Bare plasmonic metal nanoparticles: synthesis, characterisation and in vitro toxicity assessment on a liver carcinoma cell line.

Metal nanoparticles have generated great interest due to their excellent optical and chemical properties. The widely used chemical method for synthesising nanoparticles involves capping agents for colloidal stability. However, there are scarce reports on the application of metal nanoparticles synthesised without using capping agents. Hence, there is a need to develop pristine nanoparticles devoid of capping that can be used for translational research. Here, the authors developed a facile and rapid method for synthesising bare metal nanoparticles (platinum/silver/gold) that are chemically reactive and stable for a month upon storage. They synthesised bare metal nanoparticles of sub-15 nm and characterised using standard techniques (UV-VIS-NIR/DLS/zeta//TEM/XRD). They assessed the safety of the synthesised nanoparticles on the liver carcinoma cell line (HepG2). Bare gold and platinum nanoparticles were non-toxic in comparison to bare silver nanoparticles. Bare metal nanoparticles were also checked for metal detection wherein antimony, mercury and chromium were detected using bare gold and silver nanoparticles. The spectroscopic shifts of the nanoparticles when bound to metals resulted in blue and red shifting of the plasmon band, indicating the sensing of metals. These results show that bare metal nanoparticles have the potential to emerge as a promising candidate for biomedical and sensing applications.

From the Cover: Arsenic Induces Hippocampal Neuronal Apoptosis and Cognitive Impairments via an Up-Regulated BMP2/Smad-Dependent Reduced BDNF/TrkB Signaling in Rats.

Arsenic promotes hippocampal neuronal damage inducing cognitive impairments. However, mechanism arbitrating arsenic-mediated cognitive deficits remains less-known. Here, we identified that chronic exposure to environmentally relevant doses of arsenic increased apoptosis, characterized by caspase-3 activation, poly(ADP-ribose) polymerase cleavage and Terminal deoxynucleotidyl transferase dUTP nick-end labeling of rat hippocampal neurons, marked by NeuN. Investigating apoptotic mechanism through invivo and invitro studies revealed that arsenic promoted bone morphogenetic protein-2 (BMP2) expression, supported by increased BMP-receptor2 (BMPR2) and p-Smad1/5 in hippocampal neurons. BMP2-silencing and treatment with BMP antagonist, noggin, attenuated the arsenic-induced apoptosis and loss in hippocampal neurons. We then investigated whether BMP2/Smad signaling stimulated neuronal apoptosis independently or required other intermediate pathways. We hypothesized participation of brain-derived neurotrophic factor (BDNF) that promotes neuronal survival. We identified an arsenic-mediated attenuation of BDNF-dependent TrkB signaling, and observed that co-treatment with recombinant-BDNF reinstated BDNF/TrkB and reduced neuronal apoptosis. To probe whether BMP2/Smad and BDNF/TrkB pathways could be linked, we co-treated arsenic with noggin or recombinant BDNF. We detected a noggin-mediated restored BDNF/TrkB, while recombinant-BDNF failed to affect BMP2/Smad signaling. In addition, we found that TrkB-inhibitor, K252a, nullified noggin-induced protection, proving the necessity of a downstream reduced BDNF/TrKB signaling for BMP2/Smad-mediated apoptosis in arsenic-treated neurons. We further related our observations with cognitive performances, and detected noggin-mediated restoration of transfer latency time and learning-memory ability for passive avoidance and Y-Maze tests respectively in arsenic-treated rats. Overall, our study proves that arsenic promotes hippocampal neuronal apoptosis through an up-regulated BMP2/Smad-dependent attenuation of BDNF/TrkB pathway, inducing cognitive deficits.