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目的:探讨不同剂量镉与肾损伤之间的关系,从而建立单次大剂量镉致急性肾损伤的模型并进行评价。方法:将健康雄性Wiste大鼠90只随机分为0mg(对照组)、2mg、3mg、4mg、5mg、7mg共6组,大鼠一次腹腔注射氯化镉(2—7mg/kg),染镉后不同时间观察尿乙酰氨基葡糖苷酶(NAG)、尿γ—L—谷氨酰转肽酶(γ—GT)、尿蛋白、血尿素氮(BUN)含量,同时观察肾脏形态学改变。结果:随着染毒剂量的增加,大鼠的一般状态逐渐变差,同时开始死亡;尿中NAG、γ—GT、尿蛋白、血BUN随着镉中毒剂量增加而增加,并出现不同程度以肾小管损伤为主的病理改变。结论:单次大剂量镉中毒能够导致急性肾脏损伤,且呈现明显的剂量一效应关系;但镉剂量过大会出现鼠短时间死亡,可能与镉引起其它脏器的衰竭有关。
OBJECTIVE: To investigate the relationship between different doses of cadmium and renal injury, and to establish and evaluate a single model of acute renal injury induced by high dose cadmium. Methods: Ninety healthy male Wiste rats were randomly divided into 6 groups: 0mg (control group), 2mg, 3mg, 4mg, 5mg and 7mg. The rats were intraperitoneally injected with cadmium chloride (2-7mg / kg) Urine acetylglucosaminidase (NAG), urinary γ-L-glutamyl transpeptidase (γ-GT), urinary protein and blood urea nitrogen (BUN) were observed at different time points. Morphological changes of kidney were also observed. Results: With the increase of exposure dose, the general state of rats gradually became worse and began to die at the same time. The levels of NAG, γ-GT, urinary protein and blood BUN in urine increased with the increase of cadmium poisoning dose, Tubular injury-based pathological changes. CONCLUSION: A single large dose of cadmium poisoning can cause acute kidney injury with obvious dose-effect relationship. However, the short-term death of cadmium occurs when cadmium dose is excessive, which may be related to the cadmium-induced failure of other organs.