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Study · Measured the body's own peptide · 2021

2 results

Analysis by Metabolomics and Transcriptomics for the Energy Metabolism Disorder and the Aryl Hydrocarbon Receptor Activation in Male Reproduction of Mice and GC-2spd Cells Exposed to PM2.5.

Shi F, Zhang Z, Wang J, Wang Y, Deng J, Zeng Y, Zou P, Ling X, Han F, Liu J, Ao L, Cao J

Frontiers in endocrinology3 Jan 2022Cited by 12 (Europe PMC)

PMID35046903 (opens in a new tab)PMCIDPMC8761788 (opens in a new tab)DOI10.3389/fendo.2021.807374 (opens in a new tab)PepBankPUB-35046903
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Summary

Fine particulate matter (PM2.5)-induced male reproductive toxicity arouses global public health concerns. However, the mechanisms of toxicity remain unclear. This study aimed to further investigate toxicity pathways by exposure to PM2.5in vitro and in vivo through the application of metabolomics and transcriptomics. In vitro, spermatocyte-derived GC-2spd cells were treated with 0, 25, 50, 100 μg/mL PM2.5 for 48 h. In vivo, the real-world exposure of PM2.5 for mouse was established. Forty-five male C57BL/6 mice were exposed to filtered air, unfiltered air, and concentrated ambient PM2.5 in Tangshan of China for 8 weeks, respectively. The results in vitro and in vivo showed that PM2.5 exposure inhibited GC-2spd cell proliferation and reduced sperm motility. Mitochondrial damage was observed after PM2.5 treatment. Increased Humanin and MOTS-c levels and decreased mitochondrial respiratory indicated that mitochondrial function was disturbed. Furthermore, nontargeted metabolomics analysis revealed that PM2.5 exposure could disturb the citrate cycle (TCA cycle) and reduce amino acids and nucleotide synthesis. Mechanically, the aryl hydrocarbon receptor (AhR) pathway was activated after exposure to PM2.5, with a significant increase in CYP1A1 expression. Further studies showed that PM2.5 exposure significantly increased both intracellular and mitochondrial reactive oxygen species (ROS) and activated NRF2 antioxidative pathway. With the RNA-sequencing technique, the differentially expressed genes induced by PM2.5 exposure were mainly enriched in the metabolism of xenobiotics by the cytochrome P450 pathway, of which Cyp1a1 was the most significantly changed gene. Our findings demonstrated that PM2.5 exposure could induce spermatocyte damage and energy metabolism disorder. The activation of the aryl hydrocarbon receptor might be involved in the mechanism of male reproductive toxicity.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

No result from this study comes from a test of the peptide.

Natural levels measured2

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01AnimalEndogenous levelAnimal study (in vivo)Other

    In mice and cells exposed to PM2.5, levels of the body's own MOTS‑c were increased, which the authors read as disturbed mitochondrial function; the abstract does not say whether this was in mice, cells or both.

    In plain wordsIn mice and cells exposed to air pollution particles, the body's own MOTS‑c rose; the abstract does not say in which.

    Peptide
    MOTS-c
    Outcome
    IncreaseMOTS-c level after PM2.5 exposure
    Study

    mousen: not reported in source

    Mice exposed to concentrated ambient PM2.5
    Outcome group
    Mitochondrial function · Reproductive and sexual health

    Source sentences

    Summary
    Increased Humanin and MOTS-c levels and decreased mitochondrial respiratory indicated that mitochondrial function was disturbed.
    1 context sentence
    Summary · context
    Forty-five male C57BL/6 mice were exposed to filtered air, unfiltered air, and concentrated ambient PM2.5 in Tangshan of China for 8 weeks, respectively.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  2. 02AnimalEndogenous levelAnimal study (in vivo)Other

    After PM2.5 exposure, humanin levels were increased, which indicated disturbed mitochondrial function; the abstract does not state whether this was measured in mice, cells or both.

    In plain wordsIn mice or lab cells exposed to fine particles, the body's own humanin levels were higher, which pointed to disturbed mitochondrial function.

    Peptide
    Humanin
    Outcome
    IncreaseHumanin level after PM2.5 exposure
    Study

    mousen: not reported in source

    Male C57BL/6 mice and GC-2spd spermatocyte cells
    Outcome group
    Mitochondrial function · Reproductive and sexual health

    Source sentences

    Summary
    Increased Humanin and MOTS-c levels and decreased mitochondrial respiratory indicated that mitochondrial function was disturbed.
    2 context sentences
    Summary · context
    In vitro, spermatocyte-derived GC-2spd cells were treated with 0, 25, 50, 100 μg/mL PM2.5 for 48 h.
    Summary · context
    Forty-five male C57BL/6 mice were exposed to filtered air, unfiltered air, and concentrated ambient PM2.5 in Tangshan of China for 8 weeks, respectively.

    This result measures the body's own Humanin. Nobody was given the peptide. It is not evidence about taking it.

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. Versions 4 to 18Current

    28 Oct 2026, 02:02 UTC

    The same notice was added 15 times, first on 13 Oct 2026, 21:44 UTC. The status did not change between them.

    Study results updated

  2. Version 3

    13 Oct 2026, 16:31 UTC

    Study data updated · source update from Europe PMC

  3. Version 2

    9 Oct 2026, 18:17 UTC

    Study results updated

  4. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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