Silver nanoparticles (AgNPs), which have well-known antimicrobial properties, are extensively used in various medical and general applications. In spite of the widespread use of AgNPs, relatively few studies have been undertaken to determine the cytotoxic effects of AgNPs. The aim of this study was investigate how AgNPs of different sizes (4.7 and 42 nm) interact with two different tumoral human cell lines (hepatoma [HepG2] and leukemia [HL-60]). In addition, glutathione depletion, inhibition of superoxide dismutase (SOD) and reactive oxygen species (ROS) generation were used to evaluate feasible mechanisms by which AgNPs exerted its toxicity. AgNPs of 4.7 nm and 42 nm exhibited a dramatic difference in cytotoxicity. Small AgNPs were much more cytotoxic than large AgNPs. A difference in the cellular response to AgNPs was found. HepG2 cells showed a higher sensitivity to the AgNPs than HL-60. However, the cytotoxicity induced by AgNPs was efficiently prevented by NAC treatment, which suggests that oxidative stress is primarily responsible for the cytotoxicity of AgNPs. Furthermore, cellular antioxidant status was disturbed: AgNPs exposure caused ROS production, glutathione depletion and slight, but not statistically significant inactivation of SOD.

Due to their exceptional properties, gold nanoparticles (AuNPs) have shown promising medical and technological applications in the treatment of cancer and the development of antimicrobial packaging and time-temperature indicators in the food sector. However, little is known about their cytotoxicity when they come into contact with biological systems. The aim of this work was to compare the effects of three commercially available AuNPs of different sizes (30, 50 and 90 nm) on human leukemia (HL-60) and hepatoma (HepG2) cell lines. AuNP-induced cytotoxicity was dose and time-dependent, with IC50 values higher than 15 μg/mL. Nanoparticle (NP) size and cell line slightly influenced on the cytotoxicity of AuNPs, although HL-60 cells proved to be more sensitive to the cytotoxic response than HepG2. N-Acetyl-L-cysteine (NAC) protected HL-60 and HepG2 cells only against treatment with 30 nm AuNPs. In both cell types, glutathione (GSH) content was drastically depleted after 72 h of incubation with the three AuNPs (less than 30% in all cases), while the reduction of superoxide dismutase activity (SOD) activity depended on cell line. HepG2, but not HL-60 cells, exhibited a decrease of SOD activity (∼ 45% of activity). The three AuNPs also caused a two-fold elevation of reactive oxygen species (ROS) production in both cell lines. Thus, protective effect of NAC, depletion of GSH and increase of ROS appear to be determined by NP size and indicate that oxidative stress contributes to cytotoxicity of AuNPs.

The inhibitory effect of nine fruit and vegetable ethanolic extracts against the mutagenicity of N-nitrosodimethylamine (NDMA), N-nitrosopyrrolidine (NPYR), N-nitrosodibutylamine (NDBA), and N-nitrosopiperidine (NPIP) was evaluated by means of the Ames test. Licorice ethanolic extract was the only one that showed an inhibitory effect (ranging from moderate to strong) against mutagenicity of all N-nitrosamines tested. This ethanolic extract showed the greatest inhibition effect against NPIP (72%), NDMA (45%), and NPYR (39%). The greatest inhibition effect (51%) of the mutagenicity of NDBA was shown by kiwi ethanolic extract. Vegetable and fruit ethanolic extracts that exhibited an antimutagenic effect (at the range 50-2000 microg/plate), in decreasing order, against NDMA and NPYR were as follows: licorice > kiwi > carrot and licorice > broccoli > pineapple > kiwi, respectively. Decreasing orders against NDBA and NPIP were, respectively, kiwi > onion > licorice = garlic > green pepper > carrot and licorice > garlic > pineapple > carrot.

Silver compounds have been used for their medicinal properties for centuries. At present, silver nanoparticles (AgNPs) are reemerging as a viable topical treatment option for infections encountered in burns, open wounds and chronic ulcers. This study evaluated the in vitro mechanisms of two different sizes of AgNPs (4·7 and 42 nm) toxicity in normal human dermal fibroblasts. The toxicity was evaluated by observing cell viability and oxidative stress parameters. In all toxicity endpoints studied (MTT and lactate dehydrogenase assays), AgNPs of 4·7 nm were much more toxic than the large AgNPs (42 nm). The cytotoxicity of both AgNPs was greatly decreased by pre-treatment with the antioxidant N-acetyl-L-cysteine. The oxidative stress parameters showed significant increase in reactive oxygen species levels, depletion of glutathione level and slight, but not statistically significant inactivation of superoxide dismutase, suggesting generation of oxidative stress. Thus, AgNPs should be used with caution for the topical treatment of burns and wounds, medical devices etc, because their toxicity depends on the size, the smaller NPs being much more cytotoxic than the large.

Our results clearly indicate that polyphenols protect human derived cells against DNA strand breaks and oxidative DNA damage effects of NDMA, NPYR or BaP, three carcinogenic compounds which occur in the environment.