Sevoflurane exposure during the second trimester induces neurotoxicity in offspring rats by hyperactivation of PARP-1

Jiang, Qian; Zhao, Ping

doi:10.1007/s00213-022-06188-4

Cited by 5 publications

(1 citation statement)

References 70 publications

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“…Nowadays, emerging evidence has shown that maternal sevoflurane exposure during pregnancy may induce neurotoxic effects in the fetus, resulting in impaired neurodevelopment in offspring. 4 , 9 , 47 , 49 , 50 Sevoflurane is the preferred inhalation anesthetic during pregnancy and has many benefits, such as rapid induction of anesthesia and quicker awakening, 3 and modulation of its depth of anesthesia depends mainly on changing concentration. Sevoflurane at 3.0% is equivalent to a clinical concentration of 1.3–1.5 minimum alveolar concentration (MAC), which is close to the concentration commonly used in clinical practice during pregnancy and neonatal surgery.…”

Section: Discussionmentioning

confidence: 99%

Multiple sevoflurane exposures during mid‐trimester induce neurotoxicity in the developing brain initiated by 15LO2‐Mediated ferroptosis

Qian

Gao

et al. 2023

CNS Neurosci Ther

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AimsMid‐gestational sevoflurane exposure may induce notable long‐term neurocognitive impairment in offspring. This study was designed to investigate the role and potential mechanism of ferroptosis in developmental neurotoxicity induced by sevoflurane in the second trimester.MethodsPregnant rats on day 13 of gestation (G13) were treated with or without 3.0% sevoflurane, Ferrostatin‐1 (Fer‐1), PD146176, or Ku55933 on three consecutive days. Mitochondrial morphology, ferroptosis‐relative proteins, malondialdehyde (MDA) levels, total iron content, and glutathione peroxidase 4 (GPX4) activities were measured. Hippocampal neuronal development in offspring was also examined. Subsequently, 15‐lipoxygenase 2 (15LO2)‐phosphatidylethanolamine binding protein 1 (PEBP1) interaction and expression of Ataxia telangiectasia mutated (ATM) and its downstream proteins were also detected. Furthermore, Morris water maze (MWM) and Nissl's staining were applied to estimate the long‐term neurotoxic effects of sevoflurane.ResultsFerroptosis mitochondria were observed after maternal sevoflurane exposures. Sevoflurane elevated MDA and iron levels while inhibiting GPX4 activity, and resultant long‐term learning and memory dysfunction, which were alleviated by Fer‐1, PD146176, and Ku55933. Sevoflurane could enhance 15LO2‐PEBP1 interaction and activate ATM and its downstream P53/SAT1 pathway, which might be attributed to excessive p‐ATM nuclear translocation.ConclusionThis study proposes that 15LO2‐mediated ferroptosis might contribute to neurotoxicity induced by maternal sevoflurane anesthesia during the mid‐trimester in the offspring and its mechanism may be ascribed to hyperactivation of ATM and enhancement of 15LO2‐PEBP1 interaction, indicating a potential therapeutic target for ameliorating sevoflurane‐induced neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

Multiple sevoflurane exposures during mid‐trimester induce neurotoxicity in the developing brain initiated by 15LO2‐Mediated ferroptosis

Qian

Gao

et al. 2023

CNS Neurosci Ther

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Unveiling the hidden dangers: a review of non-apoptotic programmed cell death in anesthetic-induced developmental neurotoxicity

Sun,

Yisi Shan,

Cao

et al. 2024

Cell Biol Toxicol

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Anesthetic-induced developmental neurotoxicity (AIDN) can arise due to various factors, among which aberrant nerve cell death is a prominent risk factor. Animal studies have reported that repeated or prolonged anesthetic exposure can cause significant neuroapoptosis in the developing brain. Lately, non-apoptotic programmed cell deaths (PCDs), characterized by inflammation and oxidative stress, have gained increasing attention. Substantial evidence suggests that non-apoptotic PCDs are essential for neuronal cell death in AIDN compared to apoptosis. This article examines relevant publications in the PubMed database until April 2024. Only original articles in English that investigated the potential manifestations of non-apoptotic PCD in AIDN were analysed. Specifically, it investigates necroptosis, pyroptosis, ferroptosis, and parthanatos, elucidating the signaling mechanisms associated with each form. Furthermore, this study explores the potential relevance of these non-apoptotic PCDs pathways to the pathological mechanisms underlying AIDN, drawing upon their distinctive characteristics. Despite the considerable challenges involved in translating fundamental scientific knowledge into clinical therapeutic interventions, this comprehensive review offers a theoretical foundation for developing innovative preventive and treatment strategies targeting non-apoptotic PCDs in the context of AIDN.

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miR-671-5p Upregulation Attenuates Blood–Brain Barrier Disruption in the Ischemia Stroke Model Via the NF-кB/MMP-9 Signaling Pathway

et al. 2023

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Sevoflurane exposure during the second trimester induces neurotoxicity in offspring rats by hyperactivation of PARP-1

Cited by 5 publications

References 70 publications

Multiple sevoflurane exposures during mid‐trimester induce neurotoxicity in the developing brain initiated by 15LO2‐Mediated ferroptosis

Multiple sevoflurane exposures during mid‐trimester induce neurotoxicity in the developing brain initiated by 15LO2‐Mediated ferroptosis

Unveiling the hidden dangers: a review of non-apoptotic programmed cell death in anesthetic-induced developmental neurotoxicity

miR-671-5p Upregulation Attenuates Blood–Brain Barrier Disruption in the Ischemia Stroke Model Via the NF-кB/MMP-9 Signaling Pathway

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