| Sulfur dioxide (SO2), a common pollutant of urban air, can severely produce toxic symptoms in both humans and animals. It can cause respiratory tract diseases such as tracheitis, asthma, emphysema, and has close relations with lung cancer. Several studies have shown that SO2 and its derivatives could induce chromosomal aberrations, sister chromatid exchanges and micronuclei in human blood lymphocyte, bone marrow cell in mice and CHL. However, little information is available about the mechanism of sulfur dioxide toxicity to genetic materials and other large biological molecules. It has been reported that exposures to sulfur dioxide may cause increase of lipid peroxidation (LPO). Glutathione redox system as the important parts of defense systems was studied after exposure to sulfur dioxide at different concentrations. DNA damage caused by SO2 and lead acetate were also studied. Protective roles of seabuckthorn seed oil on oxidative damage caused by SO2 in liver and lung of mice were also investigated. In addition, effect of SO2 inhalation on the serum cytokine of peripheral blood was determined through the methods of molecular immunology. These studies further indicated that oxidative stress maybe plays an important role in the mechanisms of sulfur dioxide toxicity.This study was to investigate the effects of sulfur dioxide inhalation at different concentrations on some glutathione-related enzymes such as Glutathione S-transferase (GST), Glucose 6-phosphate dehydrogenase (G6PD) and Glutathione reductase (Gred) in brain, lung, heart, liver, kidney and spleen of mice by the technology of biochemical toxicology. The results were showed as follows, SO2 exposure at different concentrations caused the changes of glutathione redox system. Moreover, the activities of antioxidative enzymes and the contents of reduced glutathione (GSH) were decreased significantly in different tissues athigher concentrations of SOa. The conclusions further elucidate the damages such as metabolic alteration, membrane damage, enzyme inactivation and genetic alteration may be resulted from the change of glutathione redox system caused by SO2.Protective roles of seabuckthorn seed oil on oxidative damage induced by SO2 were also processed. In preventive groups, the levels of LPO in liver and lung were decreased and the activities of GST were increased compared with those in SO2 inhalation group. With higher dosage of seabuckthorn seed oil administrated introperitoneally (6ml/kg body weight, 8ml/kg body weight), LPO and GST changed significantly. It was showed that seabuckthorn seed oil treatment born more protective roles to lung than liver.DNA damages caused by SO2 and lead acetate were studied with the single cell microgel electrophoresis technique (or Comet assay) in order to confirm the damaging degree of lead (as an important component of atmosphere particle matter) on DNA from male mice exposed to SO2. The migrating distances of DNA of brain, lung, spleen and kidney cells of mice increased significantly, compared to the control group under conditions of single and combined poisoning of SO2 (42mg/m3) and lead acetate (0.2%), and lead could strengthen DNA damage degree by SO2 in nuclear DNA of brain, kidney, spleen cells. Damaging degree of SO2 on nuclear DNA of lung cell of mice was more severe than that of lead. The migrating distance of nuclear DNA of lung of mice in combined action group of SO2 and lead acetate had significant difference to that of lead acetate single action group (P<0.01), but no difference to SO2 single action group. It showed that both SO2 and lead acetate could induce DNA damage in mice cells and their damaging degrees were different in brain, lung, spleen, kidney, and under certain conditions, there existed significant synergistic joint action, thus could enhance mutual toxicity.Influences of SO2 inhalation on the serum cytokine of peripheral blood of mice were determined with Enzymes Linked Immunosorbant Assays (ELISA). It was showed that after exposure to SO2, the concentrations of Interleuk...
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