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A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury

A Ferret Model of Inflammation-sensitized Late Preterm Hypoxic-ischemic Brain Injury

Published on: November 19, 2019

Sevoflurane exposure triggers ferroptosis of neuronal cells initiated by the activation of ATM/p53 in the neonatal

Wanping Gu¹, Tingting Pan¹, Xuedong Wang¹

¹Department of Anesthesiology, The First Hospital of Jilin University, No. 1 Xinmin St., Changchun 130021, China.

International Immunopharmacology

|May 16, 2025

Summary

Sevoflurane anesthesia causes neonatal brain cell death via ferroptosis, a process involving iron overload and lipid peroxidation. This cell death is triggered by DNA damage and activated p53, impacting neurological development.

Keywords:

Ferroptosis JNK/p38 MAPK Neonatal brain P53 Reactive oxygen species Sevoflurane

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Area of Science:

Neuroscience
Toxicology
Cell Biology

Background:

Developmental neurotoxicity from sevoflurane is a concern, with neuronal death as a key factor.
The precise mechanisms underlying sevoflurane-induced neurotoxicity remain unclear.
Ferroptosis, a form of regulated cell death, is linked to neurological disorders and involves iron overload and lipid peroxidation.

Purpose of the Study:

To elucidate the mechanism of sevoflurane-induced neuronal death in the neonatal brain.
To investigate the role of ferroptosis in sevoflurane neurotoxicity.
To identify the molecular pathways involved in sevoflurane-induced ferroptosis.

Main Methods:

In vitro studies using HT22 cells and primary hippocampal neurons.
In vivo studies using neonatal mouse hippocampi.
Assessment of iron overload, lipid peroxidation, reactive oxygen species (ROS), and DNA damage markers.
Analysis of key signaling pathways including ATM/p53 and JNK/p38 MAPK.

Main Results:

Sevoflurane exposure induced hallmarks of ferroptosis, including iron overload and lipid peroxidation, in neuronal cells and neonatal mouse hippocampi.
Sevoflurane-induced ferroptosis was linked to ATM/p53 activation following DNA damage.
Activation of JNK/p38 MAPK pathways by sevoflurane led to ROS accumulation, DNA damage, and subsequent ferroptosis.

Conclusions:

Sevoflurane exposure triggers ferroptosis in neonatal brain neurons.
The ATM/p53 pathway, activated by JNK/p38 MAPK-mediated ROS and DNA damage, drives sevoflurane-induced ferroptosis.
These findings reveal a novel mechanism of developmental neurotoxicity by sevoflurane.