Publications (2)2.8 Total impact
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Article: Low tidal volume mechanical ventilation and oxidative stress in healthy mouse lungs.
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ABSTRACT: Mechanical ventilation (MV) itself can directly contribute to lung injury. Therefore, the aim of the present study was to investigate early biomarkers concerning oxidant/antioxidant balance, oxidative stress, and inflammation caused by short-term MV in healthy mouse lungs. Twenty male C57BL/6 mice were randomly divided into two groups: MV, submitted to low tidal volume (V T, 6 mL/kg) MV for 30 min; and spontaneous respiration (SR), used as controls. Lung homogenate samples were tested regarding the activity of various antioxidant enzymes, lipid peroxidation, and TNF-α expression. In comparison with the SR group, the MV group showed a significant decrease in the activity of superoxide dismutase (≈35%; p < 0.05), together with an increase in the activity of catalase (40%; p < 0.01), glutathione peroxidase (500%; p < 0.001), and myeloperoxidase (260%; p < 0.001), as well as a reduction in the glutathione/oxidized glutathione ratio (≈50%; p < 0.05) and an increase in TNF-α expression in the MV group. Oxidative damage, assessed by lipid peroxidation, was also greater in the MV group (45%; p < 0.05). Our results show that short-term low V T MV can directly contribute to lung injury, generating oxidative stress and inflammation in healthy mouse lungs.Jornal brasileiro de pneumologia: publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia 02/2012; 38(1):98-104. -
Article: L-NAME and L-arginine differentially ameliorate cigarette smoke-induced emphysema in mice.
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ABSTRACT: Nitric oxide (NO) represents one of the most important intra- and extracellular mediators and takes part in both biologic and pathologic processes. This study aimed to verify the treatment with an NO inhibitor and an NO substrate in pulmonary emphysema induced by cigarette smoke (CS) in a murine model. We compared N-acetylcysteine (NAC), a precursor of glutathione, to G-nitro-L-arginine-methyl ester or L-NAME (LN), which is an NO inhibitor, and to l-arginine (LA), which is a substrate for NO formation. Mice were divided into several groups: control, CS, CS + LN, CS + LA, and CS + NAC. Control and CS groups were treated daily with a vehicle, while CS + LN, CS + LA, and CS + NAC groups were treated daily with LN (60 mg/kg), LA (120 mg/kg) and NAC (200 mg/kg), respectively. The bronchoalveolar lavage was analyzed and the lungs were removed for histological and biochemical analysis. CS increases neutrophil number. Neutrophil number was lowest in CS + LN, followed by CS + LA. The lungs of CS + LN, CS + LA and CS + NAC mice were protected compared to the lungs of CS mice, but not equal to the quality of lungs in control mice. The CS group also exhibited increased oxidative stress, which was also present in the CS + LN group and to a lesser extent in the CS + LA group. Tissue inhibitor of metalloproteinase 1 and 2 increased in the CS + LN group and to a lesser extent in the CS + LA group relative to the control group. These results suggest that LN and LA treatment protected the mouse lung from CS. However, NAC treatment was more than LN and LA. We suggest that the protection conferred by LN treatment requires a balance between proteases and antiproteases, and that protection conferred by LA treatment involves the balance between oxidants and antioxidants.Pulmonary Pharmacology & Therapeutics 05/2011; 24(5):587-94. · 2.80 Impact Factor
