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

• Published in: Journal of environmental science and health. Part C, Environmental carcinogenesis & ecotoxicology reviews Environmental carcinogenesis & ecotoxicology reviews, 2011-01, Vol.29 (1), p.32-51
• Main Authors: GARRABOU, G, INORIZA, J. M, MORÉN, C, OLIU, G, MIRÓ, Ò, MARTÍ, M. J, CARDELLACH, F
• Format: Article
• Language: English
• Subjects: Acute Disease; Adolescent; Adult; Air Pollutants - toxicity; Biomarkers - metabolism; carbon monoxide; carbon monoxide (CO); Carbon Monoxide - toxicity; Carbon Monoxide Poisoning - diagnosis; Carbon Monoxide Poisoning - metabolism; Carbon Monoxide Poisoning - therapy; complications (disease); cytochrome c oxidase (COX) or mitochondrial complex IV (mtCIV); Electron Transport Complex IV - antagonists & inhibitors; Electron Transport Complex IV - metabolism; environmental science; Female; Humans; hyperbaric oxygen treatment (HBO); hypoxia; late neurological syndrome (LNS); lipid peroxidation; Lipid Peroxidation - drug effects; Male; Mitochondria - drug effects; Mitochondrial toxicity; normobaric oxygen treatment (NBO); Oxidative Stress; oxidative stress (lipid peroxidation); oxygen; Oxygen Inhalation Therapy; patients; poisoning; therapeutics; Treatment Outcome; Young Adult
• ISSN: 1532-4095; 1059-0501; 1532-4095
• DOI: 10.1080/10590501.2011.551316

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 “mitochondrially” evaluate treatment efficacy, we correlated intoxication severity and symptoms with mitochondrial function (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.