Please use this identifier to cite or link to this item: http://www.repositorio.ufop.br/handle/123456789/2103
Title: N-(2-mercaptopropionyl)-glycine but not Allopurinol prevented cigarette smoke-induced alveolar enlargement in mouse.
Authors: Pires, Karla Maria Pereira
Bezerra, Frank Silva
Machado, Mariana Nascimento
Zin, Walter Araújo
Porto, Luís Cristovão de Moraes Sobrino
Valença, Samuel dos Santos
Keywords: Cigarette
Alveolar space enlargement
Lung inflammation
Oxidative stress
Issue Date: 2011
Citation: PIRES, K. M. P. et al. N-(2-mercaptopropionyl)-glycine but not Allopurinol prevented cigarette smoke-induced alveolar enlargement in mouse. Respiratory Physiology & Neurobiology, v. 175, n.3, p.322-330, mar. 2011. Disponível em: <http://exabytetechservices.com/xml/678-all-20120605-k/23254193N.article.fulltext.000001.pdf>. Acesso em: 29 jan. 2013.
Abstract: We investigated the possible protective effects of the Allopurinol (A), N-(2-mercaptopropionyl)-glycine (M) and N-acetylcysteine (N) against lung injury caused by long-term exposure to cigarette smoke (CS) in mouse. C57BL6 mice were exposed to 12 cigarettes a day for 60 days and concomitantly treated with either one of the antioxidant drugs diluted in saline (CS + A—50 mg/kg; CS + M—200 mg/kg/day; CS + N—200 mg/kg/day). Control groups were sham-smoked (AA). Long-term CS exposure results in extensive parenchyma destruction in CS group. Both CS + N and CS + M groups showed preserved alveolar structure and showed preserved lung function when compared to CS group. Macrophage and neutrophil counts were decreased in CS + M, and CS + N groups when compared to CS group (p < 0.05). Antioxidant enzyme activities were reduced in all treated groups. CS + A showed the highest reduction in catalase activity (−25%, p < 0.01). We conclude that M treatment reduced long-term CS-induced inflammatory lung parenchyma destruction and lung function, comparable to N treatment, however, antioxidant administration did not reverse CS-induced antioxidant enzyme activity reduction.
URI: http://www.repositorio.ufop.br/handle/123456789/2103
ISSN: 15699048
metadata.dc.rights.license: O Periódico Respiratory Physiology & Neurobiology concede permissão para depósito deste artigo no Repositório Institucional da UFOP. Número da licença: 3314940932402
Appears in Collections:DECBI - Artigos publicados em periódicos

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