DNA dendrimer-templated copper nanoparticles: self-assembly, aggregation-induced emission enhancement and sensing of lead ions.

Copper nanomaterials based on DNA scaffold (DNA-Cu NMs) are becoming a novel fluorescent material, but it is still challenging to obtain highly fluorescent DNA-Cu NMs with excellent stability. In this work, we report a kind of copper nano-assemblies (Cu NASs) with aggregation-induced emission enhancement (AIEE) property using DNA dendrimers with sticky end as template. The sticky end of the DNA dendrimers induced the formation of much bigger Cu NASs with average size ranging from 131 to 264 nm, depending on the length of the DNA dendrimer sticky end from 6 bases to 27 bases. Compared with complete complementary DNA dendrimer, nearly 6-fold fluorescence enhancement was achieved using DNA dendrimer with 27 bases sticky end. Moreover, the DNA dendrimer-Cu NASs demonstrated excellent stability in serum and could be rapidly quenched by Pb2+ ions. Based on the above property, highly sensitive and selective fluorescent detection of Pb2+ ions was possible with a linear range of 2.0-100 nM and a detection limit of 0.75 nM. Due to the sensitive and rapid response to Pb2+ as well as excellent stability in complex matrix, the proposed fluorescent Cu NASs demonstrated high potential as an excellent fluorescent probe for Pb2+ in complex matrix.

Effects of duodenal redox status on calcium absorption and related genes expression in high-fat diet-fed mice.

OBJECTIVE: This study investigated whether duodenal redox imbalance induced by high-fat diet (HFD) influenced expression of genes involved in transcellular calcium absorption, thus leading to reduced intestinal calcium absorption. METHODS: Male C57BL/6 mice were randomly assigned to one of four groups with eight mice in each group. The control group consumed an ordinary diet (4.9% fat, w/w). The other three groups were fed a HFD (21.2% fat), the HFD plus 0.1% lipoic acid, or the HFD plus an additional 0.9% calcium supplement. After 9 wk, plasma and duodenal oxidative stress biomarkers including malondialdehyde, superoxide dismutase, catalase, total antioxidant capacity, reduced glutathione/oxidized glutathione ratio, and reactive oxygen species were examined. The intestinal calcium absorption state was evaluated through examining the calcium balance, bone mineral density, and calcium metabolism biomarkers. Furthermore, quantitative reverse transcription-polymerase chain reaction was carried out to analyze the changes in expression of transcellular calcium absorption-related genes. RESULTS: The HFD induced marked decreases in intestinal calcium absorption and bone mineral density of the whole body, accompanied by redox imbalance and increased oxidative damage in duodenum; duodenal expression of calbindin-D(9K), plasma membrane calcium ATPase (PMCA(1b)), and sodium-calcium exchanger was significantly down-regulated by 1.9-, 2.7-, and 1.5-fold, respectively. Furthermore, duodenal glutathione and oxidized glutathione (GSH/GSSG) ratios were strongly positively correlated with the apparent calcium absorption rate and the expression of PMCA(1b) and Calbindin-D(9K), whereas reactive oxygen species levels were negatively correlated with them. CONCLUSION: Our results demonstrated that a HFD-induced duodenal oxidation state could significantly down-regulate expression of calbindin-D(9K), PMCA(1b), and sodium-calcium exchanger, thus causing an inhibitory effect on intestinal calcium absorption.