriphenylphosphoniumUncoupling

Identifiers

PMID25416361
PMCPMC4484872
OpenAlexW1947662605

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.