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银纳米粒子诱导成年斑马鱼肝脏氧化应激和细胞凋亡。

Induction of oxidative stress and apoptosis by silver nanoparticles in the liver of adult zebrafish.

机构信息

College of Veterinary Medicine, Seoul National University, 599 Gwanak, Gwanak, Seoul, 151-742, Republic of Korea.

出版信息

Aquat Toxicol. 2010 Oct 15;100(2):151-9. doi: 10.1016/j.aquatox.2009.12.012. Epub 2009 Dec 21.

DOI:10.1016/j.aquatox.2009.12.012
PMID:20060176
Abstract

Silver nanoparticles (AgNPs) may induce deleterious effects in aquatic life on environmental release. The hepatotoxicity of AgNPs was assessed in the liver of adult zebrafish, with the aim of studying the roles of oxidative damage and apoptosis. Zebrafish were exposed to an AgNP solution in which free Ag+ ions were absent at the time of treatment. However, the metal-sensitive metallothionein 2 (MT2) mRNA was induced in the liver tissues of AgNP-treated zebrafish, suggesting that Ag+ ions were released from AgNPs after treatment. It is also possible that MT2 mRNA was induced in the liver tissues by AgNP-generated free radicals. A number of cellular alterations including disruption of hepatic cell cords and apoptotic changes were observed in histological analysis of the liver tissues. The levels of malondialdehyde, a byproduct of cellular lipid peroxidation, and total glutathione were increased in the tissues after treatment with AgNPs. The mRNA levels of the oxyradical-scavenging enzymes catalase and glutathione peroxidase 1a were reduced in the tissues. AgNP treatment induced DNA damage, as demonstrated by analysis with the double-strand break marker γ-H2AX and the expression of p53 protein in liver tissues. In addition, the p53-related pro-apoptotic genes Bax, Noxa, and p21 were upregulated after treatment with AgNPs. These data suggest that oxidative stress and apoptosis are associated with AgNP toxicity in the liver of adult zebrafish.

摘要

银纳米粒子(AgNPs)在环境释放时可能会对水生生物产生有害影响。本研究旨在评估 AgNPs 对成年斑马鱼肝脏的肝毒性,研究氧化损伤和细胞凋亡的作用。在处理时,AgNP 溶液中不存在游离的 Ag+离子,但金属敏感的金属硫蛋白 2(MT2)mRNA 在 AgNP 处理的斑马鱼肝脏组织中被诱导,这表明 Ag+离子是在处理后从 AgNPs 中释放出来的。也有可能是 AgNP 产生的自由基诱导了肝脏组织中 MT2 mRNA 的表达。在对肝脏组织的组织学分析中观察到许多细胞变化,包括肝细胞索的破坏和凋亡变化。在用 AgNPs 处理后,组织中丙二醛(细胞脂质过氧化的副产物)和总谷胱甘肽的水平增加。组织中清除活性氧的酶过氧化氢酶和谷胱甘肽过氧化物酶 1a 的 mRNA 水平降低。AgNP 处理诱导 DNA 损伤,这可以通过双链断裂标记 γ-H2AX 和肝脏组织中 p53 蛋白的表达来证明。此外,p53 相关的促凋亡基因 Bax、Noxa 和 p21 在 AgNP 处理后上调。这些数据表明,氧化应激和细胞凋亡与成年斑马鱼肝脏中的 AgNP 毒性有关。

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