Time course of inflammation, oxidative stress and tissue damage induced by hyperoxia in mouse lungs.
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2012
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In this study our aim was to investigate the time courses of inflammation, oxidative
stress and tissue damage after hyperoxia in the mouse lung. Groups of BALB⁄ c mice
were exposed to 100% oxygen in a chamber for 12, 24 or 48 h. The controls were
subjected to normoxia. The results showed that IL-6 increased progressively after 12
(P < 0.001) and 24 h (P < 0.001) of hyperoxia with a reduction at 48 h (P < 0.01),
whereas TNF-a increased after 24 (P < 0.001) and 48 h (P < 0.001). The number of
macrophages increased after 24 h (P < 0.001), whereas the number of neutrophils
increased after 24 h (P < 0.01) and 48 h (P < 0.001). Superoxide dismutase activity
decreased in all groups exposed to hyperoxia (P < 0.01). Catalase activity increased
only at 48 h (P < 0.001). The reduced glutathione ⁄ oxidized glutathione ratio
decreased after 12 h (P < 0.01) and 24 h (P < 0.05). Histological evidence of lung
injury was observed at 24 and 48 h. This study shows that hyperoxia initially causes
an inflammatory response at 12 h, resulting in inflammation associated with the oxidative
response at 24 h and culminating in histological damage at 48 h. Knowledge
of the time course of inflammation and oxidative stress prior to histological evidence
of acute lung injury can improve the safety of oxygen therapy in patients.
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NAGATO, A. C. et al. Time course of inflammation, oxidative stress and tissue damage induced by hyperoxia in mouse lungs. International Journal of Experimental Pathology, v. 93, p. 269-278, 2012. Disponível em: <https://goo.gl/7Rk1I9>. Acesso em: 19 fev. 2017.