Center for Neurosciences and Cell Biology, Department of Life Sciences, University of Coimbra, Coimbra, Portugal.
Toxicol In Vitro. 2011 Apr;25(3):664-70. doi: 10.1016/j.tiv.2011.01.004. Epub 2011 Jan 11.
The major toxicological concern associated with nanomaterials is the fact that some manufactured nanomaterials are redox active, and some particles transport across cell membranes, especially into mitochondria. Thus, evaluation of their toxicity upon acute exposure is essential. In this work, we evaluated the toxicity of silver nanoparticles (40 and 80 nm) and their effects in rat liver mitochondria bioenergetics. Wistar rat liver mitochondria demonstrate alterations in respiration and membrane potential capacities in the presence of either 40 or 80 nm silver nanoparticles. Our data demonstrated a statistically significant decrease in mitochondrial membrane potential, ADP-induced depolarization, and respiratory control ratio (RCR) upon exposure to silver nanoparticles. Our results show that silver nanoparticles cause impairment of mitochondrial function, due mainly to alterations of mitochondrial membrane permeability. This results in an uncoupling effect on the oxidative phosphorylation system. Thus, mitochondrial toxicity may have a central role in the toxicity resulting from exposure to silver nanoparticles.
与纳米材料相关的主要毒理学问题是,一些制造的纳米材料具有氧化还原活性,并且一些颗粒可以穿过细胞膜,特别是进入线粒体。因此,评估它们在急性暴露下的毒性是至关重要的。在这项工作中,我们评估了银纳米颗粒(40nm 和 80nm)的毒性及其对大鼠肝线粒体生物能学的影响。在 40nm 和 80nm 银纳米颗粒存在的情况下,Wistar 大鼠肝线粒体的呼吸和膜电位能力发生改变。我们的数据表明,暴露于银纳米颗粒后,线粒体膜电位、ADP 诱导去极化和呼吸控制比(RCR)均显著下降。我们的结果表明,银纳米颗粒会损害线粒体功能,主要是由于线粒体膜通透性的改变。这导致氧化磷酸化系统的解偶联效应。因此,线粒体毒性可能在暴露于银纳米颗粒引起的毒性中起核心作用。