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 31: 1691-1699, 2016.
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 31: 1691-1699, 2016.