ArticleAnesthesia and analgesia2014
Subclinical carbon monoxide limits apoptosis in the developing brain after isoflurane exposure.
Article in Anesthesia and analgesia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response.Pharmacological reviews · 2022Review
- Relevance of experimental paradigms of anesthesia induced neurotoxicity in the mouse.PloS one · 2019Article
- Data on the effect of sex on the size, cellular content, and neuronal density of the developing brain in mice exposed to isoflurane and carbon monoxide.Data in brief · 2017Article
- Monosialoganglioside 1 may alleviate neurotoxicity induced by propofol combined with remifentanil in neural stem cells.Neural regeneration research · 2017Article
- Carbon monoxide incompletely prevents isoflurane-induced defects in murine neurodevelopment.Neurotoxicology and teratology · 2017Article
- Hydrogen-rich saline attenuates isoflurane-induced caspase-3 activation and cognitive impairment via inhibition of isoflurane-induced oxidative stress, mitochondrial dysfunction, and reduction in ATP levels.American journal of translational research · 2017Article
- Anesthesia-Related Carbon Monoxide Exposure: Toxicity and Potential Therapy.Anesthesia and analgesia · 2016Review
- Article
- Anesthesia-Induced Neuronal Apoptosis in the Developing Retina: A Window of Opportunity.Anesthesia and analgesia · 2015Article
- Carbon monoxide modulates cytochrome oxidase activity and oxidative stress in the developing murine brain during isoflurane exposure.Free radical biology & medicine · 2015Article
- Good gas, bad gas: isoflurane, carbon monoxide, and which is which?Anesthesia and analgesia · 2014Article
- Carbon monoxide and anesthesia-induced neurotoxicity.Neurotoxicology and teratologyReview
- Neurotoxicity of anesthetics: Mechanisms and meaning from mouse intervention studies.Neurotoxicology and teratologyReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundVolatile anesthetics cause widespread apoptosis in the developing brain. Carbon monoxide (CO) has antiapoptotic properties, and exhaled endogenous CO is commonly rebreathed during low-flow anesthesia in infants and children, resulting in subclinical CO exposure. Thus, we aimed to determine whether CO could limit isoflurane-induced apoptosis in the developing brain.
methodsSeven-day-old male CD-1 mouse pups underwent 1-hour exposure to 0 (air), 5, or 100 ppm CO in air with or without isoflurane (2%). We assessed carboxyhemoglobin levels, cytochrome c peroxidase activity, and cytochrome c release from forebrain mitochondria after exposure and quantified the number of activated caspase-3 positive cells and TUNEL positive nuclei in neocortex, hippocampus, and hypothalamus/thalamus.
resultsCarboxyhemoglobin levels approximated those expected in humans after a similar time-weighted CO exposure. Isoflurane significantly increased cytochrome c peroxidase activity, cytochrome c release, the number of activated caspase-3 cells, and TUNEL positive nuclei in the forebrain of air-exposed mice. CO, however, abrogated isoflurane-induced cytochrome c peroxidase activation and cytochrome c release from forebrain mitochondria and decreased the number of activated caspase-3 positive cells and TUNEL positive nuclei after simultaneous exposure with isoflurane.
conclusionsTaken together, the data indicate that CO can limit apoptosis after isoflurane exposure via inhibition of cytochrome c peroxidase depending on concentration. Although it is unknown whether CO directly inhibited isoflurane-induced apoptosis, it is possible that low-flow anesthesia designed to target rebreathing of specific concentrations of CO may be a desired strategy to develop in the future in an effort to prevent anesthesia-induced neurotoxicity in infants and children.
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