Oxidative damage of sulfur dioxide on various organs of mice: sulfur dioxide is a systemic oxidative damage agent.

Cu,Zn-superoxide dismutase (SOD), Se-dependent glutathione peroxidase (GSH-Px), catalase (CAT), and glutathione (GSH) play an important role in attenuating free radical-induced oxidative damage. The purpose of this research was to determine (1) whether sulfur dioxide (SO(2)) increases levels of lipid peroxidation and alters intracellular redox status in multiple organs of mice, and (2) whether SO(2) is a systemic toxic agent. The effect of SO(2) on levels of thiobarbituric acid-reactive substances (TBARS) and GSH and activities of SOD, GSH-Px, and CAT were investigated in nine organs (brain, lung, heart, liver, stomach, intestine, spleen, kidney, and testis) of Kunming albino mice of both sexes. SO(2) at 20 ppm (56 mg/m(3)) was administrated to the animals of SO(2) groups in an exposure chamber for 6 h/day for 7 days while control groups were exposed to filtered air in the same condition. Results show that SO(2) inhalation decreased significantly activities of SOD and GSH-Px in all organs tested in all SO(2) groups, with respect to their corresponding control groups; CAT activities in all organs tested of both sexual mice were significantly unaltered, except CAT activities in livers were significantly lowered by SO(2); SO(2) exposure decreased significantly GSH contents and significantly increased TBARS levels of all organs tested, in comparison with their respective control groups. These results lead to two conclusions: (1) SO(2) is a systemic oxidative damage agent. It results in a significant increase in the lipid peroxidation process in all organs tested of mice of both sexes, which is accompanied by changes of antioxidant status in these organs. (2) SO(2) may cause toxicological damage to multiple organs of animals, and it is suggested that the oxidative damage produced by SO(2) inhalation may influence or promote the progression or occurrence of some disease states of various organs, not only to respiratory system. Further work is required to understand the toxicological role of SO(2) on multiple or even all organs in mammals.