| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2598902 | Toxicology Letters | 2015 | 8 Pages |
•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 1–5 h 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 3000 ppm CO in air followed by 24 h of normoxia and evaluated the possible protective influence of 100% normobaric oxygen or 100% oxygen at a pressure of 3 bar (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. 1 h 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, 1–5 h after exposure to CO.
