Antioxidant-modulated cytotoxicity of silver nanoparticles

The properties of silver nanoparticles (AgNPs) synthesized using compounds exhibiting biological activity seem to constitute an interesting issue worthy of examination. In these studies, two types of AgNPs were synthesized by a chemical reduction method using well-known antioxidants: gallic acid (GA) and ascorbic acid (AA). Transmission electron microscopy (TEM) and atomic force microscopy (AFM) revealed that the AgNPs were spherical. The average size was equal to 26 +/- 6 nm and 20 +/- 7 nm in the case of ascorbic acid-silver nanoparticles (AAgNPs) and gallic acid-silver nanoparticles (GAAgNPs), respectively. Surface-enhanced Raman spectroscopy (SERS) confirmed that the AgNPs were not stabilized by pure forms of applied antioxidants. Changes in mitochondrial activity and secretion of inflammatory and apoptosis mediators after the exposure of human promyelocytic (HL-60) and histiocytic lymphoma (U-937) cells to the AgNPs were studied to determine the impact of stabilizing layers on nanoparticle toxicity. The GAAgNPs were found to be more toxic for the cells than the AAgNPs. Their toxicity was manifested by a strong reduction in mitochondrial activity and induction of the secretion of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and caspase-9. The addition of pure antioxidants to the AgNP suspensions was found to influence their toxicity. There was a significant positive effect in the case of the mixture of AA with AAgNPs and GA with GAAgNPs. The results obtained suggest that the presence of stabilizing agents adsorbed on the surface of AgNPs is the main factor in shaping their toxicity. Nevertheless, the toxic effect can be also tuned by the introduction of free antioxidant molecules to the AgNP suspensions.

Automated summary

The study investigated the toxicity of silver nanoparticles synthesized using antioxidants on human cells, finding that GAAgNPs were more toxic than AAgNPs, with the presence of stabilizing agents being the main factor influencing toxicity.