Silver, once regarded as a safe noble metal for humans, has been widely used in industrial and commercial products, especially in nanometer biomaterials. It is now well known that Ag⁺ is biologically active and is able to interact with the cell membrane, proteins and DNA. However, very little is understood about the potential impacts of Ag⁺ at the sub-cellular level. Our work investigated the potential toxicity of Ag⁺ on mitochondria isolated from rat livers by examining the mitochondrial morphology, respiration, swelling, membrane fluidity and reactive oxygen species (ROS) generation. We observed that Ag⁺ significantly affects the mitochondrial structure and function, including mitochondrial swelling, collapse of the transmembrane potential, change of permeability and fluidity, decline of the respiratory rate, and acceleration of ROS, indicating that Ag⁺ should be seriously regarded as a potentially hazardous substance. Moreover, we conclude that Ag⁺ injures the mitochondrial structure and function by a nonspecific approach, in which the interaction is unregulated by inherent parts such as the mitochondria permeability transition pore (MPTP). These results help us learn more about the toxicity of Ag⁺ at the subcellular (mitochondrial) level and influence future biological and medical applications of Ag-based materials.

中文翻译：

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银离子通过非特异性途径 诱导线粒体功能障碍

银曾经被认为是对人类安全的贵金属，已被广泛用于工业和商业产品，特别是在纳米生物材料中。现在众所周知，Ag ⁺具有生物活性，并且能够与细胞膜，蛋白质和DNA相互作用。但是，对于亚基水平上Ag ⁺的潜在影响知之甚少。我们的工作通过检查线粒体形态，呼吸作用，肿胀，膜流动性和活性氧（ROS）生成，研究了Ag ⁺对从大鼠肝脏分离的线粒体的潜在毒性。我们观察到Ag ⁺显着影响线粒体的结构和功能，包括线粒体肿胀，跨膜电位下降，通透性和流动性变化，呼吸频率下降和ROS加速，表明Ag ⁺应该被视为潜在的有害物质。此外，我们得出结论，Ag ⁺通过一种非特异性方法损害线粒体的结构和功能，其中相互作用不受诸如线粒体通透性转换孔（MPTP）之类固有部分的调节。这些结果有助于我们更多地了解Ag ⁺在亚细胞（线粒体）水平上的毒性，并影响基于Ag的材料的未来生物学和医学应用。