The effectiveness of oxygen therapy in carbon monoxide poisoning is pressure- and time-dependent: A study on cultured astrocytes

•CO in high doses can trigger astrocytic apoptosis without necrosis.•Hyperbaric, not normobaric, oxygen inhibits CO-induced apoptosis.•Hyperbaric oxygen has the highest beneficial effect at 1–5h after CO exposure. Carbon monoxide (CO) poisoning causes neuronal and glial apoptosis that can result in...

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Bibliographic Details
Published in:Toxicology letters 2015-02, Vol.233 (1), p.16-23
Main Authors: Jurič, Damijana M., Finderle, Žarko, Šuput, Dušan, Brvar, Miran
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Astrocytes
Astrocytes - metabolism
Calpain - genetics
Calpain - metabolism
Carbon monoxide
Carbon Monoxide Poisoning - therapy
Caspase 3 - genetics
Caspase 3 - metabolism
Caspase 8 - genetics
Caspase 8 - metabolism
Caspase 9 - genetics
Caspase 9 - metabolism
Cell Survival
Cells, Cultured
Effectiveness
Exposure
Hyperbaric oxygen
Hyperbaric Oxygenation
Membrane Potential, Mitochondrial
Mitochondria - metabolism
Neuroglia
Normobaric oxygen
Poisoning
Protective
Rats
Reactive Oxygen Species - metabolism
Therapy
Toxicology
Viability
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Summary:•CO in high doses can trigger astrocytic apoptosis without necrosis.•Hyperbaric, not normobaric, oxygen inhibits CO-induced apoptosis.•Hyperbaric oxygen has the highest beneficial effect at 1–5h after CO exposure. Carbon monoxide (CO) poisoning causes neuronal and glial apoptosis that can result in delayed neurological symptoms. The damage of brain cells can be prevented by oxygen therapy. Based on the central role of astrocytes in maintaining neuronal function and viability we investigated the toxic effects of 3000ppm CO in air followed by 24h of normoxia and evaluated the possible protective influence of 100% normobaric oxygen or 100% oxygen at a pressure of 3bar (hyperbaric) against CO poisoning in these cells. CO/normoxia caused a progressive decline of viability, increase in reactive oxygen species and decline of mitochondrial membrane potential and intracellular ATP levels in cultured rat astrocytes. Increased caspase-9, caspase-8 and calpain activity converged in activation of caspase-3/7. 1h treatment with oxygen disclosed pressure- and time-dependent efficacy in restoring astrocytic mitochondrial function and the prevention of apoptosis. The protective effect was most evident when the astrocytes were exposed to hyperbaric oxygen, but not normobaric oxygen, 1–5h after exposure to CO.
ISSN:0378-4274
1879-3169
DOI:10.1016/j.toxlet.2015.01.004