Kukner Aysel, Colakoglu Neriman, Kara Haki, Oner Hakan, Ozogul Candan, Ozan Enver
Faculty of Medicine, Department of Histology and Embryology, Abant Izzet Baysal University, Golkoy-Bolu 14200, Turkey.
Biol Trace Elem Res. 2007 Nov;119(2):137-46. doi: 10.1007/s12011-007-0049-1.
Ultrastructural changes in the kidneys of rats after acute cadmium exposure and the effects of exogenous metallothionein (MT) were studied by transmission electron microscopy. Thirty-six adult Wistar rats were divided into three groups. Cadmium chloride (CdCl2) (3.5 mg/kg/day) was injected subcutaneously in the first group. In the second group, 30 micromol/kg MT was administered in addition to CdCl2. Control rats received 0.5 ml subcutaneous saline solution. Four rats from each group were killed on days 1, 3, 5, and 7 after administration of the compounds. Kidney tissues were taken and fixed in 2.5% glutaraldehyde solution for electron microscopic observations. Tissue damage in kidney increased as time passed since the administration of CdCl2 in the first group. Degeneration in the proximal and distal tubules was observed. Increased apoptosis was seen in the proximal tubules epithelium, especially on day 7. Peritubular capillaries became dilated, there was degeneration of the endothelial cells, and the amount of intertubular collagen fibers was increased. On day 1, irregular microvilli in the proximal tubules, deepening of the basal striations, and myelin figures; on day 3, multiple vesicular mitochondria and regions of edema around tubules; on days 5 and 7, increased apoptotic cell in the proximal tubules and widened rough endoplasmic reticulum of the endothelial cells of glomerular capillaries were observed. We observed that the structural alterations that increased depending on the day of Cd administration decreased after exogenous MT administration, the dilation of the peritubular capillaries persisted, and there were degenerated proximal tubules. It was established that cadmium chloride was toxic for kidney cortex and caused structural damage. Exogenous MT partly prevents CdCl2-induced damage.
通过透射电子显微镜研究急性镉暴露后大鼠肾脏的超微结构变化以及外源性金属硫蛋白(MT)的作用。将36只成年Wistar大鼠分为三组。第一组皮下注射氯化镉(CdCl₂)(3.5 mg/kg/天)。第二组除注射CdCl₂外,还给予30 μmol/kg的MT。对照大鼠皮下注射0.5 ml生理盐水溶液。在给予化合物后的第1、3、5和7天,每组处死4只大鼠。取肾脏组织并固定于2.5%戊二醛溶液中用于电子显微镜观察。第一组中,自给予CdCl₂后,肾脏组织损伤随时间增加。观察到近端和远端小管出现变性。近端小管上皮细胞凋亡增加,尤其是在第7天。肾小管周围毛细血管扩张,内皮细胞变性,肾小管间胶原纤维数量增加。第1天,近端小管微绒毛不规则、基纹加深以及出现髓鞘样结构;第3天,出现多个泡状线粒体以及小管周围水肿区域;第5天和第7天,观察到近端小管凋亡细胞增加以及肾小球毛细血管内皮细胞粗面内质网增宽。我们观察到,外源性MT给药后,随镉给药天数增加而增加的结构改变有所减少,肾小管周围毛细血管扩张持续存在,近端小管出现变性。已证实氯化镉对肾皮质有毒性并导致结构损伤。外源性MT可部分预防CdCl₂诱导的损伤。