PEGylated mesoporous silica core-shell redox-responsive nanoparticles for delivering paclitaxel to breast cancer cells.

Controlling the drug release and restricting its presence in healthy organs is extremely valuable. In this study, mesoporous silica nanoparticles (MSN) as the core, loaded with paclitaxel (PTX), were coated with a non-porous silica shell functionalized with disulfide bonds. The nanoparticles were further coated with polyethylene glycol (PEG) via disulfide linkages. We analyzed the physicochemical properties of nanoparticles, including hydrodynamic size via Dynamic Light Scattering (DLS), zeta potential, X-ray Diffraction (XRD) patterns, Fourier-Transform Infrared (FTIR) spectra, and imaging through Transmission Electron Microscopy (TEM) and Scanning Electron Microscopy (SEM). The drug release profile in two distinct glutathione (GSH) concentrations of 2 µM and 10 µM was measured. The cellular uptake of nanoparticles by MCF-7 cell line was determined using Confocal Laser Scanning Microscopy (CLSM) images and flow cytometry. Furthermore, the cell viability and the capability of nanoparticles to induce apoptosis in MCF-7 cell line were studied using the MTT assay and flow cytometry, respectively. Our investigations revealed that the release of PTX from the drug delivery system was redox-responsive. Also, results indicated an elevated level of cellular uptake and efficient induction of apoptosis, underscoring the promising potential of this redox-responsive drug delivery system for breast cancer therapy.

An updated systematic review and dose-response meta-analysis on the relation between exposure to arsenic and risk of type 2 diabetes.

Arsenic is among the most critical environmental toxicants associated with many human disorders. However, its effect on type 2 diabetes mellitus (T2DM) is contradictory. This systematic review and dose-response meta-analysis aim to update information on the association between arsenic exposure and the risk of T2DM. The sample type (drinking water, urine, blood, and nails) conducted the subgroup analysis. Evaluation of the high vs. low arsenic concentrations showed a significant association between drinking water arsenic (OR: 1.58, 95% CI: 1.20-2.08) and urinary arsenic (OR: 1.37, 95% CI: 1.24-1.51) with the risk of T2DM. The linear dose-response meta-analysis showed that each 1 µg/L increase in levels of drinking water arsenic (OR: 1.01, 95% CI: 1.00-1.01) and urinary arsenic (OR: 1.01, 95% CI: 1.00-1.02) was associated with a 1% increased risk of T2DM. The non-linear dose-response analysis indicated that arsenic in urine was associated with the risk of T2DM (Pnon-linearity<0.001). However, this effect was not statistically significant for arsenic in drinking water (Pnon-linearity=0.941). Our findings suggest that blood arsenic was not significantly linked to the increased risk of T2DM in high vs. low (OR: 1.21, 95% CI: 0.85-1.71), linear (OR: 1.04, 95% CI: 0.99-1.09), and non-linear (Pnon-linearity=0.365) analysis. Also, nail arsenic was not associated with the risk of T2DM in this meta-analysis (OR: 1.33, 95% CI: 0.69-2.59). This updated dose-response meta-analysis indicated that arsenic exposure was significantly correlated with the risk of T2DM.