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Objectives Considering the increasing applications of silver nanoparticles (AgNPs) in food- and cosmetic-related products worldwide, the aim of this study was to investigate the potential adverse health effects induced by AgNPs exposure in terms of cytotoxicity, oxidative stress, and mitochondrial injury in human A549 and HepG2 cells. Methods After a 48 h AgNPs treatment, the cell viability was measured by MTT assay. Oxidative damage was determined by assays of malondialdehyde (MDA), 8-epi-PGF2α and 8-hydroxy-2′-deoxyguanosine (8-oxo-dG). The protein expression of HSPA1A and HO-1 was analyzed by western blot analysis. Mitochondrial membrane potential (MMP) was detected by using JC-1 as fluorescent probes. The uptake and intracellular localization of AgNPs was measured by transmission electron microscopy (TEM), and cellular AgNPs was determined by inductively coupled plasma mass spectrometry (ICP-MS). Results A dose-dependent decrease in cell viability after AgNPs treatment was observed, which was associated correspondingly with oxidative damage as indicated by increases in MDA amount, 8-epi-PGF2α and 8-oxo-dG levels, HSPA1A and HO-1 expression, as well as mitochondrial injury as indicated by decreased MMP. The cellular uptake of AgNPs measured by ICP-MS analysis was correlated correspondingly with the oxidative damage and mitochondrial injury. Conclusions The dose-dependent cytotoxicity induced by AgNPs may result from an interaction of oxidative stress, DNA damage and mitochondrial injury in A549 and HepG2 cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol, 2015.

Objectives The intense commercial application of silver nanoparticles (AgNPs) has been raising concerns about their potential adverse health effects to human. This study aimed to explore the potency of AgNPs to induce GADD45α gene, an important stress sensor, and its relationships with the cytotoxicity and genotoxicity elicited by AgNPs. Methods Two established HepG2 and A549 cell lines containing the GADD45α promoter-driven luciferase reporter were treated with increasing concentrations of AgNPs for 48 hours. After the treatment, transcriptional activation of GADD45α indicated by luciferase activity, cell viability, cell cycle arrest, and levels of genotoxicity were determined. The uptake and intracellular localization of AgNPs, cellular Ag doses as well as Ag+ release were also detected. Results AgNPs could activate GADD45α gene at the transcriptional level as demonstrated by the dose-dependent increases in luciferase activity in both the reporter cells. The relative luciferase activity was greater than 12× the control level in HepG2-luciferase cells at the highest concentration tested where the cell viability decreased to 17.0% of the control. These results was generally in accordance with the positive responses in cytotoxicity, cell cycle arrest of Sub G1 and G2/M phase, Olive tail moment, micronuclei frequency, and the cellular Ag content. Conclusions The cytotoxicity and genotoxicity of AgNPs seems to occur mainly via particles uptake and the subsequent liberation of ions inside the cells. And furthermore, the GADD45α promoter-driven luciferase reporter cells, especially the HepG2-luciferase cells, could provide a new and valuable tool for predicting nanomaterials genotoxicity in humans.

Considering the increasing applications of silver nanoparticles (AgNPs) in food- and cosmetic-related products worldwide, the aim of this study was to investigate the potential adverse health effects induced by AgNPs exposure in terms of cytotoxicity, oxidative stress, and mitochondrial injury in human A549 and HepG2 cells.After a 48 h AgNPs treatment, the cell viability was measured by MTT assay. Oxidative damage was determined by assays of malondialdehyde (MDA), 8-epi-PGF2α and 8-hydroxy-2'-deoxyguanosine (8-oxo-dG). The protein expression of HSPA1A and HO-1 was analyzed by western blot analysis. Mitochondrial membrane potential (MMP) was detected by using JC-1 as fluorescent probes. The uptake and intracellular localization of AgNPs was measured by transmission electron microscopy (TEM), and cellular AgNPs was determined by inductively coupled plasma mass spectrometry (ICP-MS).A dose-dependent decrease in cell viability after AgNPs treatment was observed, which was associated correspondingly with oxidative damage as indicated by increases in MDA amount, 8-epi-PGF2α and 8-oxo-dG levels, HSPA1A and HO-1 expression, as well as mitochondrial injury as indicated by decreased MMP. The cellular uptake of AgNPs measured by ICP-MS analysis was correlated correspondingly with the oxidative damage and mitochondrial injury.The dose-dependent cytotoxicity induced by AgNPs may result from an interaction of oxidative stress, DNA damage and mitochondrial injury in A549 and HepG2 cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1691-1699, 2016.