The effects of physical exercise on the cigarette smoke-induced pulmonary oxidative response.
Studies have shown that the oxidative power of cigarettes is related to the pathogenesis of several pulmonary diseases and that regular physical exercise contributes significantly to reducing the deleterious effects of cigarettes. The objective of the present study was to investigate the therapeutic effects of physical exercise on histological and oxidative stress markers in animals exposed to cigarette smoke. Thirty-six male, eight-week-old C57BL-6 mice were divided into four groups (n = 9 for each group): control, exercise, cigarette smoke, and cigarette smoke plus exercise. The cigarette smoke (CS) groups were exposed to cigarette smoke 3 times/day (4 cigarettes/session) for 60 consecutive days. The exercise groups were submitted to swimming physical training 5 days/week for eight weeks. Forty-eight hours after the last exercise and cigarette exposure, the animals were sacrificed using cervical traction. The right lung was removed, processed, and stored for future analysis. In addition to the analysis of collagen content (hydroxyproline), oxidant production (anion superoxide), antioxidant enzyme activity (SOD and CAT), and lipid and protein oxidative damage (TBARS and Carbonylation), histological and morphological studies were performed. The results revealed that the animals exposed to cigarette smoke showed enlargement and destruction of the alveolar septum and increases in the numbers of macrophages and neutrophils, as well as in the amount of collagen. Our results also showed a decrease in the volume density of elastic fibers and an increase in the volume density of airspaces. However, physical exercise partially improved these markers. Additionally, physical exercise decreased oxidant production and increased the activity of the enzymatic antioxidant defense system, but did not reverse lipid and protein oxidative damage induced by cigarette smoke. These results suggest that physical training partially improves histological and oxidative stress parameters in the lungs of animals chronically exposed to cigarette smoke and that other therapies can contribute to potentiate these effects.
Menegali
Bruno T
BT
Exercise Biochemistry and Physiology Laboratory, Postgraduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciuma, Santa Catarina, Brazil.
Nesi
Renata T
RT
Souza
Priscila S
PS
Silva
Luciano A
LA
Silveira
Paulo C L
PC
Valença
Samuel S
SS
Pinho
Ricardo A
RA
D000818:Animals; D002374:Catalase / Q000378:metabolism; D006909:Hydroxyproline / Q000378:metabolism; D019344:Lactic Acid / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008168:Lung / Q000502:physiology*; D008264:Macrophages / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000187:drug effects; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D050050:Protein Carbonylation / Q000187:drug effects; D012907:Smoking / Q000473:pathology*; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
D013481:Superoxides; D019344:Lactic Acid; D002374:Catalase; D013482:Superoxide Dismutase; D006909:Hydroxyproline