Blue-LED assisted Photodegradation kinetics of rhodamine-6G dye, enhanced anticancer activity and cleavage of plasmids using Au-ZnO nanocomposite

The plasmonic metal doping on the UV-active metal oxide nanoparticle turns the resultant plasmonic metal-metal oxide (PMMO) into visible light active and upon exogenous illumination the photogenerated energetic charge carriers and the in situ generated reactive oxygen species (ROS, e.g. ·OH and O2−·) authoritatively enhances its biological and catalytic activity. Herein, a hexagonal rod-shaped ZnO nanoparticles (NP) precursor was prepared using the sol-gel method, which in the presence of varying concentrations of gold (0.005M, 0.01M, and 0.015M) via a greener citrate reduction method afforded a nanocrystalline Au-ZnO nanocomposite. Using which, the visible-light driven photo-degradation kinetics investigation of rhodamine-6G (R6G) dye under blue LED irradiation were carried out. The use of 20 mg 0.015-Au-ZnO completes the degradation of R6G (97.0 %, k = 6.5 X 10−3s−1 at pH 7) within 55 min while 50 mg of 0.015-Au-ZnO catalyst improves the rate of R6G degradation (15 min 97.8 %, k = 14.8 × 10−3 s−1) and it is reusable up to three cycles. The LC-MS spectra of the remains of R6G (after 15 min) identified various low molecular ions (up m/z = 65). Further, the blue-LED assisted anti-cancer studies (MTT assay) using 0.015-Au-ZnO towards human lung cancer cells (A549), breast cancer cells (SKBr3) show high anti-proliferation rate and low cytotoxicity against healthy human embryonic kidney cells (HEK-293) with an IC50 value of 65, 53 and 124 μg/mL respectively. Also, the AO-EB dual staining and DCFH-DA analysis of SKBr3 and A549 cells revealed ROS-mediated cell death via apoptosis. Moreover, plasmid cleavage studies against supercoiled pBR322 DNA result in single-stranded linear DNA without traversing the nicked circular form, suggesting the possible DNA targeting activity of Au-ZnO nanozyme. Thus, the synthesized Au-ZnO nanocomposite shows excellent photocatalytic and biological activity

Impact of Biphenyl Benzhydrazone-Incorporated Arene Ru(II) Complexes on Cytotoxicity and the Cancer Cell Death Mechanism

The biological efficacy of arene ruthenium complexes is currently of great interest due to the significance of arene moieties, chelates, and metal centers in defining and controlling their anticancer activity. The synthesis of six new arene ruthenium(II) complexes containing biphenyl benzhydrazone ligands of general composition [(η6-benzene)Ru(L)Cl] (1–3) and [(η6-p-cymene)Ru(L)Cl] (4–6, L = biphenyl benzhydrazones), and their antiproliferative properties are described in this study. The complexes have been successfully synthesized and thoroughly characterized by elemental analysis and spectral methods such as Fourier transform infrared (FT-IR), UV–vis, NMR, and high-resolution mass spectrometry (HR-MS) techniques. The coordination of azomethine nitrogen and imidolate oxygen of the hydrazone ligand to the ruthenium metal and the presence of a pseudo-octahedral geometry around the ruthenium ion were confirmed by the single-crystal X-ray diffraction (XRD) technique. Further, in vitro cytotoxicity of all of the complexes was evaluated against cancerous A549 (lung cancer), MDA-MB-231 (breast cancer), and HEPG2 (liver cancer) and noncancerous HEK-293 (human kidney) cells and was found to be good with low IC50 values compared to the standard drug cisplatin. In particular, complex 5 exhibits potential cytotoxicity against all of the cancer cells among the synthesized complexes, and this may be attributed to the hydrophobic nature of the p-cymene moiety as well as the substituent effect of the ligand. In addition, staining studies such as AO–EB and Hoechst 33342 ascertain that the complex induces the apoptosis mechanism in cancer cells. Furthermore, reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) confirm apoptosis in cancer cells via the mitochondrial pathway. Additionally, the quantification of apoptosis and ROS have been established by flow cytometry and the plate reader assay, respectively. It is worth noting that the present ruthenium complexes have significant cytotoxicity, raising the prospect of promoting potential ruthenium-based anticancer drugs over platinum drugs

A doxorubicin–platinum conjugate system: impacts on PI3K/AKT actuation and apoptosis in breast cancer cells

In recent years, the development of a nano-conjugate system for drug delivery applications has gained attention among researchers.</p

A doxorubicin–platinum conjugate system:impacts on PI3K/AKT actuation and apoptosis in breast cancer cells

In recent years, the development of a nano-conjugate system for drug delivery applications has gained attention among researchers. Keeping this in mind, in this study, we developed a doxorubicin–platinum conjugate system that targeted breast cancer cell lines. To achieve this, we developed platinum nanoparticles using polyvinylpyrrolidone (PVP). High resolution-transmission electron microscopy (HR-TEM) revealed the occurrence of octopod-shaped platinum nanoparticles. Subsequently, doxorubicin (DOX) was conjugated on the surface of the as-prepared platinum octopods via an in situ stirring method. The physicochemical characterization of the doxorubicin–platinum conjugate system revealed that the PVP of PtNPs interacts with the NH(2) group of doxorubicin via electrostatic interaction/hydrogen bonding. Besides, the doxorubicin–platinum conjugate system exhibited a sustained drug release profile within the cancer cells. Furthermore, the evaluation of the in vitro anticancer efficacy of the doxorubicin–platinum conjugate system in breast cancer cells (MCF-7 and MDA-MB-231) unveiled the induction of apoptosis via intracellular ROS and DNA damage, rather than free DOX and PtNPs. Remarkably, we also perceived that the doxorubicin–platinum conjugate system was strong enough to down-regulate the PI3K/AKT signalling pathway. As a result, the tumour suppressor gene PTEN was activated, which led to the stimulation of a mitochondrion-based intrinsic apoptotic pathway and its downstream caspases, triggering cell death. Hence, our findings suggested that a biologically stable doxorubicin–platinum conjugate system could be an imperative therapeutic agent for anticancer therapy in the near future