Multifunctional Cu2-xTe Nanocubes Mediated Combination Therapy for Multi-Drug Resistant MDA MB 453.

Hypermethylated cancer populations are hard to treat due to their enhanced chemo-resistance, characterized by aberrant methylated DNA subunits. Herein, we report on invoking response from such a cancer lineage to chemotherapy utilizing multifunctional copper telluride (Cu2-XTe) nanocubes (NCs) as photothermal and photodynamic agents, leading to significant anticancer activity. The NCs additionally possessed photoacoustic and X-ray contrast imaging abilities that could serve in image-guided therapeutic studies.

Facile synthesis of CdTe@GdS fluorescent-magnetic nanoparticles for tumor-targeted dual-modal imaging.

Multimodal imaging has made great contribution for diagnosis and therapy of disease since it can provide more effective and complementary information in comparison to any single imaging modality. The design and fabrication of fluorescent-magnetic nanoparticles for multimodal imaging has rapidly developed over the years. Herein, we demonstrate the facile synthesis of GdS coated CdTe nanoparticles (CdTe@GdS NPs) as multimodal agents for fluorescence (FL) and T1-weighted magnetic resonance (MR) imaging. These nanoparticles obtain both prominent fluorescent and paramagnetic properties by coating the GdS shell on the surface of CdTe core via a simple room-temperature route in aqueous solution directly. It is shown that the as-prepared CdTe@GdS NPs have high quantum yield (QY) value of 12% and outstanding longitudinal relaxation rate (r1) of 11.25 mM s(-1), which allow them to be employed as FL/MR dual-modal imaging contrast agents. They also exhibit small particle size of 5 nm, excellent colloidal stability and low cellular toxicity for concentrations up to 750 µg mL(-1). In addition, with the conjugation of folic acid, the nanoparticles were successfully used for tumor-targeted FL/MR dual-modal imaging in vitro and in vivo.

Intracellular diagnostics: hunting for the mode of action of redox-modulating selenium compounds in selected model systems.

Redox-modulating compounds derived from natural sources, such as redox active secondary metabolites, are currently of considerable interest in the field of chemoprevention, drug and phytoprotectant development. Unfortunately, the exact and occasionally even selective activity of such products, and the underlying (bio-)chemical causes thereof, are often only poorly understood. A combination of the nematode- and yeast-based assays provides a powerful platform to investigate a possible biological activity of a new compound and also to explore the "redox link" which may exist between its activity on the one side and its chemistry on the other. Here, we will demonstrate the usefulness of this platform for screening several selenium and tellurium compounds for their activity and action. We will also show how the nematode-based assay can be used to obtain information on compound uptake and distribution inside a multicellular organism, whilst the yeast-based system can be employed to explore possible intracellular mechanisms via chemogenetic screening and intracellular diagnostics. Whilst none of these simple and easy-to-use assays can ultimately substitute for in-depth studies in human cells and animals, these methods nonetheless provide a first glimpse on the possible biological activities of new compounds and offer direction for more complicated future investigations. They may also uncover some rather unpleasant biochemical actions of certain compounds, such as the ability of the trace element supplement selenite to induce DNA strand breaks.

Acute pulmonary toxicity of copper gallium diselenide, copper indium diselenide, and cadmium telluride intratracheally instilled into rats.

Acute toxicity studies were conducted on copper gallium diselenide (CGS), copper indium diselenide (CIS), and cadmium telluride (CT), three novel compounds used in the photovoltaic and semiconductor industries. Female Sprague-Dawley rats (six rats/dose) were administered 0, 12, 25, 50, or 100 mg/kg body wt of CGS, CIS, or CT by intratracheal instillation. At 72 hr after treatment, body weight gain was significantly decreased in the 100 mg/kg CIS group and in all CT dose groups. Lung weights were increased in most chemical-treated rats, with CT causing the greatest increase. Total numbers of cells in bronchoalveolar lavage fluid (BALF) were significantly increased in treated rats and were greatest in the 100 mg/kg CIS group. Differential cell counts of BALF demonstrated a marked decrease in the percentage of alveolar macrophages and an increase in the percentage of polymorphonuclear leukocytes in all dose groups of all three chemicals. Slight to moderate increases in lactate dehydrogenase activity were observed in BALF from CGS- and CIS-treated rats; marked increases were observed in CT-treated rats. BALF protein was significantly increased in rats treated with CIS and CT. Microscopic examination revealed lymphoid hyperplasia in lungs of rats treated with all three chemicals. CT caused necrosis of the terminal bronchiolar epithelium and epithelium of the alveolar duct region with inflammation, prominent fibrin exudates, and type II cell hyperplasia. CGS and CIS also caused intraalveolar inflammation and type II cell hyperplasia, but did not cause the necrosis and fibrin exudate observed in lungs of CT-treated rats. Based on changes in lung weight, BALF indices, and histopathology, CT was the most toxic for the lung; CIS had intermediate toxicity and CGS was the least toxic. The solubilities of CGS and CIS were relatively low and similar at both pH levels and do not readily explain the observed differences in pulmonary toxicity. The solubility of CdTe was considerably greater than that of CGS and CIS and likely contributed to the greater toxicity of this compound.

Amounts of twelve elements required to induce selenium-vitamin E deficiency in ducklings.

Mortality and myopathy of selenium-vitamin E (Se-E) deficiency was produced, in a concentration-dependent pattern, during a 4-week study of 750 ducklings fed a commercial duck starter mash that contained adequate amounts of Se and E, and supplemented with multiple amounts of Ag (50 to 3,000 mg/kg of feed, as acetate), Zn (3,000 to 6,000 mg/kg, as sulfate), Cd (10 to 500 mg/kg, as sulfate), Te (25-500 mg/kg, as tetrachloride), Co (100 to 1,000 mg/kg, as chloride), Cu (500 to 1,500 mg/kg, as sulfate), Hg (200 to 400 mg/kg, as chloride), and Sn (1,000 mg/kg, as chloride). Also, feeding supplements of Pb (500 mg/kg, as acetate), As (600 mg/kg, as sodium arsenilate), Fe (5,000 mg/kg, as sulfate), and S (5,000 mg/kg, as sodium sulfite) produced a low-to-medium frequency of lesions of Se-E deficiency. In ducklings with muscle lesions, the gizzard was most often affected (84.2%), followed in decreasing order by skeletal muscles (69.7%), intestine (34.9%), and heart (23.0%). The frequency of skeletal muscle lesions was high in birds fed Ag, and myocardial necrosis was frequent in ducklings fed Te and Hg. Ducklings affected with myopathy were reluctant to stand. Subcutaneous edema, with or without hemorrhages, and pale areas of myonecrosis in gizzard, skeletal muscles, intestine, and heart were seen at necropsy. Birds fed Te and Hg often had hydropericardium and hemorrhagic myocardial necrosis. Seemingly, addition of many elements to a Se-E adequate commercial diet will increase the requirement for Se-E. In our duckling model, minimal amounts shown to induce Se-E deficiency were 50 mg of Ag/kg, 3,000 mg of Zn/kg, 10 mg of Cd/kg, 25 mg of Te/kg, 1200 mg of Co/kg, 500 mg of Cu/kg, 200 mg of Hg/kg, 1,000 mg of Sn/kg, 500 mg of Pb/kg, 600 mg of As/kg, 5,000 mg of Fe/kg, and 5,000 mg of S/kg.