Mechanisms and therapeutic targets of carbon monoxide poisoning: A focus on reactive oxygen species.

Autor: Wang T; Department of Neurology, The First Hospital of Lanzhou University, Lanzhou, 730000, China. Electronic address: tjwth05@163.com., Zhang Y; Department of Radiology, The First Hospital of Lanzhou University, Lanzhou, 730000, China.
Jazyk: angličtina
Zdroj: Chemico-biological interactions [Chem Biol Interact] 2024 Nov 01; Vol. 403, pp. 111223. Date of Electronic Publication: 2024 Sep 03.
DOI: 10.1016/j.cbi.2024.111223
Abstrakt: Carbon monoxide (CO) poisoning presents a substantial public health challenge that necessitates the identification of its pathological mechanisms and therapeutic targets. CO toxicity arises from tissue hypoxia-ischemia secondary to carboxyhemoglobin formation, and cellular damage mediated by CO at the cellular level. The mitochondria are the major targets of neuronal damage caused by CO. Under normal physiological conditions, mitochondria produce reactive oxygen species (ROS), which are byproducts of aerobic metabolism. While low ROS levels are crucial for essential cellular functions, including signal transduction, differentiation, responses to hypoxia and immunity, transcriptional regulation, and autophagy, excess ROS become pathological and exacerbate CO poisoning. This review presents the evidence of elevated ROS being associated with the progression of CO poisoning. Antioxidant treatments targeting ROS removal have been proven effective in mitigating CO poisoning, underscoring their therapeutic potential. In this review, we highlight the latest advances in the understanding of the role and the clinical implications of ROS in CO poisoning. We focus on cellular sources of ROS, the molecular mechanisms underlying mitochondrial oxidative stress, and potential therapeutic strategies for targeting ROS in CO poisoning.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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