Mesoporous organosilicas with highly-content tyrosine framework as extractive phases for non-steroidal anti-inflammatory drugs in aquatic media.

BACKGROUND: Attentions regarding ordered mesoporous silica materials (OMSs), with large specific surface areas and narrow pore size distribution, which are prepared via self-assembly techniques, have been raised in sorption, separation, and sample preparation. However, in order to extend and improve their applications, a functionalization step is required. Organic units can be anchored on the inner or outer surface as well as in the silica wall framework by co-condensation-, grafting-, and periodic mesoporous organosilica (PMO) preparation approaches. Apparently, by synthesizing PMO with extensive and flexible organic bridging groups within the mesoporous wall, an efficient extractive phase can be achieved. RESULTS: We employed tyrosine amino acid to synthesize a PMO-based extractive phase. The FT-IR, 1H NMR, HR-ESI-MS, Low angle-XRD, TEM, FESEM, BET, and EDX-MAP analyses confirmed the successful synthesis of PMO within the salt-assisted templating method. A comprehensive study on sorption behavior of PMO was performed and its efficiency was evaluated against the grafting and co-condensation methods. Then, it was implemented to the pipette tip-micro solid phase extraction (PT-µ-SPE) of widely used non-steroidal anti-inflammatory drugs (NSAIDs) in water/wastewaters. Limits of detection and quantification were obtained in the range of 0.1-1.5 and 0.3-5 µg L-1, respectively. The calibration plots are linear in the 1-1000, 3-1000, 10-750, and 3-750 µg L-1, respectively. The intra-and inter-day precision at 50 and 200 µg L-1 levels are 2.9-7.1 % and 3.5-8%, while recoveries are between 84 and 111 %. SIGNIFICANCE: High-capacity tyrosine functionalized PMO with 2D hexagonal symmetry silica mesoporous structures found to be highly efficient extractive media. Despite the bulkiness and flexibility of the bridging group within the mesoporous wall, the synthesis condition was optimized in order to load more organic content in the PMO structure. The PMO performance was superior over organically modified ordered mesoporous silica materials prepared by the grafting and co-condensation methods.

A New Approach for Determining the Minimum Concentration of Proanthocyanidin for Preservation of Collagen in H Dentin.

PURPOSE: Introducing a minimum concentration and clinically relevant application time for grape seed extract (GSE) proanthocyanidin as a dentin preserver. MATERIALS AND METHODS: Dentin beams were demineralized in 10% phosphoric acid for 24h. Then, the following groups were prepared: G1: no treatment, G2: 2% CHX + 1min, G3: 1% GSE + 1min, G4: 1% GSE +5min, G5: 2% GSE + 1min, G6: 2% GSE + 5min, G7: 5% GSE + 1min and G8: 5% GSE + 5min. After 30 days, MALDI-TOF mass spectrometry was used to confirm the availability of digested peptide fragments and monitor the pattern of collagen digestion. Gravimetric assessment and HPLC-UV were utilized for quantitative measurement of dentin destruction. Glycine quantities were considered as measures of collagen digestion. RESULTS: 7% to 25% loss of dry mass was measured in experimental groups. Regarding the liberated Glycine, GSE dose- and time-responses were observed, so that, 5% GSE showed considerable protecting effect on collagen compared to 1 and 2% GSE (P⟨0.001) and 5min GSE application could establish superior dentin preservation compared to 1min application (P⟨0.001). CONCLUSION: 5-minute treatment of dentin at 2% GSE and above is essential for protecting the demineralized dentin collagen against biodegradation.

Cytotoxicity, oxidative stress, and apoptosis in K562 leukemia cells induced by an active compound from pyrano-pyridine derivatives.

Recent studies have reported the potential of pyrano-pyridine compounds in inhibiting cell growth and apoptosis induction in cancer cells. Here, we investigated the effect of new pyrano-pyridine derivatives on proliferation, oxidative damages, and apoptosis in K562 leukemia cells. Among different tested compounds, we found 8-(4-chlorobenzylidene)-2-amino-4-(4-chlorophenyl)-5, 6, 7, 8-tetrahydro-6-phenethyl-4H-pyrano-[3,2-c]pyridine-3-carbonitrile (4-CP.P) as the most effective compound with IC50 value of 20 µM. Gel electrophoresis, fluorescence microscopy, and flow cytometry analyses indicated the apoptosis induction ability of 4-CP.P in K562 cells. Further analyses revealed that 4-CP.P induces significant increase in cellular reactive oxygen species production, lipid peroxidation, protein oxidation, and total thiol depletion. Interestingly, while 4-CP.P significantly increased the activity of superoxide dismutase, it reduced the catalase activity in a time-dependent manner. These data propose that 4-CP.P treatment causes free radicals accumulation that ultimately leads to oxidative stress condition and apoptosis induction. Therefore, we report the 4-CP.P as a novel, potent compound as a chemotherapeutic agent in cancer treatment.