Silver nanoparticles are among the most significant diagnostic and therapeutic agents in the field of nanomedicines. In the current study, the green chemistry approach was made to optimize a cost-effective synthesis protocol for silver nanoparticles from the aqueous extract of the important anticancer plant Fagonia indica. We investigated the anticancer potential and possible involvement of AgNPs in apoptosis. The biosynthesized AgNPs are stable (zeta potential, -16.3mV) and spherical with a crystal size range from 10 to 60nm. The MTT cell viability assay shows concentration-dependent inhibition of the growth of Michigan Cancer Foundation-7 (MCF-7) cells (IC₅₀, 12.35μg/mL). In addition, the fluorescent microscopic analysis shows activation of caspases 3 and 9 by AgNPs that cause morphological changes (AO/EB assay) in the cell membrane and cause nuclear condensation (DAPI assay) that eventually lead to apoptotic cell death (Annexin V/PI assay). It was also observed that AgNPs generate reactive oxygen species (ROS) that modulate oxidative stress in MCF-7 cells. This is the first study that reports the synthesis of a silver nanoparticle mediated by Fagonia indica extract and evaluation of the cellular and molecular mechanism of apoptosis.

The wide scale use of copper oxide nanoparticles (CuONPs) due to their unique properties and important applications in magnetic, thermal, electrical, sensor devices, and cosmetics makes human beings more prone to the exposure of CuONPs and its potential adverse effects. Exposure to such nanoparticles is mainly through skin and inhalation. Therefore, the aim of the present study was to assess the apoptotic and genotoxic potential of CuONPs (50 nm) in the human skin epidermal (HaCaT) cells and its underlying mechanism of cellular toxicity. Significant decreases in cell viability were observed with CuONPs exposure in a dose- and time-dependent manner and also induced significant reduction in glutathione and induction in lipid peroxidation, catalase, and superoxide dismutase in HaCaT cells. A significant increase in caspase-3 activity was observed with CuONPs exposure in HaCaT cells indicating apoptosis. Apoptosis or necrosis was confirmed with fluorescent staining (acridine orange and propidium iodide). The CuONPs also induced DNA damage that was mediated by oxidative stress. This study investigating the effects of CuONPs in human skin cells has provided valuable insights into the mechanism of potential toxicity induced by CuONPs.

Introduction: Extensive use of metallic nanomaterials in different areas of agriculture and commercial products induce significant harmful effects on human health and the environment. In the current study, we synthesized an eco-friendly approach silver nanoparticles (AgNPs) using root extracts of Beta vulgaris L. Methods: The synthesized green silver nanoparticles (gAgNPs) were characterized by dynamic light scattering (DLS) and high-resolution transmission electron microscope (HR-TEM). The gAgNPs had a round shape and the mean size was 20− 50 nm. The cytotoxic effects of gAgNPs were determined in human hepatic normal (CHANG) and cancer (HUH-7) cells by using tetrazolium salt (MTT) and lactate dehydrogenase (LDH) assays for 24 h. Results and Discussion: It was clear from the observations of this experiment that higher concentrations of gAgNPs reduce cell viability. The production of reactive oxygen species (ROS) was evaluated by using DCFDA. The gAgNPs induced more ROS in the HuH-7 cells than in the CHANG cells. The fragmentation of DNA was evaluated by alkaline single-cell gel electrophoresis and the maximum DNA strand breakage was found at a higher concentration exposure of gAgNPs for 24 h. It is important to notice that the HuH-7 cells showed an increased sensitivity to gAgNPs than the CHANG cells. The apoptotic and necrotic effects of gAgNPs on both the cells were evaluated using annexin-V-FITC and propidium iodide staining. An increased count of apoptotic and necrotic cells was found following a higher concentration exposure of gAgNPs. The apoptotic protein expression in these cells due to gAgNPs exposure was determined using immunoblotting techniques and the level of Bcl2 was decreased. However, the expression of BAX and protein was increased in both cells. Conclusion: Therefore, it can be concluded that higher concentrations of gAgNPs may induce significant cytotoxicity and cause DNA damage and apoptosis.

Cadmium exposure induces nephrotoxicity by mediating oxidative stress, inflammation, and apoptosis. The purpose of this study was to examine the protective effect of royal jelly on Cd-induced nephrotoxicity. Adult male mice were distributed randomly into 4 clusters: untreated, royal jelly-treated (85 mg/kg, oral), CdCl₂-treated (6.5 mg/kg, intraperitoneal), and pretreated with royal jelly (85 mg/kg) 2 h before CdCl₂ injection (6.5 mg/kg, intraperitoneal) for seven consecutive days. Cd concentration in the renal tissue and absolute kidney weight of the Cd-treated mice were significantly higher than those of control group. The levels of kidney function markers, kidney injury molecules-1 (KIM-1), metallothionein, lipid peroxidation, nitric oxide, tumor necrosis factor-α, interleukin-1β, and the apoptosis regulators Bax and caspases-3 also increased significantly in the renal tissue of Cd-treated mice, whereas the levels of glutathione, antioxidant enzyme activities, and the apoptosis inhibitor Bcl-2 were significantly reduced in the renal tissue of Cd-treated group. Histopathological studies showed vacuolation and congested glomeruli in the kidney tissue of Cd-treated mice. However, all aforementioned Cd-induced changes were attenuated by pretreatment with royal jelly. We therefore concluded that royal jelly attenuated Cd-induced nephrotoxicity and it is suggested that this nephroprotective effect could be linked to its ability to promote the nuclear factor erythroid 2–related factor 2 (Nrf2)/antioxidant responsive element (ARE) pathway.