摘要:铅(Pb)是柔软而且延展性强的重金属,有毒。铅是生活中常见的环境污染物,对肾脏也具有的毒性。铅通过肾小管上皮细胞排出时,一部分铅会进入细胞核,在肾小管上皮细胞核里形成铅-蛋白复合物从而使肾小管功能障碍,严重时可导致慢性肾功能障碍。本论文研究原花青素和铅对小鼠肾脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)及过氧化氢酶(CAT)活性的影响。实验小鼠分成五组:对照组;醋酸铅组;醋酸铅+原花青素组(100 mg);醋酸铅+原花青素组(200 mg);原花青素组。铅暴露模型是通过给于小鼠饮用250mg/kg的醋酸铅饮用水建立,实验进行了3个月,测定SOD,CAT和GSH-PX的活性,研究原花青素对铅造成小鼠肾脏SOD,CAT和GSH-PX活力的影响。结果显示:铅对小鼠肾脏影响严重,导致SOD,CAT和GSH-PX活性偏低,而原花青素对铅的这种作用具有有效的抑制作用,有效文持SOD,CAT和GSH-PX活性处于正常水平。说明原花青素对铅诱导的肾脏氧化损伤具有保护作用。 38405 毕业论文关键词:小鼠,肾脏,铅,原花青素,GSH-PX,CAT,SOD
Effect of Procyanidins on activities of SOD, GPX, CAT in kidney exposed to lead
Abstract: lead (Pb) is soft and good extension of heavy metals and toxic. Lead can induced injury to kidney in the life of the environmental pollutants. Lead through the renal tubular epithelial cells, part of the lead to enter the nucleus, the formation of lead can induced renal tubular epithelial cells protein complexes to renal tubular dysfunction, serious when can cause chronic renal dysfunction. In this study, The protective effect of procyanidins on lead-induced kidney injury in mice was studied. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and catalase (CAT) were assaied. Experimental mice pided into 5 groups: control group; Lead acetate group; Lead+procyanidins group (100 mg); Lead+procyanidins group (200 mg). Lead exposure model is to drink 250 mg/kg of lead acetate in mice drinking water was established, the experiment for three months. CAT and GSH-PX activity. The results showed that lead induced injury to kidney of mice. Activities of SOD, CAT and GSH-PX decreased after exposed to lead. However, procyanidins has effective inhibitory effect and effectively maintain SOD, CAT and GSH-PX activity in the normal level.
Keywords:Mice; Kidney; Lead; Kidney; GSH-PX; CAT; SOD
目录
引言 1
1.材料与方法 2
1.1供试材料 2
1.1.1实验动物 2
1.1.2实验试剂 2
1.1.3实验设备 4
1.2.1 样本预处理 4
1.2.2 样本采集 5
1.2.3 肾脏组织的生化功能测定 5
2.实验结果 7
2.1死亡率 7
2.2肾脏体重比 7
2.3 CAT、SOD 及GSH-PX活力的测定 8
2.3.1过氧化氢酶(CAT)活力的测定 8
2.3.2超氧化物歧化酶((SOD )活力的测定 9
2.3.3谷胱甘肽过氧化物酶(GSH-PX )活力的测定 9
3.讨论 10
4.致谢 12
参考文献 12