Venter Chantelle, Oberholzer Hester Magdalena, Cummings Franscious Riccardo, Bester Megan Jean
Department of Anatomy, Faculty of Health Sciences, University of Pretoria, Private Bag x323, Arcadia, 0007, South Africa.
Electron Microscope Unit, University of the Western Cape, Private Bag X17, Bellville, 7535, South Africa.
Microsc Res Tech. 2017 Aug;80(8):878-888. doi: 10.1002/jemt.22877. Epub 2017 Apr 12.
Heavy metal pollution has increased in the last decades. Water sources are contaminated and human exposure is often long term exposure to variable amounts of different metals. In this study, male Sprague-Dawley rats were exposed via oral gavage for 28 days to cadmium (Cd) and chromium (Cr), alone and in combination at concentrations 1000 times the human World Health Organization's acceptable water limits. Rat equivalent dosages were used. Blood markers of liver and kidney function were measured, changes to cellular morphology was determined with transmission electron microscopy and the intracellular metal localisation was determined with the electron energy-loss spectroscopy and energy filtered transmission electron microscopy analysis. Both Cd and Cr caused changes to the nuclear and mitochondrial membranes and irregular chromatin condensation of hepatocytes. Cr exposure caused dilation of the rough endoplasmic reticulum (rER). The combination caused nuclear and mitochondrial membrane damage as well as irregular chromatin condensation. In the kidney tissue, Cd caused irregular chromatin condensation in the cells of the proximal convoluted tubule (PCT). Cr caused changes to the outer nuclear and mitochondrial membrane and chromatin structure. The combination group caused membrane damage, irregular chromatin condensation and rER changes in the PCT. All the metal groups showed damage to the endothelial cells and pedicles, but not to the mesangial cells. Cd and Cr bio-accumulation was observed in the nucleus, mitochondria and rER of the liver and kidney and therefore are responsible for the cellular observed damage that can cause functional changes to the tissues and organs.
在过去几十年中，重金属污染有所增加。水源受到污染，人类往往长期接触不同数量的各种金属。在本研究中，雄性斯普拉格-道利大鼠通过口服灌胃的方式，单独或联合接触镉（Cd）和铬（Cr），浓度为世界卫生组织规定的人类可接受水限量的1000倍。采用大鼠等效剂量。检测肝肾功能的血液标志物，用透射电子显微镜确定细胞形态变化，并用电子能量损失谱和能量过滤透射电子显微镜分析确定细胞内金属定位。镉和铬均导致肝细胞核膜和线粒体膜发生变化，肝细胞染色质出现不规则凝聚。铬暴露导致粗面内质网（rER）扩张。联合暴露导致核膜和线粒体膜损伤以及染色质不规则凝聚。在肾组织中，镉导致近端肾小管（PCT）细胞染色质不规则凝聚。铬导致核外膜和线粒体膜以及染色质结构发生变化。联合暴露组导致PCT细胞膜损伤、染色质不规则凝聚和rER变化。所有金属组均显示内皮细胞和蒂受到损伤，但系膜细胞未受损伤。在肝脏和肾脏的细胞核、线粒体和rER中观察到镉和铬的生物蓄积，因此它们是导致观察到的细胞损伤的原因，而这种损伤会导致组织和器官的功能变化。
