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Study · In vitro (cells) · 2008

2 results

Do mitochondriotropic antioxidants prevent chlorinative stress-induced mitochondrial and cellular injury?

Whiteman M, Spencer JP, Szeto HH, Armstrong JS

Antioxidants & redox signaling1 Mar 2008Cited by 31 (Europe PMC)

PMID18052717 (opens in a new tab)DOI10.1089/ars.2007.1879 (opens in a new tab)PepBankPUB-18052717
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study2

2 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In human fetal liver cells, MitoQ and SS31 significantly protected against HOCl-induced mitochondrial damage at concentrations of 25 nM or more.

    In plain wordsIn cells, SS31 and MitoQ protected mitochondria from damage by the oxidant HOCl at low (25 nanomolar or more) concentrations.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseHOCl-induced mitochondrial damage
    Study

    humann: not reported in source

    Human fetal liver cells exposed to HOCl
    Outcome group
    Mitochondrial function · Liver
    Studied dose
    Dose not stated

    Measurements

    Effective concentration
    ≥ 25 nM
    HOCl-induced mitochondrial damage

    Source sentences

    Summary
    In this current study, we show that recently developed mitochondria-targeted antioxidants (MitoQ and SS31) significantly protected against HOCl-induced mitochondrial damage and cell death at concentrations >or=25 nM.
    1 context sentence
    Summary · context
    Since mitochondria are key mediators of apoptosis and necrosis, we hypothesized that mitochondriotropic antioxidants could limit HOCl-mediated intracellular oxidative injury to human fetal liver cells, preserve mitochondrial function, and prevent cell death.
  2. 02LabIn vitro (cells)Efficacy outcome

    In human fetal liver cells, MitoQ and SS31 significantly protected against HOCl-induced cell death at concentrations of 25 nM or more.

    In plain wordsIn cells, SS31 and MitoQ protected liver cells from death caused by the oxidant HOCl at low (25 nanomolar or more) concentrations.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseHOCl-induced cell death
    Study

    humann: not reported in source

    Human fetal liver cells exposed to HOCl
    Outcome group
    Cell viability and death · Liver
    Studied dose
    Dose not stated

    Measurements

    Effective concentration
    ≥ 25 nM
    HOCl-induced cell death

    Source sentences

    Summary
    In this current study, we show that recently developed mitochondria-targeted antioxidants (MitoQ and SS31) significantly protected against HOCl-induced mitochondrial damage and cell death at concentrations >or=25 nM.
    1 context sentence
    Summary · context
    Since mitochondria are key mediators of apoptosis and necrosis, we hypothesized that mitochondriotropic antioxidants could limit HOCl-mediated intracellular oxidative injury to human fetal liver cells, preserve mitochondrial function, and prevent cell death.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

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