Skip to content

Study · Animal study (in vivo) · mouse · 2018

6 results

Contradictory effects of mitochondria- and non-mitochondria-targeted antioxidants on hepatocarcinogenesis by altering DNA repair in mice.

Wang B, Fu J, Yu T, Xu A, Qin W, Yang Z, Chen Y, Wang H

Hepatology (Baltimore, Md.)7 Jan 2018Cited by 25 (Europe PMC)

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 study6

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

  1. 01AnimalAnimal study (in vivo)Safety outcome

    In mouse models of chemical hepatocarcinogenesis, SS‑31 facilitated tumorigenesis, whereas the non-mitochondria-targeted antioxidants NAC and Trolox prevented it.

    In plain wordsIn mice, SS‑31 made liver tumors more likely, while two other antioxidants (NAC and Trolox) prevented tumors.

    Outcome
    IncreaseHepatocarcinogenesis (tumorigenesis)
    Study

    mousen: not reported in source

    Mouse chemical hepatocarcinogenesis models
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Utilizing mouse models of chemical hepatocarcinogenesis
    1 context sentence
    Summary · context
    administration of mitochondria-targeted antioxidants SS-31 (the mitochondria-targeted peptide) and Mito-Q (a derivative of ubiquinone) facilitated tumorigenesis.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mouse hepatocarcinogenesis models, RNA sequencing showed that SS‑31 and NAC caused very different changes in oxidation-reduction state and DNA damage response.

    In plain wordsIn mice, SS‑31 and NAC changed gene activity for oxidation state and DNA damage response in very different ways.

    Outcome
    MixedOxidation-reduction state and DNA damage response (RNA sequencing)
    Study

    mousen: not reported in source

    Mouse chemical hepatocarcinogenesis models
    Comparator
    NAC
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    RNA sequencing revealed that NAC and SS-31 caused very different changes in the oxidation-reduction state and DNA damage response.
    1 context sentence
    Summary · context
    Utilizing mouse models of chemical hepatocarcinogenesis
  3. 03LabIn vitro (cells)Mechanism

    In DEN-treated primary hepatocytes, SS‑31 aggravated DNA damage, whereas NAC and Trolox alleviated it.

    In plain wordsIn cells, SS‑31 made DNA damage worse, while NAC and Trolox reduced it.

    Outcome
    IncreaseDNA damage in DEN-treated primary hepatocytes
    Study

    n: not reported in source

    DEN-treated primary hepatocytes
    Comparator
    NAC and Trolox
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.
  4. 04LabIn vitro (cells)Mechanism

    In DEN-treated primary hepatocytes, SS‑31 inactivated ATM/ATR, whereas NAC and Trolox activated them.

    In plain wordsIn cells, SS‑31 switched off the DNA repair proteins ATM and ATR, while NAC and Trolox switched them on.

    Outcome
    DecreaseATM/ATR activation in DEN-treated primary hepatocytes
    Study

    n: not reported in source

    DEN-treated primary hepatocytes
    Comparator
    NAC and Trolox
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.
  5. 05LabIn vitro (cells)Mechanism

    In mouse hepatocarcinogenesis models, SS‑31 treatment altered the localization of ATM between mitochondria and nuclei; direction not stated.

    In plain wordsIn mice, SS‑31 changed where the DNA repair protein ATM sits between mitochondria and nuclei.

    Outcome
    Direction not reportedATM localization between mitochondria and nuclei
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Localization of ATM between mitochondria and nuclei was altered after NAC and SS-31 treatment.

Studies that did not test the peptide alone1

In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Elamipretide (SS-31).

  1. 06AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Mechanism

    In DEN-induced hepatocellular carcinoma in mice, reactivation of p-ATR blocked the tumor promotion caused by SS‑31.

    In plain wordsIn mice, switching p-ATR back on blocked the extra liver tumor growth seen with SS‑31.

    Outcome
    DecreaseSS-31-promoted DEN HCC after p-ATR reactivation
    Study

    mousen: not reported in source

    Mouse DEN hepatocellular carcinoma model
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    In contrast, reactivation of p-ATR blocked SS-31-promoted DEN HCC.

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

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

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.