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目的观察亚慢性砷暴露对大鼠红细胞蛋白的影响及其氧化损伤的可能机制。方法将健康体重为160~180 g的40只雌雄各半的SD大鼠按体重随机分为对照组,低、中和高剂量砷染毒组共4组,每组按照自由饮水的方法染毒,每组的染毒剂量分别为0、10、60和360μg/L。动物染毒2个月,腹主动脉采血。MEK-6318K全自动血细胞分析仪分析不同组大鼠红细胞参数:红细胞数(RBC)、血红蛋白(HGB)、红细胞压积(HCT)、平均红细胞体积(MCV)、平均红细胞血红蛋白含量(MCH)、平均红细胞血红蛋白浓度(MCHC)、红细胞宽度变异系数(RDW);用还原型谷胱甘肽(GSH)试剂盒采用酶联免疫吸附法(Elisa)测定血浆中的谷胱甘肽含量;采用western-blot的方法分析比较各组大鼠红细胞band-3蛋白和血红蛋白a1链(Hb A1)蛋白质含量。结果与对照组相比,各个染毒组大鼠红细胞参数差异均无统计学意义(P>0.05);高剂量砷染毒组band-3和Hb A1含量明显高于对照组,差异有统计学意义(P<0.05);中和高剂量砷染毒组的GSH含量明显少于对照组和低剂量砷染毒组,差异有统计学意义(P<0.05)。结论亚慢性砷暴露可以引起大鼠红细胞蛋白含量差异及氧化损伤。
Objective To observe the effect of subchronic arsenic exposure on erythrocyte protein and its possible mechanism of oxidative damage. Methods 40 male and half female SD rats weighing 160-180 g were randomly divided into control group, low, medium and high dose arsenic poisoning group, 4 rats in each group were exposed to drinking water freely The dose of each group was 0, 10, 60 and 360 μg / L, respectively. Animals were poisoned for 2 months, blood was drawn from the abdominal aorta. MEK-6318K automatic hematology analyzer was used to analyze the red blood cell parameters of different groups: RBC, HGB, HCT, MCV, MCH, mean Erythrocyte hemoglobin concentration (MCHC), coefficient of variation of erythrocyte width (RDW); glutathione (GSH) kit using enzyme-linked immunosorbent assay (Elisa) determination of plasma glutathione content; using western-blot Methods The levels of red blood cell band-3 protein and hemoglobin a1 chain (Hb A1) in rats were analyzed. Results Compared with the control group, there was no significant difference in erythrocyte parameters between the three groups (P> 0.05). The content of band-3 and Hb A1 in high dose arsenic exposure group was significantly higher than that in the control group (P <0.05). The content of GSH in medium and high dose arsenic exposure group was significantly lower than that in control group and low dose arsenic exposure group (P <0.05). Conclusion Subchronic arsenic exposure can cause red blood cell protein content and oxidative damage in rats.