betadex and 2-thiomalic-acid

A hydrophilic interaction chromatography (HILIC) strategy is considered as an efficient strategy for efficient glycopeptide enrichment. Here, a novel hydrophilic material (denoted as magCDP@Ada-MSA) was constructed through host-guest interaction between crosslinked β-cyclodextrin (β-CD) polymers and mercaptosuccinic acid (MSA) derived adamantane. On the one hand, crosslinked β-CD polymers have great hydrophilicity due to their abundant hydrophilic hydroxyl groups. On the other hand, the hydrophilic functional molecule MSA was introduced into crosslinked β-CD polymers through host-guest interaction for further hydrophilic modification of the material. Hydroxyl groups in crosslinked β-CD polymers and carboxyl groups in MSA together endow the material with excellent hydrophilicity and good affinity toward glycopeptides. The prepared hydrophilic material demonstrated rapid magnetic separation (within 5 s) and reusability (at least 10 cycles). Thanks to the above advantages, magCDP@Ada-MSA showed satisfactory performance for the specific enrichment of glycopeptides (selectivity, 1 : 500 molar ratios of HRP/BSA and sensitivity, 0.1 fmol μL

Topics: Adamantane; beta-Cyclodextrins; Cellulose; Cyclodextrins; Glycopeptides; Humans; Hydrophobic and Hydrophilic Interactions; Polymers; Thiomalates

Cadmium telluride quantum dots (CdTe QDs) have been proposed to induce oxidative stress, which plays a crucial role in CdTe QDs-mediated mitochondrial-dependent apoptosis in human umbilical vein endothelial cells (HUVECs). However, the direct interactions of CdTe QDs with HUVECs and their potential impairment of other organelles like endoplasmic reticulum (ER) in HUVECs are poorly understood. In this study, we reported that the negatively charged CdTe QDs (-21.63±0.91 mV), with good dispersity and fluorescence stability, were rapidly internalized via endocytosis by HUVECs, as the notable internalization could be inhibited up to 95.52% by energy depletion (NaN3/deoxyglucose or low temperature). The endocytosis inhibitors (methyl-β-cyclodextrin, genistein, sucrose, chlorpromazine, and colchicine) dramatically decreased the uptake of CdTe QDs by HUVECs, suggesting that both caveolae/raft- and clathrin-mediated endocytosis were involved in the endothelial uptake of CdTe QDs. Using immunocytochemistry, a striking overlap of the internalized CdTe QDs and ER marker was observed, which indicates that QDs may be transported to ER. The CdTe QDs also caused remarkable ER stress responses in HUVECs, confirmed by significant dilatation of ER cisternae, upregulation of ER stress markers GRP78/GRP94, and activation of protein kinase RNA-like ER kinase-eIF2α-activating transcription factor 4 pathway (including phosphorylation of both protein kinase RNA-like ER kinase and eIF2α and elevated level of activating transcription factor 4). CdTe QDs further promoted an increased C/EBP homologous protein expression, phosphorylation of c-JUN NH2-terminal kinase, and cleavage of ER-resident caspase-4, while the specific inhibitor (SP600125, Z-LEVD-fmk, or salubrinal) significantly attenuated QDs-triggered apoptosis, indicating that all three ER stress-mediated apoptosis pathways were activated and the direct participation of ER in the CdTe QDs-caused apoptotic cell death in HUVECs. Our findings provide important new insights into QDs toxicity and reveal potential cardiovascular risks for the future applications of QDs.

Topics: Apoptosis; beta-Cyclodextrins; Cadmium Compounds; Colchicine; eIF-2 Kinase; Endocytosis; Endoplasmic Reticulum Chaperone BiP; Endoplasmic Reticulum Stress; Fluorescence; Genistein; Heat-Shock Proteins; Human Umbilical Vein Endothelial Cells; Humans; Quantum Dots; Tellurium; Thiomalates