亚硒酸钠对镉和汞肝肾氧化损伤影响的实验研究

Experimental studying the effects of sodium selenite on oxidative damage of liver and kidney induced by cadmium and mercury

目的:观察一次染镉和汞对大鼠肝、肾组织氧化损伤作用,探讨亚硒酸钠预处理对镉和汞氧化损伤的影响。方法:Wister大鼠48只,随机分成6组,每组8只,第1组为染镉实验对照组,第2组为单纯染镉组,第3组为亚硒酸钠预处理组,第4组为染汞实验对照组,第5组为单纯染汞组,第6组为亚硒酸钠预处理干预组。第1、4组大鼠先腹腔注射生理盐水,2 h后皮下注射生理盐水。第2组大鼠先腹腔注射生理盐水,2 h后皮下注射35μmol/kg氯化镉溶液。第3组大鼠先腹腔注射10μmol/kg亚硒酸钠溶液,2 h后皮下注射35μmol/kg氯化镉溶液。第5组大鼠先腹腔注射生理盐水,2 h后皮下注射2.5 mg/kg HgCl2溶液,第6组大鼠先腹腔注射20μmol/kg亚硒酸钠溶液,2 h后皮下注射2.5 mg/kg HgCl2溶液。染毒24 h后测定肝、肾皮质镉或汞、谷胱甘肽、丙二醛含量和谷胱甘肽过氧化物酶活性。结果:与对照组比较,单纯染镉组大鼠肝GSH、MDA含量显著升高,GSH—Px活性显著下降。Na2SeO3预处理组肝、肾皮质GSH和镉含量显著降低,肝脏GSH—Px活性及肾皮质MDA含量显著升高。单纯染汞组大鼠肝、肾皮质及尿汞含量均显著高于对照组。单纯染汞组肝MDA含量显著高于对照组,GSH含量和GSH—Px活性显著低于对照组。Na2SeO3预处理组的肝脏GSH含量和GSH—Px活性均较单纯染汞组升高,有显著性差异。单纯染汞组肾皮质MDA含量显著高于对照组,GSH含量和GSH—Px活性显著降低。Na2SeO3预处理组中肾皮质MDA含量低于单纯染汞组,GSH—Px含量高于单纯染汞组。结论:给大鼠一次染镉和汞,可以对肝和肾脏产生明显的氧化损伤作用。亚硒酸钠对急性染镉和汞所致肝肾损伤具有一定的拮抗作用,其机制可能与增加内源性GSH、使GSH—Px活性增强以及清除自由基能力提高有关。

Objective：To study the oxidative damage of liver and kidney induced by cadmium and mercury administrated once and to observe the effects of sodium selenite （Na2SeO3） pretreatment on the oxidative damage of liver and kidney of rats exposed to cadmium and mercury. Methods：48 Wistar rats were divided into six groups. Control group was injected se with NaCl ;Cadmium chloride group was injected sc with 35μmol/kg CACl2 ; Others were pretreated by administering ip injection of 10μmol/kg Na2SeO3 2 hour before the injection of CdCl2. The mercury group rats were subcutaneously （se） injected with 2.5 mg/kg HgCl2. The Na2SeO3pretreatment group rats were injected with 20 μmol/kg Na2SeO3 by abdominal cavity, and then two hours later sc administrated with 2.5 mg/kg HgCl2. The control group rats were sc injected with saline at corresponding time. 24 hours after the last injection, liver and kidney cortex were collected. MDA and GSH contents in liver and renal cortex as well as GSH--Px acivities were measured. Results： Compared with control group, Cd contents in both liver and renal cortex with Cd alone were obviously increased. GSH, MDA contents in liver were increased significantly and GSH--Px activities were obviously decreased with CA alone. The pretreatment of Na2SeO3 decreased the GSH and Cd contents in both liver and renal cortex significantly. It also obviously increased GSH--Px activities in liver and MDA contents in renal cortex as compared with those given Cd alone. The concentrations of GSH, GSH--Px in the liver were higher significantly than 2.5 mg/ kg HgCl2 group. The content of MDA in liver was significantly lower than 2.5 mg/kg HgCl2 group. The concentration of GSH--Px in renal cortex of Na2SeO3 pretreatment rats was higher than that of 2.5 mg/kg HgCl2 groups alone. The others had no different with 2. 5 mg/kg HgCl2 groups. Conclusions： Na2SO3 pretreatment had antagonistic effects on oxidative damage in liver induced by cadmium and mercury, which may relate to increase the content of GSH and the activities of GSH--Px.