摘要
本文研究结果表明:肾功能受损以前,尿镉仅以小分子镉复合物(MMS-Cd,MW<1000)的形式排泄;当肾皮质镉超过其临界浓度并引发肾功能障碍后,尿镉排泄急刷增加,其绝大多数以金属硫蛋白结合镉(MT-Cd,MW=10000)的形式排泄,且MMS-Cd仍继续增加;随着肾损害的加重,尿中又相继出现中、高分子量蛋白结合镉(MMWP-Cd,MW=25000～64500,HMWP-Cd,MW>65000)。但MT-Cd是肾脏受损后尿镉的主要排泄形式,始终占尿镉总量的55～75%。正常动物尿锌主要以MMS-Zn形式排泄(占90%以上);肾损害严重时期方有尿锌的显著升高,且系HMWP-Zn排泄增多所致。
Molecular weight distribution of Cd, Zn compounds in the urine of rats subacutely exposed to cadmium were investigated by Sephadex G-75 column chromatography and atomic absorption spectroscopy. The results showed that urinary cadmium was excreted only in the form of binding with micromolecular weight substances (MMS-Cd. MW<1000) before renal dysfunction was found. Whenever, renal cortex cadmium burden exceeded the critical concentration, and renal function became impaired, cadmium in urine increased markedly and except the MMS-Cd, most of urinary cadmium was excreted in the form of binding with metallothionein (MT-Cd, MW=10000). Following the development of renal damage, cadmium bound to middle, high molecular weight proteins (MMWP-Cd, MW: 25000～64500 and HMWP-Cd, MW>65000) occurred in the urine in succession. However, MT-Cd was still the major form of cadmium in urine, approximately 55～75% of the total cadmium. Urinary zinc in control animals excreted in the form of MMS-Zn (not less than 90%). When severe renal damage appeared, urinary zinc was significantly elevated due to obvious increase of HMWP-Zn.
出处
《职业医学》
1990年第5期258-261,319,共4页
China Occupational Medicine
关键词
镉
锌
肾损害
尿
大鼠
cadmium
Cd, Zn-compounds
urine
renal damage
rat
