Oxidative damage induced by cigarette smoke exposure in mice: impact on lung tissue and diaphragm muscle,

Abstract

OBJECTIVE: To evaluate oxidative damage (lipid oxidation, protein oxidation, thiobarbituric acid-reactive substances [TBARS], and carbonylation) and inflammation (expression of phosphorylated AMP-activated protein kinase and mammalian target of rapamycin [p-AMPK and p-mTOR, respectively]) in the lung parenchyma and diaphragm muscles of male 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): a control 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 30 days. In CS-exposed mice (compared with control mice), the greatest differences (increases) in TBARS levels were observed on day 7 in diaphragm-muscle, compared with day 45 in lung tissue; the greatest differences (increases) in carbonyl levels were observed on day 7 in both tissue types; and sulfhydryl levels were lower, in both tissue types, at all time points. In lung tissue and diaphragm muscle, p-AMPK expression exhibited behavior similar to that of TBARS. Expression of p-mTOR was higher than the control value on days 7 and 15 in lung tissue, as it was on day 45 in diaphragm muscle. CONCLUSION: Our data demonstrate that CS exposure produces oxidative damage, not only in lung tissue but also (primarily) in muscle tissue, having an additional effect on respiratory muscle, as is frequently observed in smokers with COPD.

Impaired calcium signaling in muscle fibers from intercostal and foot skeletal muscle in a cigarette smoke-induced mouse model of COPD

“…Importantly, this mouse model is a valuable tool for further examination of the role of smoking in the systemic pathogenesis in COPD, such as respiratory [62][63][64] and skeletal muscle atrophy and dysfunction. [31][32][33] In conclusion, in this report, we demonstrate the effects of chronic cigarette exposure on actionpotential induced Ca 21 transients in intercostal and intrinsic foot muscles. The intrinsic muscles of the foot are important for ambulation and balance in bipeds and quadrupeds, including humans and small mammals.…”

“…Nevertheless, whole‐body cigarette smoke exposure has been previously demonstrated to produce emphysematous mice, with alveolar destruction and airspace enlargement, the hallmarks of emphysema. Importantly, this mouse model is a valuable tool for further examination of the role of smoking in the systemic pathogenesis in COPD, such as respiratory and skeletal muscle atrophy and dysfunction …”

“…Muscle tissues were isolated from control and 6 month whole‐body cigarette smoke‐exposed mice. This 6‐month whole‐body cigarette smoke exposure is known to cause muscle dysfunction in different species, including mice . The procedures for isolating single muscle fibers were previously described in detail .…”

“…This 6-month wholebody cigarette smoke exposure is known to cause muscle dysfunction in different species, including mice. [31][32][33] The procedures for isolating single muscle fibers were previously described in detail. 34 In brief, intercostal (combined internal and external) and FDB muscles were dissected and enzymatically digested, then mechanically triturated with a polished glass pipette.…”

Effects of passive inhalation of cigarette smoke on structural and functional parameters in the respiratory system of guinea pigs

“… 26 , 35 Carlos et al, 26 in a study in which male (C57BL/6) mice were exposed to smoke from 12 cigarettes a day for 7, 15, 30, 45, and 60 days, identified that the oxidative stress induced by cigarette smoke caused changes in the lungs and in the diaphragm. Those authors added that the oxidative stress caused by exposure to cigarette smoke occurs first in the skeletal muscle and subsequently in the lung tissue.…”