Meng Ziqiang
Institute of Environmental Medicine and Toxicology, Department of Life Sciences, Shanxi University, Taiyuan, People's Republic of China.
Inhal Toxicol. 2003 Feb;15(2):181-95. doi: 10.1080/08958370304476.
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.
铜锌超氧化物歧化酶（SOD）、硒依赖型谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）和谷胱甘肽（GSH）在减轻自由基诱导的氧化损伤中发挥着重要作用。本研究的目的是确定：（1）二氧化硫（SO₂）是否会增加小鼠多个器官的脂质过氧化水平并改变细胞内氧化还原状态；（2）SO₂是否为一种全身性毒性剂。研究了SO₂对雌雄昆明白化小鼠九个器官（脑、肺、心、肝、胃、肠、脾、肾和睾丸）中硫代巴比妥酸反应性物质（TBARS）水平、GSH水平以及SOD、GSH-Px和CAT活性的影响。将SO₂组动物置于暴露室中，以20 ppm（56 mg/m³）的浓度，每天暴露6小时，持续7天，而对照组在相同条件下暴露于过滤空气中。结果显示，与相应对照组相比，所有SO₂组中所有测试器官的SOD和GSH-Px活性均显著降低；除肝脏中的CAT活性因SO₂而显著降低外，两性小鼠所有测试器官中的CAT活性均无显著变化；与各自对照组相比，SO₂暴露显著降低了所有测试器官的GSH含量，并显著提高了TBARS水平。这些结果得出两个结论：（1）SO₂是一种全身性氧化损伤剂。它导致雌雄小鼠所有测试器官的脂质过氧化过程显著增加，并伴有这些器官抗氧化状态的变化。（2）SO₂可能对动物的多个器官造成毒理学损伤，提示吸入SO₂产生的氧化损伤可能影响或促进各个器官某些疾病状态的进展或发生，而不仅限于呼吸系统。需要进一步开展工作以了解SO₂在哺乳动物多个甚至所有器官中的毒理学作用。
