Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis.

By M. Piao, K. Kang, I. Lee, Hye Sun Kim, Suhkmann Kim, Jeong-Yun Choi, Jinhee Choi, J. Hyun. Toxicology Letters, 2011

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A systematic review on silver nanoparticles-induced cytotoxicity: Physicochemical properties and perspectives (2017, positive): “Effect of Ag-NPs on mitochondrial membrane permeability could cause loss of mitochondrial integrity, which may regulate JNK mediated caspase dependent apoptosis [60].”
The effect of particle size on the cytotoxicity, inflammation, developmental toxicity and genotoxicity of silver nanoparticles. (2011, result): “In our study, L929 fibroblasts were more sensitive to the effects of 20 nm nanoparticles, which is similar to what was reported for human liver cells [10].”
Molecular Toxicity Mechanism of Nanosilver (2014, background): “[19,83,85,103,106], but some used aquatic species [24,25,35,42] and organisms [20e23,26,43,45].”
Biological Synthesis of Nanoparticles from Plants and Microorganisms. (2016, background): “The possible anticancer mechanism of nanoparticles is related to their size and shape, which are associated with the generation of reactive oxygen species (ROS), causing damage to cellular components [82].”
The role of surface charge in cellular uptake and cytotoxicity of medical nanoparticles (2012, neutral): “The increase in mitochondrial membrane permeability was induced either by disruption of the respiratory chain or by changes in Bax and Bcl-2 expression, which lead to disruption of mitochondrial metabolism, increased ROS production, adenosine diphosphate-induced depolarization, release of cytochrome”