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金属和金属氧化物纳米颗粒的毒性主要针对肝细胞和肾细胞的线粒体。

Metallic and metallic oxide nanoparticles toxicity primarily targets the mitochondria of hepatocytes and renal cells.

机构信息

Nanobiology Unit, Faculty of Sciences, Jerash University, Jordan.

College of Science, King Saud University, Riyadh, Saudi Arabia.

出版信息

Toxicol Ind Health. 2024 Dec;40(12):667-678. doi: 10.1177/07482337241282860. Epub 2024 Sep 17.

Abstract

Nanoparticles (NPs) are utilized in various applications, posing potential risks to human health, tissues, cells, and macromolecules. This study aimed to investigate the ultrastructural alterations in hepatocytes and renal tubular cells induced by metallic and metal oxide NPs. Adult healthy male Wistar albino rats () were divided into 6 ( = 7) control and 6 treated groups ( = 7). The rats in the treated groups exposed daily to silver NPs, gold NPs, zinc oxide NPs, silicon dioxide NPs, copper oxide NPs, and ferric oxide NPs for 35 days. The members of the control group for each corresponding NPs received the respective vehicle. Liver and kidney tissue blocks from all rats were processed for Transmission Electron Microscopy (TEM) examinations. The hepatocytes and renal tubular cells of all NPs-treated rats demonstrated mitochondrial ultrastructural alterations mainly cristolysis, swelling, membrane disruption, lucent matrices, matrices lysis, and electron-dense deposits. However, other organelles demonstrated injury but to a lesser extent in the form of shrunken nuclei, nuclear membrane indentation, endoplasmic reticulum fragmentation, cellular membranes enfolding, brush border microvilli disruption, lysosomal hyperplasia, ribosomes dropping, and peroxisome formation. One may conclude from the findings that the hepatocytes and the renal tubular cells mitochondria are the main targets for nanoparticles toxicity ending in mitochondrial disruption and cell injury. Further studies taking into account the relation of mitochondrial ultrastructural damage with a weakened antioxidant defense system induced by chronic exposure to nanomaterials are needed.

摘要

纳米粒子(NPs)在各种应用中得到了广泛的应用,对人类健康、组织、细胞和生物大分子都存在潜在的风险。本研究旨在探讨金属和金属氧化物 NPs 诱导的肝细胞和肾小管细胞的超微结构改变。成年健康雄性 Wistar 白化大鼠()分为 6 个(=7)对照组和 6 个处理组(=7)。处理组大鼠每天暴露于银 NPs、金 NPs、氧化锌 NPs、二氧化硅 NPs、氧化铜 NPs 和氧化铁 NPs 中 35 天。每个相应 NPs 对照组的成员接受相应的载体。所有大鼠的肝和肾组织块均进行透射电子显微镜(TEM)检查。所有 NPs 处理组大鼠的肝细胞和肾小管细胞均显示线粒体超微结构改变,主要为嵴溶解、肿胀、膜破裂、透明基质、基质溶解和电子致密沉积物。然而,其他细胞器也受到了损伤,但程度较轻,表现为细胞核皱缩、核膜内陷、内质网碎片化、细胞膜折叠、刷状缘微绒毛破坏、溶酶体增生、核糖体脱落和过氧化物酶体形成。从研究结果可以得出结论,肝细胞和肾小管细胞的线粒体是纳米颗粒毒性的主要靶标,导致线粒体破坏和细胞损伤。需要进一步研究,考虑到慢性暴露于纳米材料引起的线粒体超微结构损伤与抗氧化防御系统减弱之间的关系。

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