The development of nanotechnology has led to the increased production of zinc oxide nanoparticles (ZnO‐NPs) and their application in a wide variety of everyday products. It creates the need for a full assessment of their safety for humans. The aim of the study was to assess the toxic effects of ZnO‐NPs on model human cells of the immune system: U‐937, HL‐60, HUT‐78, and COLO‐720L. Particular attention was paid to the direct interaction of the nanoparticles with membrane lipids and the role of zinc ions in the mechanism of their toxicity. Cell viability, lipid peroxidation, cell membrane integrity, and the amount of zinc ions released from nanoparticles were tested. Disruption in cell metabolism was noted for ZnO‐NPs concentrations from 6.25 mg/L. Contact with ZnO‐NPs caused lipid peroxidation of all cells and correlated with membrane disruption of HL‐60, HUT‐78, and COLO‐720L cells. Model monolayers (Langmuir technique) were used to assess the interaction of the nanoparticles with the studied lipids. Physicochemical parameters, such as the area per molecule at maximal layer compression, the pressure at which the monolayer collapses, and the static compression modulus, were calculated. The models of the HL‐60 and U‐937 cell membranes under ZnO‐NPs treatment reacted in a different way. It has also been shown that Zn2+ are not the main causative factor of ZnO‐NPs toxicity. Investigating the early stages of mechanism of nanoparticles toxicity will allow for a more complete risk assessment and development of methods for a safer synthesis of engineering nanomaterials.
Silver nanoparticles (AgNPs) prepared and stabilized by diverse biologically active substances seem to be especially useful in diverse biological and medical applications. The combination of AgNPs with bioactive substances, such as antioxidants, can lead to the development of new systems of desired anticancer properties. In this research, AgNPs were prepared with the use of diverse antioxidant combinations including gallic acid (GA), (−)‐epicatechin‐3‐gallate (EGCG), and caffeine (CAF). The insightful physicochemical characteristic revealed that each type of AgNPs exhibited spherical shape, comparable size distribution and negative surface charge. Surface‐enhanced Raman spectroscopy (SERS) delivered the information about the chemistry of AgNP stabilizing layers, which turned out to be a crucial factor tuning toxicity of AgNPs toward murine B16 melanoma cells (B16‐F0) and human skin melanoma (COLO 679) cells. EGCGAgNPs were the most cytotoxic among all the investigated AgNPs. They strongly reduced the activity of mitochondria, damaged cell membrane integrity, and penetrated inside the cells causing DNA damage. In turn, the toxicity of GAAgNPs strongly manifested via the induction of oxidative stress in the cells. It was found that CAFGAAgNPs exhibited the lowest toxicity toward the melanoma cells, which proved that a proper combination of antioxidants enable to prepare AgNPs of differentiated toxicity. It was established that human skin melanoma cells were significantly more sensitive to AgNPs than the murine melanoma cells.
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