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Neuronal Cell Death Modalities and Protective Mechanisms Induced By Sevoflurane: A Narrative Review.
Teodora Oltean1, Sean Ostlund1, Joseph Rinehart1
1From the Department of Anesthesiology and Perioperative Care, University of California Irvine, Irvine, California.
Sevoflurane anesthesia may cause long-term neurotoxic effects, including cognitive impairment, primarily through neuronal cell death. This review examines sevoflurane
Area of Science:
- Neuroscience
- Anesthesiology
- Toxicology
Background:
- Sevoflurane is a common inhaled anesthetic used in surgeries for adults and children.
- Neurotoxic long-term effects, such as cognitive impairment, have been associated with sevoflurane exposure in both pediatric and adult populations.
- Neuronal cell death is a key mechanism underlying sevoflurane-induced neurotoxicity.
Purpose of the Study:
- To review and analyze existing animal and clinical data on the neurotoxic potential of sevoflurane.
- To investigate the effects of sevoflurane on the developing and aged brain.
- To highlight cell death modalities and propose strategies to mitigate neurotoxicity.
Main Methods:
- Comprehensive review of published animal and clinical studies.
- Analysis of data investigating sevoflurane's impact on neuronal cell death.
- Examination of mechanisms including apoptosis, ferroptosis, necroptosis, pyroptosis, mitochondrial dysfunction, and oxidative stress.
Main Results:
- Sevoflurane exposure is linked to various forms of neuronal cell death.
- Mitochondrial dysfunction and oxidative stress are implicated in sevoflurane-mediated neurotoxicity.
- The review identifies specific cell death pathways involved in neurological function alteration.
Conclusions:
- Distinct cell death modalities play a critical role in sevoflurane-induced neurotoxicity, particularly in vulnerable populations.
- Understanding these mechanisms is crucial for developing strategies to minimize adverse neurological outcomes.
- Further research is needed to refine protective interventions against sevoflurane neurotoxicity.
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