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

The best oxygen therapy for acute carbon monoxide poisoning (ACOP) remains un established. Reported mitochondrial complex IV (mtCIV) inhibition, together with car boxyhaemoglobin (COHb)-induced hypoxia, may influence acute clinical symptoms andoutcome. 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 de pending 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 advocatesfor 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 develop ment.