Carbon Monoxide: A Pleiotropic Redox Regulator of Life and Death

Despite recent technological progress, carbon monoxide poisoning is still one of the leading causes of domestic and industrial morbidity and mortality. The brain is particularly vulnerable to CO toxicity, and thus the majority of survivors develop delayed movement and cognitive complications. CO bin...

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Bibliographic Details
Published in:Antioxidants 2024-09, Vol.13 (9), p.1121
Main Authors: Abramov, Andrey Y, Myers, Isabella, Angelova, Plamena R
Format: Article
Language:English
Subjects:
Antioxidants
Brain
Carbon monoxide
Carbon monoxide poisoning
Cell death
CO toxicity
Cytochrome
Enzymes
Erythrocytes
Glucose
Health aspects
Hemoglobin
Homeostasis
Hypoxia
Metabolism
Methylene blue
Mitochondria
Morbidity
Mortality
neuron
Neurons
Oxidative stress
Oxygenation
Physiology
Poisoning
Proteins
Reactive oxygen species
Reperfusion
Review
Toxicity
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Summary:Despite recent technological progress, carbon monoxide poisoning is still one of the leading causes of domestic and industrial morbidity and mortality. The brain is particularly vulnerable to CO toxicity, and thus the majority of survivors develop delayed movement and cognitive complications. CO binds to haemoglobin in erythrocytes, preventing oxygen delivery to tissues, and additionally inhibits mitochondrial respiration. This renders the effect of CO to be closely related to hypoxia reperfusion injury. Oxygen deprivation, as well as CO poisoning and re-oxygenation, are shown to be able to activate the production of reactive oxygen species and to induce oxidative stress. Here, we review the role of reactive oxygen species production and oxidative stress in the mechanism of neuronal cell death induced by carbon monoxide and re-oxygenation. We discuss possible protective mechanisms used by brain cells with a specific focus on the inhibition of CO-induced ROS production and oxidative stress.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox13091121