急性氯化镉中毒肾损害大鼠尿γ－谷氨酰转换酶及其同工酶

大鼠一次ｉｐ氯化镉（１．５～１２．２ｍｇ·ｋｇ－１），染镉前和染毒后ｄ１，ｄ３，ｄ５观察尿β２－微球蛋白（β２－ＭＧ），Ｎ－乙酰－β－氨基葡萄糖苷酶（ＮＡＧ），尿蛋白，肾小球滤过率（ＧＦＲ）和尿γ－谷氨酰转换酶（ＧＧＴ）及其同工酶，同时观察肾脏形态学改变．结果大鼠尿中β２－ＭＧ，ＮＡＧ和蛋白排出增加，９．２ｍｇ·ｋｇ－１以上组ＧＦＲ下降，形态学检查发现以肾小管损害为主的病理改变．大鼠尿ＧＧＴ异常增加并出现异常ＧＧＴ同工酶区带．

Rat urinary γ-glutamyltransferase and its isoenzyme in cadmium chloride-induced acute nephropathy

Sixty male Wistar rats were divided into six groups, one control and five groups treated with 1.5-12.2 mg·kg -1 CdCl 2 ip. Urinary β 2 -microglobulin, N-acetyl-β-D-glucosaminidase, total γ-glutamyltransferase (GGT), glomerular filtration rate and protein were significantly increased and glomerular filtration rate was decreased among cadmium treated rats. Light microscopy of kidney revealed morphological changes mainly in the epithelial cells of the proximal tubules. There were three bands of GGT isoenzymes in the urine and the renal cortex homogenate of cadmium treated rats, while two bands of GGT isoenzymes in controls. The change of GGT isoenzyme seems to be a more sensitive index of cadmium-induced nephropathy compared to urinary total GGT. The significance of the change of GGT isoenzyme needs further studies and GGT isoenzymes may be served as a new tool to study of the mechanism of cadmium-induced nephrotoxicity.