Lung injury-dependent oxidative status and chymotrypsin-like activity of skeletal muscles in hamsters with experimental emphysema.
BACKGROUND
Peripheral skeletal muscle is altered in patients suffering from emphysema and chronic obstructive pulmonary disease (COPD). Oxidative stress have been demonstrated to participate on skeletal muscle loss of several states, including disuse atrophy, mechanical ventilation, and chronic diseases. No evidences have demonstrated the occurance in a severity manner.


METHODS
We evaluated body weight, muscle loss, oxidative stress, and chymotrypsin-like proteolytic activity in the gastrocnemius muscle of emphysemic hamsters. The experimental animals had 2 different severities of lung damage from experimental emphysema induced by 20 mg/mL (E20) and 40 mg/mL (E40) papain.


RESULTS
The severity of emphysema increased significantly in E20 (60.52 ± 2.8, p < 0.05) and E40 (52.27 ± 4.7; crossed the alveolar intercepts) groups. As compared to the control group, there was a reduction on body (171.6 ± 15.9 g) and muscle weight (251.87 ± 24.87 mg) in the E20 group (157.5 ± 10.3 mg and 230.12 ± 23.52 mg, for body and muscle weight, respectively), which was accentuated in the E40 group (137.4 ± 7.2 g and 197.87 ± 10.49 mg, for body and muscle weight, respectively). Additionally, the thiobarbituric acid reactive substances (TBARS), tert-butyl hydroperoxide-initiated chemiluminescence (CL), carbonylated proteins, and chymotrypsin-like proteolytic activity were elevated in the E40 group as compared to the E20 group (p < 0.05 for all comparisons). The severity of emphysema significantly correlated with the progressive increase in CL (r = -0.95), TBARS (r = -0.98), carbonyl proteins (r = -0.99), and chymotrypsin-like proteolytic activity (r = -0.90). Furthermore, augmentation of proteolytic activity correlated significantly with CL (r = 0.97), TBARS (r = 0.96), and carbonyl proteins (r = 0.91).


CONCLUSIONS
Taken together, the results of the present study suggest that muscle atrophy observed in this model of emphysema is mediated by increased muscle chymotrypsin-like activity, with possible involvement of oxidative stress in a severity-dependent manner.
Laboratory of Free Radicals and Pathophysiology, Department of General Pathology, Londrina, Brazil.
Jair
J
Tonon
Alessandra Lourenço
AL
Cecchini
Cláudia Roberta
CR
Brunnquell
Sara Santos
SS
Bernardes
Rubens
R
Cecchini
Flávia Alessandra
FA
Guarnier
D000818:Animals; D001835:Body Weight; D002918:Chymotrypsin / Q000378:metabolism*; D006224:Cricetinae; D004195:Disease Models, Animal; D008168:Lung / Q000473:pathology; D008297:Male; D008647:Mesocricetus; D018482:Muscle, Skeletal / Q000201:enzymology* / Q000473:pathology; D009133:Muscular Atrophy / Q000201:enzymology / Q000209:etiology* / Q000473:pathology; D009929:Organ Size; D018384:Oxidative Stress; D010206:Papain; D050050:Protein Carbonylation; D011656:Pulmonary Emphysema / Q000139:chemically induced / Q000150:complications* / Q000201:enzymology / Q000473:pathology; D012720:Severity of Illness Index; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D020122:tert-Butylhydroperoxide / Q000378:metabolism
D017392:Thiobarbituric Acid Reactive Substances; D020122:tert-Butylhydroperoxide; D002918:Chymotrypsin; D010206:Papain