Highly selective chemosensor for the sensitive detection of Hg2+ in aqueous media and its cell imaging application.

The deleterious toxicity of Hg2+ on ecological and biological system makes it crucial for the precise monitoring of Hg2+. Herein, we prepared a novel "turn-on" chemosensor N'-(4-(methylthio)butan-2-ylidene) rhodamine B hydrazide (denoted as MTRH) by a simple two-step reaction. MTRH exhibited an ultra-low detection limit (LOD) in fluorescence measurement of Hg2+ in pure aqueous media, which was estimated to be 1.3 × 10-9 mol·L-1. Moreover, the proposed chemosensor holds the ability of visualizing Hg2+ by the distinct color change of the solution. The corresponding recognition mechanism was investigated by Job's plots, mass spectrometry and DFT calculation analysis. Importantly, the characteristics such as high sensitivity, low cytotoxicity and good biocompatibility of MTRH exhibited in the application of detecting Hg2+ in real water sample and bioimaging of intracellular Hg2+ prove that MTRH is a promising tool to evaluate the levels of Hg2+ in complex biological systems.

A novel benzotriazole derivative inhibits proliferation of human hepatocarcinoma cells by increasing oxidative stress concomitant mitochondrial damage.

Benzotriazole derivatives have been shown to be able to induce growth inhibition in cancer cells. In the present study, we synthesized bioactive compound, 3-(1H-benzo [d] [1,2,3] triazol-1-yl)-1-(4-methoxyphenyl)-1-oxopropan-2-yl benzoate (BmOB), which is a novel benzotriazole derivative. BmOB displayed anti-proliferative effects on several human tumor cell lines. Human hepatocarcinoma BEL-7402 cell line was selected as a model to illustrate BmOB's inhibition effect and its potential mechanism, since it was the highest susceptible cell line to BmOB. It was shown that treatment with BmOB resulted in generation of reactive oxygen species, disruption of mitochondrial membrane potential (DeltaPsim), and cell death in BEL-7402 cells. BmOB induced cytotoxicity could be prevented by antioxidant vitamin C and mitochondrial permeability transition inhibitor cyclosporine A. cyclosporine A could also protect the BmOB induced collapse of DeltaPsim in BEL7402 cells, while vitamin C did not show similar effects. The results suggest that BmOB could inhibit BEL-7402 cell proliferation, and the cell death may occur through the modulation of mitochondrial functions regulated by reactive oxygen species. It appears that collapse of DeltaPsim prior to intracellular reactive oxygen species arose during the cytotoxic process in our experimental system.