[Ex vivo analysis of mitochondrial function in patients attended in an emergency department due to carbon monoxide poisoning].
OBJECTIVE
Many experimental studies in animals have demonstrated that carbon monoxide (CO) has the ability to bind to complex IV of the mitochondrial respiratory chain (MRC) inhibiting its function. It is unknown, however, if this situation is also present in patients who are admitted to an emergency department because of acute CO poisoning. The objective of this study was to evaluate from different points of view whether or not mitochondrial function is abnormal in patients admitted because of an acute CO poisoning.


METHODS
Ten patients with an acute CO poisoning admitted in an emergency department were included in the study. Initial carboxyhemoglobin was 20.4 (6)%. Seven of these patients received hyperbaric-oxygen therapy. In all the patients, lymphocytes from 20 mL of blood were obtained at admission (t0), and at days 3-5 (t1), and 10-14 (t2). Mitochondrial content was estimated through citrate synthase activity (nmol/min/mg protein). Enzymatic activity of complexes III and IV (both containing cytochromes) as well as oxidative activities were measured. Lipid peroxidation was ascertained by means of cis-parinaric acid fluorescence. All the values were given as absolute values, and were corrected according to the mitochondrial content (relative values). The results were compared with the control values obtained from 130 historical normal individuals.


RESULTS
During acute poisoning (t0), there were no changes in mitochondrial content. On the other hand, there was a significant inhibition of the enzymatic activity of complexes III and IV, and a decrease in all oxidative activities, considering both absolute and relative values. Although all the activities showed a trend to recuperation with time (t1 y t2), statistical significance was only observed for complex IV and for the oxydative activity stimulated with glutamate.


CONCLUSIONS
In the present study we confirm that an inhibition of the MRC can be demonstrated ex vivo in patients attended in an emergency department due to acute CO poisoning. The inhibition is still present 14 days after the acute event. This mitochondrial dysfunction may play a pathogenic role in the persisting or delayed sings and symptoms that these patients occasionally refer.
Miró
Oscar
O
Unidad de Urgencias. Medicina. Laboratorio de Funcionalismo Mitocondrial. Grupo de Investigación Muscular. Servicio de Medicina Interna. Hospital Clínic de Barcelona. Barcelona. España. omiro@clinic.ub.es
Alonso
Josep R
JR
López
Sònia
S
Beato
Anna
A
Casademont
Jordi
J
Cardellach
Francesc
F
D000328:Adult; D002249:Carbon Monoxide Poisoning / Q000378:metabolism* / Q000503:physiopathology; D004630:Emergencies; D005260:Female; D006801:Humans; D008297:Male; D008928:Mitochondria / Q000502:physiology*