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Hypobaric-hypoxia-induced pulmonary damage in rats ameliorated by antioxidant erdosteine

Free radical-mediated injury to lung and pulmonary vasculature is an important mechanism in hypoxia-induced lung damage. In this study, we aimed to investigate the potential protective effects of erdosteine as an antioxidant agent on hypobaric hypoxia-induced pulmonary hypertension. Adult male rats...

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Published in:Acta histochemica 2006-01, Vol.108 (1), p.59-68
Main Authors: Uzun, Özge, Balbay, Öner, Üstündagˇ Çomunogˇlu, Nil, Yavuz, Özlem, Nihat Annakkaya, Ali, Güler, Selver, Silan, Coşkun, Erbaş, Mete, Arbak, Peri
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Language:English
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Summary:Free radical-mediated injury to lung and pulmonary vasculature is an important mechanism in hypoxia-induced lung damage. In this study, we aimed to investigate the potential protective effects of erdosteine as an antioxidant agent on hypobaric hypoxia-induced pulmonary hypertension. Adult male rats were assigned randomly to three groups. The first group of rats was exposed to hypobaric–hypoxia and the second group was treated with erdosteine (20 mg/kg, daily) for 2 weeks, during which time they were in a hypoxic chamber. These groups were compared with normoxic controls. All rats were sacrificed after 2 weeks. The hypoxia-induced increase in right ventricle to left ventricle plus septum weight ratio (from 0.20±0.01 to 0.26±0.01) was reduced significantly in the erdosteine-treated group (0.23±0.01). Malondialdehyde levels were elevated (from 0.33±0.11 to 0.59±0.02) and total antioxidant status was not changed significantly (from 1.77±0.42 to 2.61±0.23) by hypoxia. In contrast to the hypoxia-exposed group, malondialdehyde levels were significantly decreased in the erdosteine-treated group (0.37±0.02). Total antioxidant status (4.03±0.22) was significantly higher in erdosteine-treated rats when compared to non-treated rats. Histopathological examination demonstrated that erdosteine prevented inflammation and protected lung parenchyma and pulmonary endothelium of hypoxia-exposed rats.
ISSN:0065-1281
1618-0372
DOI:10.1016/j.acthis.2006.01.001