A new murine oxidative stress model associated with senescence.

A murine oxidative stress model was established via ozone inhalation, which was identified by detection of the response of antioxidant defense system, levels of oxidative products and effects of natural antioxidants on this model. Male BALB/c mice were exposed to 1.2 mg/m(3) ozone for 10 h per day. The control group was exposed to flowing air. From inhaling ozone, mice were killed at day 5, 10, 15 and 20, respectively. Exposure to ozone made mice show the increase of malondialdehyde (MDA) contents in heart, kidney and liver, as well as 8-OHdG levels in urine, and resulted in cytological nuclear concentration in brain neurons or thymocytes. Ozone exposure also impaired antioxidative capacity such as the decrease of total antioxidation capacity (TAC) in sera, reduced glutathione (GSH) in sera or thymus and glutathione-S-transferase (GST) activity in spleen or thymus but not in liver. Correlation analysis showed the significant inverse correlation (r=-0.894, P<0.05) between thymus weight index and inhalation doses of ozone. Meanwhile, thymocyte in model mice proliferated more poorly than normal controls. Catechin and clove extract could reverse parts of changes above induced by ozone inhalation. These results suggest that exposure to ozone can result in an increased production of reactive oxygen species in vivo, which causes oxidative stress. The mice under oxidative stress showed senescence-related alterations in physiological parameters as well. Taken together, our data demonstrates that an oxidative stress model in mice has been successfully established by ozone inhalation, which would be helpful to probe the relationship between oxidative stress and senescence and evaluate effects of antioxidants.