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目的研究不同浓度SO2吸入染毒对运动大鼠心肺组织超氧化物歧化酶(SOD)活力、还原型谷胱甘肽(GSH)及丙二醛(MDA)含量的影响,探讨SO2污染对运动者心肺组织损伤的机制。方法48只SD雄性大鼠随机分为8组:空白对照组、单纯运动组、低污染运动组、低污染安静组、中污染运动组、中污染安静组、高污染运动组和高污染安静组。除了空白对照组和单纯运动组,其余各组均置于不同浓度SO2污染环境中(低、中、高污染组SO2浓度分别为5、10、15mg/m3),运动组大鼠进行跑轮运动(8m/min,2h/d,共10d)。24h后处死大鼠,取心肺组织匀浆后立即进行抗氧化酶和脂质过氧化水平测定。结果肺组织SOD活力在高污染运动组、高污染安静组、中污染运动组、中污染安静组、低污染运动组较空白对照组显著降低(P<0.05);心组织SOD活力却出现单纯运动组、中污染安静组升高而高污染安静组、高污染运动组下降的变化趋势(P<0.05)。心肺组织的GSH含量中污染安静组升高而高污染运动组、高污染安静组、中污染运动组下降(P<0.05)。MDA水平各实验组较安静对照组显著升高(P<0.05)。同一浓度污染环境中运动组与安静组相比,SOD活力、GSH含量显著降低,MDA水平显著升高(P<0.05),且存在剂量-效应关系。结论SO2污染可引起大鼠心肺组织的氧化损伤,而SO2污染对运动大鼠心肺组织的氧化损伤效应比安静组更明显。
Objective To investigate the effects of SO2 inhalation on the activities of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) in heart and lung tissue of trained rats, Mechanism of cardiopulmonary tissue injury. Methods 48 SD male rats were randomly divided into 8 groups: blank control group, simple exercise group, low-pollution exercise group, low-pollution quiet group, moderate pollution exercise group, moderately-contaminated exercise group, . Except for the blank control group and simple exercise group, the remaining groups were placed in different concentrations of SO2 pollution environment (SO2 concentrations of low, medium and high pollution groups were 5,10,15 mg / m3), exercise group rats running wheel exercise (8m / min, 2h / d, a total of 10d). The rats were sacrificed 24h later, and the levels of antioxidant enzymes and lipid peroxidation were determined immediately after cardioplegia. Results SOD activity in lung tissue was significantly lower in high-pollution exercise group, high-pollution quiet group, middle-pollution exercise group, middle-pollution safety group and low-pollution exercise group as compared with blank control group (P <0.05) Group, in the quiescent group increased pollution and high pollution quiet group, high pollution movement group decreased the trend (P <0.05). The level of GSH in cardiopulmonary tissues was increased in the quiescent group and was lower in the polluted group, the polluted group and the polluted group (P <0.05). The level of MDA in each experimental group was significantly higher than that in the quiet control group (P <0.05). Compared with the quiet group, SOD activity, GSH content and MDA level were significantly increased (P <0.05) in the same concentration of polluted environment, and there was dose-effect relationship. Conclusion Sulfur dioxide (SO2) pollution can cause oxidative damage in the heart and lung tissue of rats, while the oxidative damage of SO2 in heart and lung tissue of rats is more obvious than that in the quiet group.