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.

中文翻译：

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吸入二氧化硫对小鼠大脑和肝脏的氧化损伤。

二氧化硫（SO（2））对硫代巴比妥酸反应性物质（TBARS）的水平，还原型谷胱甘肽（GSH）的水平以及铜锌超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GPx）和过氧化氢酶活性的影响（CAT）在昆明两性白化小鼠的大脑和肝脏中进行了研究。将SO（2）以不同的浓度（22、56和112 mg / m（3））分别在不同的暴露室中对SO（2）组的动物施用6 h / day，共7天，而对照组则暴露于过滤空气在相同条件下。我们的结果表明，SO（2）引起小鼠脑和肝脏中脂质过氧化和抗氧化状态的变化。在所有测试浓度下都暴露于SO（2）会导致小鼠脑和肝中TRARS水平的显着增加。为了大脑 这些抗氧化酶的活性和谷胱甘肽水平在低浓度下不会被SO（2）改变，除了雄性小鼠大脑中谷胱甘肽水平显着增加外；但是，较高浓度的SO（2）会导致GSH含量和这些抗氧化酶活性的显着降低。对于肝脏，相对于对照动物，所有测试浓度下的SO（2）均显着降低了SOD的活性。SO（2）倾向于降低GPx和CAT的活性，但只有SO（2）暴露于较高浓度（56和112 mg / m（3））引起的GPx和CAT活性降低具有统计学意义。SO（2）也倾向于降低GSH的水平，但仅以112 mg / m（3）引起两只性小鼠肝脏中GSH的显着降低。不料，SO（2）在小鼠的大脑和肝脏中不同浓度引起的这些抗氧化酶活性的降低并未遵循线性的剂量反应曲线。在许多方面，SO（2）分别以22、56和112 mg / m（3）在小鼠的大脑和肝脏中引起的每种抗氧化酶（SOD或GPx或CAT）活性降低的百分比相似。这些结果得出结论，SO（2）的暴露可能对小鼠的大脑和肝脏造成氧化损伤，而SO（2）是哺乳动物的大脑和肝脏的毒素，而不仅是呼吸系统的毒素。需要进一步的工作来了解SO（2）对人类和动物的多个甚至所有器官的毒理作用。SO（2）以22、56和112 mg / m（3）在小鼠的大脑和肝脏中引起的每种抗氧化酶（SOD或GPx或CAT）的活性降低百分比相似。这些结果得出结论，SO（2）的暴露可能对小鼠的大脑和肝脏造成氧化损伤，而SO（2）是哺乳动物的大脑和肝脏的毒素，而不仅是呼吸系统的毒素。需要进一步的工作来了解SO（2）对人类和动物的多个甚至所有器官的毒理作用。SO（2）以22、56和112 mg / m（3）在小鼠的大脑和肝脏中引起的每种抗氧化酶（SOD或GPx或CAT）的活性降低百分比相似。这些结果得出结论，SO（2）的接触会导致小鼠大脑和肝脏的氧化损伤，而SO（2）是哺乳动物的大脑和肝脏的毒素，而不仅是呼吸系统的毒素。需要进一步的工作来了解SO（2）对人类和动物的多个甚至所有器官的毒理作用。