Acute exposure of ozone induced pulmonary injury and the protective role of vitamin E through the Nrf2 pathway in Balb/c mice.

Ozone (O3) in the lower atmosphere is generally derived from various sources of human activity. It has become a major air pollutant in China and has been shown to adversely affect the health of humans and animals. We undertook a study to ascertain the molecular mechanism of ozone induced lung injury in mice and tried to demonstrate the protective mechanism of vitamin E. In this study, mice were exposed to clean air and three different concentrations of ozone. Oxidative stress (reactive oxygen species and malondialdehyde) and Th cytokines in the lung, serum IgE, as well as histopathological examination and the airway hyper-responsiveness (AHR) test were used to reflect inflammation and damage to the lungs of ozone-exposed mice. We then chose an effective concentration of ozone and combined treatment with vitamin E (VE) to explore the underlying mechanism of ozone-induced lung damage. The results of immunological and inflammatory biomarkers (total-immunoglobulin (Ig) E and Th cytokines) as well as histopathological examination and AHR assessment supported the notion that high doses of ozone (>0.5 ppm) could induce inflammation and lung injury in mice and that this induction was counteracted by concurrent administration of VE. The elimination of oxidative stress, the reduced Th2 responses and Ig production, and the relief of lung damage were proposed to explain the molecular mechanism of ozone induced lung injury. We also showed that VE, an antioxidant that enhanced the expression of Nrf2 and up-regulated the antioxidant genes HO-1 and NQO1, could decrease the levels of oxidative stress and alleviate ozone-induced lung injury.