Oxidative damage of sulfur dioxide on various organs of mice: Sulfur dioxide is a systemic oxidative damage agent
Oxidative damage of sulfur dioxide on various organs of mice: Sulfur dioxide is a systemic oxidative damage agent
复制标题
DOI：
10.1080/08958370304476
复制
发表时间：
2003-02-01
影响因子：
2.1
通讯作者：
Meng, ZQ
中科院分区：
文献类型：
--
作者：
Meng, ZQ
铜锌超氧化物歧化酶(SOD)、硒依赖的谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)和谷胱甘肽(GSH)在减轻自由基氧化损伤中起重要作用。本研究的目的是确定(1)二氧化硫(SO2)是否增加小鼠多器官的脂质过氧化水平和改变细胞内氧化还原状态，以及(2)二氧化硫是否是一种全身性毒物。研究了SO2对昆明种白化小鼠脑、肺、心、肝、胃、肠、脾、肾、睾丸等9个脏器组织中硫代巴比妥酸反应物质(TBARS)、谷胱甘肽(GSH)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性的影响。给SO2组动物吸入20ppm(56 mg/m(3))的SO2，每天6小时，连续7天，对照组暴露在相同条件下的过滤空气中。结果表明，与相应对照组相比，SO2暴露组小鼠各器官组织中的SOD和GSH-Px活性均显著降低；与各自的对照组相比，SO2暴露组小鼠各器官组织中的CAT活性除肝脏CAT活性显著降低外，其余各器官组织中的CAT活性均无显著变化；这些结果得出两个结论：(1)SO2是一种全身性氧化损伤物质。其结果是，无论性别，受试小鼠的所有器官的脂质过氧化过程都显著增加，并伴随着这些器官中抗氧化状态的变化。(2)SO2可对动物多个器官造成毒性损伤，提示吸入SO2所产生的氧化损伤可能影响或促进各器官某些疾病状态的进展或发生，而不仅仅是呼吸系统。要了解二氧化硫对哺乳动物多个甚至所有器官的毒理作用，还需要进一步的工作。
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 (SO2) increases levels of lipid peroxidation and alters intracellular redox status in multiple organs of mice, and (2) whether SO2 is a systemic toxic agent. The effect of SO2 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. SO2 at 20 ppm (56 mg/m(3)) was administrated to the animals of SO2 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 SO2 inhalation decreased significantly activities of SOD and GSH-Px in all organs tested in all SO2 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 SO2; SO2 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) SO2 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) SO2 may cause toxicological damage to multiple organs of animals, and it is suggested that the oxidative damage produced by SO2 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 SO2 on multiple or even all organs in mammals.