Shibasaki T, Ohno I, Ishimoto F, Sakai O
Second Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan.
Nihon Jinzo Gakkai Shi. 1993 Aug;35(8):913-7.
Male Syrian hamsters were used to evaluate cadmium (Cd)-induced nephrotoxicity. Furthermore, they were treated with polyaspartic acid (PAA) in an attempt to prevent renal damage due to Cd. To induce renal proximal tubular damage, the hamsters were administered a single subcutaneous injection of cadmium chloride (CdCl2) at the dose of 3 mg/kg body weight. Within 24 hours, they exhibited significant proteinuria and an increased urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG). Renal histological changes consisted of degenerative changes in renal tubule cells, irregularly shaped nuclei with marginated chromatin and rounded mitochondria. The administration of PAA did not improve creatinine clearance or urinary protein excretion. The concentration of Cd in the renal tissue showed a gradual increase on day 3 following cadmium exposure. Cadmium nephrotoxicity appears to be more severe in Syrian hamsters than in rats or mice. Thus, this animal model appears to be excellent for studying Cd-induced nephrotoxicity.
雄性叙利亚仓鼠被用于评估镉(Cd)诱导的肾毒性。此外,它们接受了聚天冬氨酸(PAA)治疗,试图预防因镉导致的肾损伤。为诱导肾近端小管损伤,给仓鼠皮下注射一次氯化镉(CdCl2),剂量为3毫克/千克体重。在24小时内,它们出现了显著的蛋白尿,并且N-乙酰-β-D-氨基葡萄糖苷酶(NAG)的尿排泄增加。肾脏组织学变化包括肾小管细胞的退行性变化、染色质边缘化的不规则形状细胞核和圆形线粒体。PAA的给药并未改善肌酐清除率或尿蛋白排泄。镉暴露后第3天,肾组织中的镉浓度逐渐升高。镉肾毒性在叙利亚仓鼠中似乎比在大鼠或小鼠中更严重。因此,这种动物模型似乎非常适合用于研究镉诱导的肾毒性。