Zinc-chitosan nanoparticles induced apoptosis in human acute T-lymphocyte leukemia through activation of tumor necrosis factor receptor CD95 and apoptosis-related genes.

Chitosan (CS), a novel biomaterial is widely used as a drug nano-carrier for cancer treatments. Towards this aim, anticancer and antibacterial activities of CS-nanoparticles-linked zinc (Zn-CSNPs) were evaluated. The particle size of CSNPs was lowered (113.09 nm) compared to Zn-CSNPs (160.7 nm). Both nanoparticles (CSNPs and Zn-CSNPs) were spherical in shape, polydispersive and homogenous. Fourier transforms infrared spectrophotometer (FTIR) and energy dispersive X-ray spectroscopy (EDX) analysis confirmed the different molecular arrangement of NPs and the presence of Zn in Zn-CSNPs and CS in both NPs, respectively. Zn-CSNPs had higher inhibitory activity against tested pathogens with a minimal inhibitory concentration (MIC) of 9.25-13.5 μg·mL-1 and showed the complete inhibition of Staphylococcus aureus and Escherichia coli. Zn-CSNPs have triggered the apoptosis through activation of first apoptosis signal receptor/cluster of differentiation 95 (Fas/CD95), and apoptotic-regulatory genes and caused 65-70% of cellular damage in human acute T-lymphocyte leukemia (6T-CEM) cells. Overall, internalizing properties of Zn from CSNPs is a promising therapeutic approach to treat Zn-deficiency related diseases particularly human acute leukemia (HAL).