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Hyperoxia‐induced a time‐dependent lung oxidative stress in BALB/c mice
Author(s) -
Valenca Samuel S,
Nagato Akinori C,
Bezerra Frank S,
Lopes Alan A,
Santos Thiago,
Lanzetti Manuella,
Porto Luis Cristovao
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.572.5
Subject(s) - hyperoxia , oxidative stress , chemistry , malondialdehyde , hydroxyproline , lung , bronchoalveolar lavage , catalase , myeloperoxidase , superoxide dismutase , andrology , endocrinology , medicine , inflammation , biochemistry
The effects of hyperoxia in mouse lung are unclear. Our aim was to study lung oxidative responses of hyperoxia in 12, 24 and 48 h in mouse. Thirty mice were exposed to 100% of oxygen for 12, 24 or 48 h. Control group was exposed to normoxia (CG). After exposure mice were sacrificed, bronchoalveolar lavage (BAL) performed and lungs were removed for histological and biochemical analysis. We observed an increase (p<0.001) of total leukocytes in BAL (cells x103/ml) in 48h when compared with CG. Myeloperoxidase (mU/mg ptn) was increased in 24h (p<0.001) and 48h (p<0.05) when compared with CG. Catalase activity (U/mg ptn) was increased in 48h (p<0.001) when compared with CG. Nitrite was increased in 12h and 24h (p<0.001) when compared with CG. The ratio GSH/GSSG (nM/mg ptn) was reduced in 12h and 24h (p<0.05) when compared with CG. Positive cells for TNF‐á was observed in 24h and 48h when compared with CG. Alveolar septa were thickened in 48h, but red blood cells in alveoli were observed in all times of exposure to hyperoxia. MMP‐2 and MMP‐9 activity was increased progressively at 12, 24h and 48 h when compared with CG. The levels of malondialdehyde (nM/mg ptn ‐ p<0.05) and hydroxyproline (ng/mg ptn ‐ p<0.001) were increased in 12h and 24h when compared with CG. Our results indicate harmful effects of hyperoxia mainly at 24 and 48 h with clear evidence of oxidants/antioxidants imbalance. Supported by FAPERJ and CNPq.