大鼠亚慢性铬染毒引起的肾损害  

Subchronic chromate-induced renal damage in rats

作　　者：何兴轩[1] 郭卫星[2] 王翔朴[2] 

机构地区：[1]湖南医科大学劳动卫生职业病学教研室 [2]环境医学研究室,长沙410078

出　　处：《中国药理学与毒理学杂志》1991年第2期144-148,共5页Chinese Journal of Pharmacology and Toxicology

摘　　要：30只Wistar♂大鼠ip K_2Cr_2O_7 1.06mgCr^(6+)/kg,每周5次,连续12wk。肾脏出现明显的形态和功能异常,早期肾小管上皮细胞出现变性,尿中N-乙酰-β-D-氨基葡萄糖苷酶(NAG)、溶菌酶(LZM)和蛋白质的含量分别在染毒d2,3和5wk时显著增加;晚期肾小管上皮细胞出现广泛变性和坏死,尿中碱性磷酸酶(ALP)、γ-谷氨酰移换酶(γ-GT)和葡萄糖的含量分别在染毒d6,10和10wk时明显增加,GFR在染毒7wk开始下降。尿铬主要以低分子铬结合物(LW-Cr,5000道尔顿)形式排出。尿铬与肾损害程度显著相关,尿LZM、尿蛋白和GFR出现异常的尿铬临界浓度分别为5.90,7.57和9.36μg/mg肌酐。肾脏铬的蓄积则以高分子铬结合物(HM-Cr,65000道尔顿)和与尿铬相似的LM-Cr两种形式存在,主要蓄积在肾皮质。肾铬与肾损害相关密切,尿LZM和尿蛋白出现异常的肾皮质铬临界浓度分别为36.7ppm和41.8ppm。Thirty male Wistar rats were treated with K2Cr2O7 (1.0 mg Cr6+ / kg body weight) ip, 5 d a week for 12 wk. Apparent morphological and functional changes of the kidneys were found as follows: the degeneration of the renal tubular epithelial cells in the early stages, the significant increase of the urinary excretion of N-acetyl-β-glucosaminidase (NAG), lysozyme and protein in 2, 3 and 5 wk after injection, the extensive degeneration and necrosis of the renal tubular epithelial cells in the final stages, the significant elevations of alkaline phosphatase (ALP), ν-glutamyltranspeptidase (ν-GT) and glucose in urine in 6, 10 and 10 wk after injection, and a decline of GFR in 7 wk after ip injection. Chromium-binding low molecular weight substance (LM-Cr, 5000) wasthe main form of chromium in urine. The critical concentrations of chromium in urine for the abnormal changes of urinary lysozyme, protein and GFR were 5.90, 7.57 and 9.36 μg/mg creatinine, respectively. Chromium accumulation in the renal cortex was found in two forms: the chromium-binding high molecular weight substance (HM-Cr, 65 000) and LM-Cr. The critical concentrations of chromium in the renal cortex were 36.7 and 41.8 ppm respectively due to the significant increase of the urinary excretion of lysozyme and protein.

关 键 词：铬中毒 肾损伤 病理 病因 

分 类 号：R595.206[医药卫生—内科学]