Abstract
Cigarette smoking is the main cause of chronic obstructive pulmonary disease (COPD). Diaphragm injury is observed in patients with COPD. However, the potential role of smoking in triggering or perpetuating muscle injury is unknown. The present study was aimed at evaluating the potential role of commercial tobacco smoke as a direct cause of skeletal muscle injury in experimental conditions. Seventy Wistar rats (170 - 250 g) were assigned to smoking (n = 49) or non-smoking (n = 21) groups. The smoking groups were submitted to a single or multiple (i.e., five or thirty) daily sessions of cigarette smoking in an inhalatory chamber (time length: 2 h each session). The level of exposure was constant and assessed by CO concentrations (50 ppm) and serum cotinine analysis. Animals submitted to a single smoke exposure and the corresponding controls were euthanized in groups at 0 h, 2 h, 4 h, 24 h or 48 h after completing the exposure. Animals submitted to multiple exposures were euthanized at 0 h after smoking. Samples from vastus lateralis muscle were obtained and processed for assessing cell injury and selected protein expression. Monoclonal anti-albumin antibodies were used to identify muscle fibers with sarcolemmal (membrane) injury. Subcellular muscle injury was assessed using transmission electron microscopy (EM). MyoD, myogenin and α-tubulin were immunodetected using western blot techniques. Exposure to cigarette smoke associated with significant membrane damage (mean relative difference (MRD) with controls: +181%, p = 0.004) and sarcomere disruptions (MRD: +226%, p = 0.001). Expression of MyoD and myogenin (normalized to α-tubulin) were significantly increased at 4 h and remained increased at 48 h post-exposure. We conclude that not only a single but also consecutive exposure to tobacco smoke have acute deleterious effects on peripheral muscle structure. A rapid induction of subrogate markers of skeletal muscle stress and repair processes associates to sarcolemmal and sarcomere damage.
Highlights
Chronic obstructive pulmonary disease (COPD), mainly induced by tobacco smoking, represents a major cause of disability and mortality in all countries, resulting in an important economic and social burden [1]
Single sessions of smoking associated with a significant increase of serum cotinine from 0.5 ± 0.3 to 8.3 ± 8.3 ng/ml (p < 0.0001) and carboxihemoglobin concentration
Given that cigarette smoking is the main cause of COPD, we hypothesized that gases and particulate matter from cigarette smoke could be involved in the susceptibility to prolonged cellular and molecular disturbances found in these patients [1]
Summary
Chronic obstructive pulmonary disease (COPD), mainly induced by tobacco smoking, represents a major cause of disability and mortality in all countries, resulting in an important economic and social burden [1]. Skeletal muscle dysfunction (i.e., decreased in strength or endurance) is one of the relevant extrapulmonary impairments frequently found in patients with COPD. This dysfunction is not merely a descriptive finding but has clinical relevance: muscle dysfunction relates to increased need for medical assistance and decreased survival of COPD patients [3]-[6]. A limited improvement in exercise capacity has been demonstrated when COPD patients receive pulmonary or combined heart-lung transplant [7]-[9]
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