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A simple method of synthesis of a stable bimetallic copper-silver nano-particle (CuAg-NP) was developed by successive reduction of Cu(NO) and AgNO, using hydrazine hydrate as the reducing agent and gelatin and poly-vinyl pyrrolidone (PVP) as the capping agents. The round-shaped particles were of a core-shell structure with a core of Cu atoms surrounded by a shell of Ag atoms. The size and the mol. wt. of the NPs were (100 ± 10) nm and (820 ± 157) Kd, respectively; the particles were crystalline in nature and 90% of the precursors Cu(NO) and AgNO were converted to the NPs. The particles were more toxic to cancer cells than normal cells; the dose of the NPs (4-5 μg ml), that killed about 75% of the different human cancer cell lines viz, HepG2 (liver cancer), A549 (lung cancer) and AGS (stomach cancer), killed only about 22.5% of the normal cell lines viz, WRL68 (liver) and WI38 (lung). Therefore, the NP may be developed as a potent anticancer drug in future. The more detailed study on the cytotoxicity of the CuAg-NP on the HepG2 cell line revealed that the particles caused cell cycle arrest in a G2/M phase, depolarization of mitochondrial membrane potential, translocation of phosphatidylserine residues from inner to outer leaflets of cell membrane and DNA degradation; these phenomena confirmed that the NP-induced cell death was apoptotic in nature.

This study was initiated to resolve the ambiguity of contradictory pro-oxidant (toxic) and antioxidant (protective) effects of cerium oxide nanoparticles (CeONPs) taking zebrafish as a model system. To carry out the investigation, different CeONPs having different surface charges (+ve/−ve) with similar shapes and sizes were synthesized at different pH conditions (acidic/basic) using different capping agents (lysine/citrate). Our findings show that the alteration of the capping agent or pH had a profound effect on the biological activity of CeONPs. CeONPs synthesized at alkaline pH showed almost no toxic effect on zebrafish larvae; on the contrary, CeONPs synthesized at acidic pH were found to be toxic, leading to mortality, morphological changes, and abnormal swimming behavior of the larvae and altered levels of reactive oxygen species (ROS), mitochondrial membrane potential, and DNA degradation in larval cells. Moreover, the level of toxicity further increased on coating the NPs with positively charged capping agents. Thus, the study will be very useful in designing CeONPs for killing or protecting biological cells as needed.

SIRT2, an NAD+-dependent histone deacetylase, has been shown to play a pivotal role in various physiological processes, however, its role in cancer is currently controversial. In recent years, SIRT2 has been described as both a tumor suppressor and oncogene with divergent expression and function in various malignancies. Using murine allograft melanoma models, our results suggest increased systemic expression of SIRT2 promotes tumor progression. In this study, SIRT2-overexpressing mice exhibited enhanced tumor growth and larger tumor volumes compared to their wild-type littermates. Mechanistically, systemic overexpression of SIRT2 reduces the number of tumor-infiltrating natural killer (NK) cells and suppresses NK cell function and proliferation within the tumor microenvironment (TME). Furthermore, despite the enhancing effect of NK cell depletion on tumor volume and growth rate in wild-type littermate mice, this effect was diminished in SIRT2-overexpressing mice. Lastly, pharmacological inhibition of SIRT2 increases NK cell tumor infiltration and suppresses allograft melanoma tumor growth. The findings of this study identify a dynamic functional interaction between systemic SIRT2 and NK cell activity, which controls melanoma tumor progression. Given the recent renewed interest in NK-cell-mediated immunotherapy response, SIRT2 could present a new opportunity to mediate immunotherapy response and resistance.

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Compared to Boldine (Bol), NBol had better ability of drug carriage and protective potentials (29.00% approximately) against Cisplatin-induced toxicity. Combinational therapeutic use of PLGA-NBol can reduce unwanted Cisplatin-induced cellular toxicity facilitating use of Cisplatin.