Oxidative damage of sulfur dioxide inhalation on lungs and hearts of mice

Abstract

Effects of sulfur dioxide (SO 2) on concentrations of thiobarbituric acid-reactive substances (TBARS) and reduced glutathione (GSH), activities of Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were investigated in lungs and hearts of Kunming albino mice of both sexes. The mice of SO 2 groups were exposed to various concentrations (22, 56, and 112 mg/m 3) of SO 2 in separate exposure chambers for 6 h/day for 7 days, whereas control groups were exposed to filtered air under otherwise the same conditions. Our results show that SO 2 caused lipid peroxidation and changes of antioxidative status in both lungs and hearts of mice. Exposure to SO 2 at all concentrations tested caused a significant increase of TBARS and a significant decrease in GSH content in lungs and hearts of mice, with the exception of GSH content in the hearts of female mice. For lungs, SO 2 at low concentrations significantly increased SOD and GPx activities, whereas at high concentrations it significantly decreased these same activities in mice of both sexes. For hearts, SO 2 at all tested concentrations significantly decreased activities of SOD from mice of both sexes, as well as that of GPx from male mice, but the decrease of GPx activities in hearts from female mice was statistically insignificant. SO 2 inhalation tended to decrease activities of CAT in lungs and hearts from mice of both sexes, whereas only the decrease of CAT activities caused by SO 2 in lungs from male mice was statistically significant, at 112 mg/m 3. The results also show a gender difference in oxidative stress and antioxidation status caused by SO 2 exposure. These results lead us to conclude that SO 2 exposure can cause oxidative damage to lungs and hearts of mice, and SO 2 is toxic not only to the respiratory system, but to the heart as well. Additional work is required to understand the toxicological role of SO 2 on many or even all mammalian organs.