壳聚糖对镉致大鼠肝脏线粒体氧化损伤的影响

Protective effects of chitosan on cadmium-induced oxidative damage in liver mitochondria of rats

目的探讨壳聚糖对镉染毒大鼠肝脏线粒体氧化损伤的影响。方法将40只清洁级健康SD大鼠随机分为5组,分别为对照组、0.8 mg/kg氯化镉组和低、中、高剂量干预(20、100、500 mg/kg壳聚糖+0.8 mg/kg氯化镉)组,每组8只,雌雄各半。干预组采用灌胃方式给予壳聚糖;2 h后,采用腹腔注射方式染毒氯化镉,每天1次,连续染毒7 d。对照组和0.8 mg/kg氯化镉组先灌胃蒸馏水,2 h后,对照组腹腔注射生理盐水,氯化镉组腹腔注射氯化镉溶液。测定大鼠肝脏线粒体中超氧化物歧化酶(SOD)活力和还原型谷胱甘肽(GSH)含量。结果与对照组比较,氯化镉组、低、高剂量干预组雌雄大鼠肝线粒体SOD活力、GSH含量以及中剂量干预组雄性大鼠肝线粒体GSH含量均下降,差异有统计学意义(P<0.05)。与氯化镉组比较,仅中剂量干预组大鼠肝线粒体SOD活力升高,差异有统计学意义(P<0.05);各剂量干预组和氯化镉组大鼠肝线粒体GSH含量均无明显变化。结论壳聚糖对镉致大鼠肝脏线粒体氧化损伤具有一定拮抗作用。

Objective To investigate the protective effects of chitosan on cadmium-induced oxidative damage in liver mitochondria of rats. Methods A total of 40 clean SD rats （male：female= 1：1） were randomly divided into five groups,namely the control group,0.8 mg/kg CdCl2 group and 20,100,500 mg/kg chitosan＋0.8 mg/kg CdCl2 groups respectively,eight animals in each group. The rats in control group were treated with distilled water through garage and followed by normal saline（NS） through intraperitoneal injection. The rats in 0.8 mg/kg CdCl2 group were treated with distilled water as the control first and was injected intraperitoneally with 0.8 mg/kg CdCl2 after 2 h. The rats in each chitosan intmwention group were injected intraperitoneally with 0.8 mg/kg body weight CdCl2, after 2 hours, chitosan was given at the doses of 20,100 and 500 mg/kg body weight respectively through gavage. The animals in all groups were treated once a day for seven consecutive days. The SOD activities were determinmed by the pyrogallol autoxidation method,the GSH contents were measured by the chromogenic DTNB method in mitochondria. Results Compared with control group,the SOD activity and the GSH content in mitochondria decreased in 0.8 mg/kg CdCl2 group,the SOD activities decreased in 20 and 500 mg/kg chitosan＋0.8 mg/kg CdCI2 group, GSH levels were also decreased in 0.8 mg/kg CdCl2 group and each dose of chitosan＋0.8 mg/kg CdCl2 group male rats and 20 mg/kg chitosan＋0.8 mg/kg CdCl2 group female rats significantly （P〈0.05）. Compared with 0.8 mg/kg CdCl2 group, the SOD activity was only increased in the 100 mg/kg chitosan＋0.8 mg/kg CdCl2 group rats significantly （P〈0.05）. But the mitochondrial GSH content did not change significantly in each dose cadmium chloride group. Conclusion Exposure to 0.8 mg/kg CdCI2 can cause liver mitochondrial oxidative damage in rats ,which can be antagonized by chitosan. Key words： Cadmium ; Chitosan ; Mitochondria; Superoxide dismutase; Glutathione