Oxidative stress response to carbon monoxide intoxication and the effect of normobaric and hyperbaric oxygen on it

Background: Carbon monoxide (CO) is the leading agent of injury and death by poisoning worldwide. Delayed neurological sequels (DNS) are seen in up to 50% of the CO intoxicated patients. The toxic effects of CO which produces DNS have been attributed to oxidative stress induced by hypoxia. Normobaric oxygen is the routine therapy of CO intoxicaton but the use of hyperbaric oxygen (HBO) therapy remains controversial. Besides that HBO therapy has been shown to reduce the risk of DNS after CO poisoning. We conducted a prospective study to identify the role of normobaric and hyperbaric oxygen on the oxidative stress and lipid peroxidation. We aimed to compare these results of two treatment modalities to discuss oxidative stress as the possible way of effect of hyperbaric oxygen therapy on DNS. Methods: Patients who were admitted to our Emergency Department and diagnosed as CO intoxication were studied prospectively between 1st January and 30th June 2012. Patients were divided in to two treatment groups depending on their indications. The normobaric oxygen (NBO) treatment group received 4-6 hours of oxygen by a reservoir mask. Hyperbaric oxygen (HBO) treatment group was received hyperbaric oxygen therapy started as soon as possible and continued 5 daily treatments at 2.4 ATA for 120 minutes. The control group was consisted of healthy individuals who were admitted to the emergency unit with minor traumas. All blood samples were taken in the treatment groups when diagnosed and in the control group at admittance. Other samples were taken from the patients soon after the NBO and first HBO therapy (1st day) and at the fifth day of HBO or 5 days after NBO therapy. The NOS activities, TBARS, SOD, CAT and GST were studied in these samples. Results: 95 patients were diagnosed as CO intoxication. 81 of them and another 24 healthy volunteers were studied. The NBO group was consisted of 56 patients and the HBO group was consisted of 25 patients. NOS and TBARS levels were significantly higher and SOD, CAT, GST levels were lower when compared with the control group at the admittance. Although there was an increase in TBARS levels at the end of the first treatments, it decreased at the 5th day in the HBO group but still remained higher from controls. NOS levels were significantly decreased at the first day of the both treatment groups. SOD and CAT levels showed a trend of increase which was not statistically significant. There were no differences in the GST levels of each treatment group. Conclusions: Although these results have shown oxidative stress and lipid peroxidation in CO intoxicated patients, it appeared to be poor to reinforce the superiority of the effect of HBO therapy on these parameters.