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Study · Animal study (in vivo) · mouse · 2022

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Mitochondria-Related Ferroptosis Drives Cognitive Deficits in Neonatal Mice Following Sevoflurane Administration.

Zhang P, Chen Y, Zhang S, Chen G

Frontiers in medicine22 Jul 2022Cited by 41 (Europe PMC)

PMID35935755 (opens in a new tab)PMCIDPMC9355652 (opens in a new tab)DOI10.3389/fmed.2022.887062 (opens in a new tab)PepBankPUB-35935755
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Summary

Multiple sevoflurane exposure may result in cognitive deficits in neonatal animals. This study attempted to investigate the potential mechanism of sevoflurane-induced neurotoxicity in developing hippocampus. Neonatal animals received sevoflurane anesthesia, then the behavioral tests and Golgi-Cox staining were employed to detect the effect of sevoflurane inhalation in adult mice. And the mitochondrial function was evaluated using MitoSOX staining, Fluo calcium indicators, mitochondrial permeability transition pore (mPTP) assay, and JC-1 probe after sevoflurane administration. Meanwhile, mitochondrial lipid hydroperoxide and ferroptosis were measured by MitoPeDPP and Mito-FerroGreen signals following sevoflurane exposure. Moreover, the ferroptosis and behavioral performance were assessed after deferiprone (DFP) treatment. The results showed that sevoflurane administration induced cognitive impairment accompanied by reducing dendritic length, density, and nodes. Additionally, sevoflurane exposure elevated mitochondrial ROS production and cytoplasm calcium levels, triggered the opening of mPTP, and decreased the mitochondrial membrane potential (MMP). However, supplement of elamipretide (SS-31) effectively reversed mitochondrial dysfunction. Mitochondrial lipid hydroperoxide production was increased after sevoflurane administration, whereas Fer-1 treatment reduced lipid hydroperoxide formation. Sevoflurane exposure induced mitochondrial iron overload, whereas Mito-Tempo treatment reduced iron accumulation. Prussian blue staining showed that the hippocampal iron deposition was apparently increased after sevoflurane inhalation. Additionally, the ferroptosis-related protein expression (including ACSL4, COX2, GPX4, and FTH1) was significantly changed, whereas DFP effectively suppressed ferroptosis and enhanced sevoflurane-induced behavioral malfunction. These findings demonstrated that sevoflurane administration elicited mitochondrial dysfunction and iron dyshomeostasis and eventually resulted in cognitive impairments, whereas protecting mitochondrial function and chelating neurotoxic iron effectively reversed these pathological processes.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In neonatal mice exposed to sevoflurane, elamipretide (SS‑31) reversed mitochondrial dysfunction.

    In plain wordsIn mice exposed to sevoflurane as newborns, elamipretide reversed damage to mitochondria.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseSevoflurane-induced mitochondrial dysfunction
    Study

    mousen: not reported in source

    Neonatal mice exposed to sevoflurane
    Outcome group
    Mitochondrial function · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    supplement of elamipretide (SS-31) effectively reversed mitochondrial dysfunction.
    1 context sentence
    Summary · context
    Neonatal animals received sevoflurane anesthesia, then the behavioral tests and Golgi-Cox staining were employed to detect the effect of sevoflurane inhalation in adult mice.

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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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