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Eur Respir J 2004; 23:214-218
Copyright ©ERS Journals Ltd 2004


Reversible inhibition of mitochondrial complex IV activity in PBMC following acute smoking

J-R. Alonso, F. Cardellach, J. Casademont and Ò. Miró

Mitochondrial Research Laboratory, Muscle Research Unit, Dept of Internal Medicine, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and University of Barcelona, Barcelona, Catalonia, Spain

CORRESPONDENCE: Ò. Miró, Muscle Research Unit, Dept of Internal Medicine, Hospital Clínic, Villarroel 170, 08036, Barcelona, Catalonia, Spain. Fax: 34 932279365. E-mail: omiro@clinic.ub.es

Keywords: carbon monoxide toxicity, cytochrome oxidase, mitochondrial diseases, smoking

Received: April 6, 2003
Accepted September 22, 2003

This study was supported by Promoción General del Conocimiento PM99-0038 and Premi Fi de Residència 1999 of Hospital Clínic i Provincial de Barcelona.

Smoking causes a decrease of mitochondrial complex IV activity in chronic smokers. However, it is not known if this toxic effect is due to the acute effect of cigarette smoke itself or is a secondary phenomenon related to other smoking factors.

The study assessed mitochondrial respiratory chain function in peripheral blood mononuclear cells of 15 healthy nonsmoker individuals before smoking (t0), immediately after smoking five cigarettes in 45 min (t1) and 24 h later (t2). Blood carboxyhaemoglobin (COHb) and carbon monoxide concentrations in exhaled air (COEA) were determined to ascertain smoke inhalation status.

After acute smoking, COHb increased from 0.5±0.3% to 3.3±1.5%, and COEA from 2.9±2.5 to 26.1±9.9 ppm. Complex II and III enzyme activities did not change along the study. Complex IV activity showed a 23% inhibition at t1 but returned to initial (t0) levels at t2. A decay in oxygen consumption was observed after the correction for mitochondrial content. Lipid peroxidation of cell membranes remained unchanged.

Short-time smoking causes an acute and reversible mitochondrial complex IV inhibition in human mononuclear cells. These results suggest that smoke itself is one of the causes for the decrease of complex IV activity observed in chronic smokers.




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