Gold nanoparticles induced cloudy swelling to hydropic degeneration, cytoplasmic hyaline vacuolation, polymorphism, binucleation, karyopyknosis, karyolysis, karyorrhexis and necrosis in the liver.
Gold nanoparticles induced cloudy swelling to hydropic degeneration, cytoplasmic hyaline vacuolation, polymorphism, binucleation, karyopyknosis, karyolysis, karyorrhexis and necrosis in the liver.
复制标题
DOI：
10.1186/1476-511x-10-166
复制
发表时间：
2011-09-22
影响因子：
4.5
通讯作者：
Jarrar BM
中科院分区：
文献类型：
--
作者：
Abdelhalim MA;Jarrar BM
纳米颗粒（NPs）由于其不寻常的物理化学性质，可能对器官、组织、细胞、亚细胞和蛋白质水平造成不良影响。纳米技术的进步已经确定了许多生物和生物医学应用的有前途的候选人。本研究的目的是研究金纳米颗粒（GNP）对肝组织的粒径，剂量和暴露时间的影响，试图涵盖和了解毒性及其潜在的治疗和诊断用途。将总共70只健康雄性Wistar-Kyoto大鼠暴露于GNP，接受50或100 μ l大小（10、20和50 nm）的GNP输注3或7天，以研究GNP对肝组织的颗粒大小、剂量和暴露持续时间的影响。与相应的对照大鼠相比，暴露于GNP剂量已经在肝细胞、门静脉三联体和血窦中产生了改变。肝细胞的变化主要是空泡至水肿变性、胞浆透明空泡化、多态性、双核化、核固缩、核溶解、核破裂和坏死。肝细胞肿胀可能是由于膜功能紊乱导致水和Na+大量流入（由于GNP效应），伴随溶酶体水解酶泄漏，导致细胞质变性和大分子拥挤。水肿变性是离子和液体稳态导致细胞内水增加的结果。GNP处理的大鼠肝细胞胞浆空泡肿胀可能指示GNP诱导的急性和亚急性肝损伤。双核化是细胞损伤的结果，是一种常见于再生细胞的染色体增生。诱导的组织学改变可能是由于GNP毒性导致的肝细胞损伤的指示，GNP毒性变得无法处理由这些NP引起的代谢和结构紊乱引起的累积残留物。这些变化是大小依赖性的，较小的诱导的影响最大，并与接触的时间GNP。肝细胞胞质变性和核破坏的出现可能表明GNP与肝组织的蛋白质和酶相互作用，干扰抗氧化防御机制并导致活性氧（ROS）的产生，这反过来可能诱导肝细胞中的应激以经历萎缩和坏死。GNP作为一种治疗和诊断工具的潜在作用需要更多的组织形态学、组织化学和超微结构研究。
Nanoparticles (NPs) can potentially cause adverse effects on organ, tissue, cellular, subcellular and protein levels due to their unusual physicochemical properties. Advances in nanotechnology have identified promising candidates for many biological and biomedical applications. The aim of the present study was to investigate the particle-size, dose and exposure duration effects of gold nanoparticles (GNPs) on the hepatic tissue in an attempt to cover and understand the toxicity and their potential therapeutic and diagnostic use. A total of 70 healthy male Wistar-Kyoto rats were exposed to GNPs received 50 or 100 ul of GNPs infusion of size (10, 20 and 50 nm for 3 or 7 days) to investigate particle-size, dose and exposure duration effects of GNPs on the hepatic tissue. In comparison with respective control rats, exposure to GNPs doses has produced alterations in the hepatocytes, portal triads and the sinusoids. The alterations in the hepatocytes were mainly vacuolar to hydropic degeneration, cytopasmic hyaline vacuolation, polymorphism, binucleation, karyopyknosis, karyolysis, karyorrhexis and necrosis. The hepatocytes swelling might be exhibited as a result of disturbances of membranes function that lead to massive influx of water and Na+ due to GNPs effects accompanied by leakage of lysosomal hydrolytic enzymes that lead to cytoplasmic degeneration and macromolecular crowding. Hydropic degeneration is a result of ion and fluid homestasis that lead to an increase of intracellular water. The vacuolated swelling of the cytoplasm of the hepatocytes of the GNPs treated rats might indicate acute and subacute liver injury induced by the GNPs. Binucleation represents a consequence of cell injury and is a sort of chromosomes hyperplasia which is usually seen in regenerating cells. The induced histological alterations might be an indication of injured hepatocytes due to GNPs toxicity that became unable to deal with the accumulated residues resulting from metabolic and structural disturbances caused by these NPs. These alterations were size-dependent with smaller ones induced the most effects and related with time exposure of GNPs. The appearance of hepatocytes cytoplasmic degeneration and nuclear destruction may suggest that GNPs interact with proteins and enzymes of the hepatic tissue interfering with the antioxidant defense mechanism and leading to reactive oxygen species (ROS) generation which in turn may induce stress in the hepatocytes to undergo atrophy and necrosis. More histomorphologcal, histochemical and ultrastrucural investigations are needed in relation of the application of GNPs with their potential role as a therapeutic and diagnostic tool.