四氯化碳诱发大鼠肝损伤对镉肾脏毒性的影响

Effects of CCl_4induced hepatic damage on cadmium nephrotoxicity in rats

目的探讨肝损伤对镉肾毒性的影响。方法大鼠腹腔注射ＣｄＣｌ２（含镉０．５ｍｇ／ｋｇ）染毒，第４周末通过灌胃给予ＣＣｌ４９００ｍｇ／ｋｇ，观察大鼠肝、肾功能的变化。结果肝损伤使尿蛋白含量增高和肾小管坏死等肾脏病变提前出现。ＣＣｌ４仅引起一过性的肝损害而未见任何肾功能指标的异常。ＣｄＣｌ２＋ＣＣｌ４联合处理组肾镉临界浓度（７１．５０μｇ／ｇ）明显低于ＣｄＣｌ２组（１００．５５μｇ／ｇ）或ＣＣｌ４＋ＣｄＣｌ２联合处理组（１０３．８０μｇ／ｇ，Ｐ＜０．０５），表明镉染毒大鼠的肝损害能促进镉性肾病的发生和发展，并提高肾脏对镉毒作用的敏感性。结论肝脏功能状态在慢性镉中毒性肾病中起重要的作用。

The present study was designed to investigate the effects of hepatic damage on the pathogenesis of Cd nephrotoxicity in rats.Experimental rats were divided into 3 groups:(1)CdCl_2 group,rats were injected ip with CdCl_2 at the dosage of 0.5 mg Cd^2+/kg a day,3 times a week,up to 10 weeks;(2)CdCl_2+CCl_4 group,rats were administered CCl_4 900 mg/kg at the end of the 4th week;(3)CCl4+CdCl2 group,rats were given CCl4 900 mg/kg 2 times before CdCl_2 treatment in the 1st week.Renal pathological changes,such as increase of urinary protein excretion,proximal tubular cells necrosis in CdCl_2+CCl_4 group were detected earlier and appeared more serious than those in either CdCl_2 or CCl_4+CdCl_2 group.CCl_4 only caused temporary hepatic dysfunction but no renal injury sign was observed.The critical Cd concentration in renal cortex was markedly lower in CdCl_2+CCl_4 group than in either CdCl_2 or CCl_4+CdCl_2 group(71.50 μg/g vs 100.55 μg/g or 103.80 μg/g respectively).These results indicated that hepatic injury may enable the kidney of Cdloaded rats to be more sensitive to cadmium toxicity and promote the pathogenesis of cadmium nephrotoxicity.