Mitochondrial Injury in Human Acute Carbon Monoxide Poisoning: The Effect of Oxygen Treatment

作者：Garrabou G^*; Inoriza J M; Moren C; Oliu G; Miro O; Marti M J; Cardellach F

来源：Journal of Environmental Science and Health Part C-Environmental Carcinogenesis & Ecotoxicology Reviews, 2011, 29(1): 32-51.

DOI：10.1080/10590501.2011.551316

• Mitochondrial toxicity
• carbon monoxide (CO)
• hyperbaric oxygen treatment (HBO)
• normobaric oxygen treatment (NBO)
• cytochrome c oxidase (COX) or mitochondrial complex IV (mtCIV)
• oxidative stress (lipid peroxidation)
• late neurological syndrome (LNS)

The best oxygen therapy for acute carbon monoxide poisoning (ACOP) remains unestablished. Reported mitochondrial complex IV (mtCIV) inhibition, together with carboxyhaemoglobin (COHb)-induced hypoxia, may influence acute clinical symptoms and outcome. To omitochondriallyo evaluate treatment efficacy, we correlated intoxication severity and symptoms with mitochondrial mtCIV activity) and oxidative stress (lipid peroxidation) in 60 poisoned patients and determined ACOP recovery depending on either normobaric or hyperbaric oxygen therapy along a 3-month follow-up. In the present article we positively evaluate mtCIV as a good marker of ACOP recovery, treatment effectiveness, and late neurological syndrome development, which advocates for hyperbaric oxygen therapy as the treatment of choice. However, we discourage its usefulness as a severity marker because of its excessive sensitivity. We additionally evaluate oxidative stress role and prognostic factors for neurological sequelae development.

• 出版日期2011