Piscator M, Björck L, Nordberg M
Acta Pharmacol Toxicol (Copenh). 1981 Jul;49(1):1-7. doi: 10.1111/j.1600-0773.1981.tb00862.x.
Male rabbits were exposed to cadmium during 16 weeks by subcutaneous injections of either 0.25 mg or 0.5 md Cd as cadmium chloride per kg body weight 3 times per week. beta 2-microglobulin (beta 2-m) and creatinine in serum, cadmium in blood, as well as total protein, creatinine, beta 2-m and cadmium in urine were determined before exposure and after 3 and 7 weeks of exposure. Measurements were also made at 19 weeks, 3 weeks after the last exposure. During exposure, there was a slight increase in the serum beta 2-m/creatinine ratio among rabbits with the highest exposure, while no effect of the cadmium burden could be observed once exposure had ceased. Urinary excretion of beta 2-m was related to urinary pH, which appeared to be the case also for excretion of total protein. In the high exposure group, a significant increase in urinary beta 2-m excretion, indicative of renal tubular dysfunction was seen after 7 weeks of exposure. This was, however, not related to serum beta 2-m levels. It was concluded that before renal damage has occurred even heavy cadmium exposure has very little influence on serum beta 2-m levels.
雄性兔子通过皮下注射,以每千克体重0.25毫克或0.5毫克氯化镉的剂量,每周3次,连续16周暴露于镉环境中。在暴露前以及暴露3周和7周后,测定血清中的β2-微球蛋白(β2-m)和肌酐、血液中的镉,以及尿液中的总蛋白、肌酐、β2-m和镉。在最后一次暴露3周后的第19周也进行了测量。在暴露期间,暴露量最高的兔子血清中β2-m/肌酐比值略有增加,而一旦暴露停止,未观察到镉负荷的影响。β2-m的尿排泄与尿液pH值有关,总蛋白的排泄情况似乎也是如此。在高暴露组中,暴露7周后可见尿β2-m排泄显著增加,表明存在肾小管功能障碍。然而,这与血清β2-m水平无关。得出的结论是,在肾脏损伤发生之前,即使是重度镉暴露对血清β2-m水平的影响也很小。