Supplementation with vitamins C and E improves mouse lung repair

Valença, Samuel Santos; Bezerra, Frank Silva; Romana‐Souza, Bruna; Paiva, Rojane Oliveira; Monte‐Alto‐Costa, Andréa; Pôrto, Luís Cristóvão

doi:10.1016/j.jnutbio.2007.08.004

Cited by 28 publications

(10 citation statements)

References 37 publications

(52 reference statements)

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“…The mice were subjected to these four-cigarette treatments three times per day (morning, noon, and afternoon), resulting in 72 min of CS exposure (12 cigarettes per day). ( 16 ) Each cigarette smoked produced 300 mg/m 3 of total particulate matter in the exposure chamber. ( 3 ) The animals were sacrificed by cervical dislocation at 24 h after the final CS exposure.…”

Section: Methodsmentioning

confidence: 99%

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

et al. 2014

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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.

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Section: Methodsmentioning

confidence: 99%

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

et al. 2014

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“…For differential cell counts, 100 μl of BALF were smeared on glass slides, then dried and stained using rapid panoptic staining (Laborclin, Paraná, Brazil). Two hundred cells per animal were classified as neutrophils, macrophages or lymphocytes and expressed as a percentage of recovered cells (Valença et al. 2008).…”

Section: Methodsmentioning

confidence: 99%

Bark extract of Bathysa cuspidata attenuates extra‐pulmonary acute lung injury induced by paraquat and reduces mortality in rats

Novaes

Gonçalves

Cupertino

et al. 2012

Int J Experimental Path

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This study investigated the effect of the bark extract of Bathysa cuspidata on paraquat (PQ)-induced extra-pulmonary acute lung injury (ALI) and mortality in rats. ALI was induced with a single dose of PQ (30 mg/kg, i.p.), and animals were treated with B. cuspidata extract (200 and 400 mg/kg). Analyses were conducted of survival, cell migration, lung oedema, malondialdehyde, proteins carbonyls, catalase, superoxide dismutase, histopathology and the stereology of lung tissue. Rats exposed to PQ and treated with 200 and 400 mg of the extract presented lower mortality (20% and 30%), compared with PQ alone group (50%). Furthermore, lung oedema, septal thickening, alveolar collapse, haemorrhage, cell migration, malondialdehyde and proteins carbonyl levels decreased, and catalase and superoxide dismutase activity were maintained. These results show that the bark extract of B. cuspidata reduced PQ-induced extra-pulmonary ALI and mortality in rats and suggest that these effects may be associated with the inhibition of oxidative damage.

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“…Of human SODs, Cu/Zn-SOD accounts for 80% of all SOD activities within the lung (Kinnula and Crapo, 2003). Altered levels of expression and activity of SOD were observed in both patients with COPD and animals treated with elastase or CS (animal models for COPD) (Kondo et al, 1994;Daga et al, 2003;Valenca et al, 2008), and transgenic mice expressing Cu/Zn-SOD were resistant to elastase-or CSinduced pulmonary emphysema (Foronjy et al, 2006). Furthermore, transgenic mice expressing another type of SOD, extracellular SOD, or knockout mice for this protein were resistant or sensitive, respectively, to elastase-or CS-induced pulmonary emphysema through attenuating oxidative fragmentation of extracellular matrix (Yao et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Effect of Lecithinized Superoxide Dismutase on Pulmonary Emphysema

Tanaka

Tanaka²,

Miyazaki³

et al. 2011

J Pharmacol Exp Ther

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No medication exists that clearly improves the mortality of chronic obstructive pulmonary disease (COPD). Oxidative molecules, in particular superoxide anions, play important roles in the COPD-associated abnormal inflammatory response and pulmonary emphysema, which arises because of an imbalance in proteases and antiproteases and increased apoptosis. Superoxide dismutase (SOD) catalyzes the dismutation of superoxide anions. Lecithinized human Cu/Zn-SOD (PC-SOD) has overcome a number of the clinical limitations of SOD, including low tissue affinity and low stability in plasma. In this study, we examine the effect of PC-SOD on elastase-induced pulmonary emphysema, an animal model of COPD. The severity of the pulmonary inflammatory response and emphysema in mice was assessed by various criteria, such as the number of leukocytes in the bronchoalveolar lavage fluid and the enlargement of airspace. Not only intravenous administration but also inhalation of PC-SOD suppressed elastase-induced pulmonary inflammation, emphysema, and dysfunction. Inhalation of PC-SOD suppressed the elastase-induced increase in the pulmonary level of superoxide anions and apoptosis. Inhalation of PC-SOD also suppressed elastase-induced activation of proteases and decreased in the level of antiproteases and expression of proinflammatory cytokines and chemokines. We also found that inhalation of PC-SOD suppressed cigarette smokeinduced pulmonary inflammation. The results suggest that PC-SOD protects against pulmonary emphysema by decreasing the pulmonary level of superoxide anions, resulting in the inhibition of inflammation and apoptosis and amelioration of the protease/antiprotease imbalance. We propose that inhalation of PC-SOD would be therapeutically beneficial for COPD.

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Supplementation with vitamins C and E improves mouse lung repair

Cited by 28 publications

References 37 publications

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

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

Bark extract of Bathysa cuspidata attenuates extra‐pulmonary acute lung injury induced by paraquat and reduces mortality in rats

Therapeutic Effect of Lecithinized Superoxide Dismutase on Pulmonary Emphysema

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