Oxidative damage of sulfur dioxide inhalation on brains and livers of mice.

The effects of sulfur dioxide (SO(2)) on levels of thiobarbituric acid reactive substances (TBARS), levels of reduced glutathione(GSH) and the activities of Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) were investigated in brains and livers of Kunming albino mice of both sexes. SO(2) at different concentrations (22, 56 and 112 mg/m(3)) was administered to animals of SO(2) groups in different exposure chambers for 6 h/day for 7 days, while control groups were exposed to filtered air in the same condition. Our results show that SO(2) caused lipid peroxidation and changes of antioxidative status in brains and livers of mice. Exposure to SO(2) at all concentrations tested caused significantly the increase of TRARS levels in brains and livers of mice. For the brains, activities of these antioxidant enzymes and levels of GSH were significantly unaltered by SO(2) at low concentrations, except significant increase of GSH levels in the brains of male mice; however, SO(2) at higher concentrations caused significantly decreases of GSH levels and activities of these antioxidant enzymes. For livers, SO(2) at all concentrations tested decreased significantly activities of SOD relative to control animals; SO(2) tended to decrease activities of GPx and CAT, but only the decreases of GPx and CAT activities caused by SO(2) exposures of higher concentrations (56 and 112 mg/m(3)) were statistically significant. SO(2) also tended to decrease levels of GSH, but only at 112 mg/m(3) caused significantly decrease of GSH levels in livers of both sexual mice. Unexpectedly, the decreases of activities of these antioxidative enzymes caused by SO(2) at different concentrations in brains and livers of mice did not follow a linear dose-response curves. In many respects, the decreased percentages of the activities of each antioxidative enzyme (SOD or GPx or CAT) caused by SO(2) at 22, 56 and 112 mg/m(3) in brains and livers of mice were similar. These results lead to conclusion that SO(2) exposure can caused oxidative damage to brains and livers of mice, and SO(2) is a toxin to brain and liver of mammals, not only to respiratory system. Further work is required to understand toxicological role of SO(2) on multiply or even all organs in human and animal.