| Abstract: | OBJECTIVE: To evaluate oxidative damage (lipid oxidation, protein oxidation, thiobarbituricacid-reactive substances [TBARS], and carbonylation) and inflammation (expressionof phosphorylated AMP-activated protein kinase and mammalian target of rapamycin[p-AMPK and p-mTOR, respectively]) in the lung parenchyma and diaphragm muscles ofmale C57BL-6 mice exposed to cigarette smoke (CS) for 7, 15, 30, 45, or 60 days.METHODS: Thirty-six male C57BL-6 mice were divided into six groups (n = 6/group): acontrol group; and five groups exposed to CS for 7, 15, 30, 45, and 60 days,respectively. RESULTS: Compared with control mice, CS-exposed mice presented lower body weights at 30days. In CS-exposed mice (compared with control mice), the greatest differences(increases) in TBARS levels were observed on day 7 in diaphragm-muscle, comparedwith day 45 in lung tissue; the greatest differences (increases) in carbonyllevels were observed on day 7 in both tissue types; and sulfhydryl levels werelower, in both tissue types, at all time points. In lung tissue and diaphragmmuscle, p-AMPK expression exhibited behavior similar to that of TBARS. Expressionof p-mTOR was higher than the control value on days 7 and 15 in lung tissue, as itwas on day 45 in diaphragm muscle. CONCLUSION: Our data demonstrate that CS exposure produces oxidative damage, not only in lungtissue but also (primarily) in muscle tissue, having an additional effect onrespiratory muscle, as is frequently observed in smokers with COPD. |
