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Emerging cellular-based therapies in carbon monoxide poisoning

Jang, David H. ; Piel, Sarah LU orcid ; Greenwood, John C. ; Ehinger, Johannes K. LU orcid and Kilbaugh, Todd J. (2021) In American Journal of Physiology - Cell Physiology 321(2). p.269-275
Abstract

Carbon monoxide (CO) is an odorless and colorless gas with multiple sources that include engine exhaust, faulty furnaces, and other sources of incomplete combustion of carbon compounds such as house fires. The most serious complications for survivors of consequential CO exposure are persistent neurological sequelae occurring in up to 50% of patients. CO inhibits mitochondrial respiration by specifically binding to the heme a3 in the active site of CIV-like hydrogen sulfide, cyanide, and phosphides. Although hyperbaric oxygen remains the cornerstone for treatment, it has variable efficacy requiring new approaches to treatment. There is a paucity of cellular-based therapies in the area of CO poisoning, and there have been... (More)

Carbon monoxide (CO) is an odorless and colorless gas with multiple sources that include engine exhaust, faulty furnaces, and other sources of incomplete combustion of carbon compounds such as house fires. The most serious complications for survivors of consequential CO exposure are persistent neurological sequelae occurring in up to 50% of patients. CO inhibits mitochondrial respiration by specifically binding to the heme a3 in the active site of CIV-like hydrogen sulfide, cyanide, and phosphides. Although hyperbaric oxygen remains the cornerstone for treatment, it has variable efficacy requiring new approaches to treatment. There is a paucity of cellular-based therapies in the area of CO poisoning, and there have been recent advancements that include antioxidants and a mitochondrial substrate prodrug. The succinate prodrugs derived from chemical modification of succinate are endeavored to enhance delivery of succinate to cells, increasing uptake of succinate into the mitochondria, and providing metabolic support for cells. The therapeutic intervention of succinate prodrugs is thus potentially applicable to patients with CO poisoning via metabolic support for fuel oxidation and possibly improving efficacy of HBO therapy.

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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Carbon monoxide, Cellular therapies, Mitochondria, Respiration, Succinate prodrug
in
American Journal of Physiology - Cell Physiology
volume
321
issue
2
pages
269 - 275
publisher
American Physiological Society
external identifiers
  • pmid:34133239
  • scopus:85111546061
ISSN
0363-6143
DOI
10.1152/ajpcell.00022.2021
project
Mitochondrial dysfunction in drug and chemical toxicity: mechanism, target identification and therapeutic development
language
English
LU publication?
yes
id
77b920c8-ed45-42b1-90cd-278fb937eba3
date added to LUP
2021-08-27 11:59:34
date last changed
2024-06-15 15:13:51
@article{77b920c8-ed45-42b1-90cd-278fb937eba3,
  abstract     = {{<p>Carbon monoxide (CO) is an odorless and colorless gas with multiple sources that include engine exhaust, faulty furnaces, and other sources of incomplete combustion of carbon compounds such as house fires. The most serious complications for survivors of consequential CO exposure are persistent neurological sequelae occurring in up to 50% of patients. CO inhibits mitochondrial respiration by specifically binding to the heme a<sub>3</sub> in the active site of CIV-like hydrogen sulfide, cyanide, and phosphides. Although hyperbaric oxygen remains the cornerstone for treatment, it has variable efficacy requiring new approaches to treatment. There is a paucity of cellular-based therapies in the area of CO poisoning, and there have been recent advancements that include antioxidants and a mitochondrial substrate prodrug. The succinate prodrugs derived from chemical modification of succinate are endeavored to enhance delivery of succinate to cells, increasing uptake of succinate into the mitochondria, and providing metabolic support for cells. The therapeutic intervention of succinate prodrugs is thus potentially applicable to patients with CO poisoning via metabolic support for fuel oxidation and possibly improving efficacy of HBO therapy.</p>}},
  author       = {{Jang, David H. and Piel, Sarah and Greenwood, John C. and Ehinger, Johannes K. and Kilbaugh, Todd J.}},
  issn         = {{0363-6143}},
  keywords     = {{Carbon monoxide; Cellular therapies; Mitochondria; Respiration; Succinate prodrug}},
  language     = {{eng}},
  number       = {{2}},
  pages        = {{269--275}},
  publisher    = {{American Physiological Society}},
  series       = {{American Journal of Physiology - Cell Physiology}},
  title        = {{Emerging cellular-based therapies in carbon monoxide poisoning}},
  url          = {{http://dx.doi.org/10.1152/ajpcell.00022.2021}},
  doi          = {{10.1152/ajpcell.00022.2021}},
  volume       = {{321}},
  year         = {{2021}},
}