53 research outputs found
Camel Milk Triggers Apoptotic Signaling Pathways in Human Hepatoma HepG2 and Breast Cancer MCF7 Cell Lines through Transcriptional Mechanism
Few published studies have reported the use of crude camel milk in the treatment of stomach infections, tuberculosis and cancer. Yet, little research was conducted on the effect of camel milk on the apoptosis and oxidative stress associated with human cancer. The present study investigated the effect and the underlying mechanisms of camel milk on the proliferation of human cancer cells using an in vitro model of human hepatoma (HepG2) and human breast (MCF7) cancer cells. Our results showed that camel milk, but not bovine milk, significantly inhibited HepG2 and MCF7 cells proliferation through the activation of caspase-3 mRNA and activity levels, and the induction of death receptors in both cell lines. In addition, Camel milk enhanced the expression of oxidative stress markers, heme oxygenase-1 and reactive oxygen species production in both cells. Mechanistically, the increase in caspase-3 mRNA levels by camel milk was completely blocked by the transcriptional inhibitor, actinomycin D; implying that camel milk increased de novo RNA synthesis. Furthermore, Inhibition of the mitogen activated protein kinases differentially modulated the camel milk-induced caspase-3 mRNA levels. Taken together, camel milk inhibited HepG2 and MCF7 cells survival and proliferation through the activation of both the extrinsic and intrinsic apoptotic pathways
High-throughput sensing microtiter plate for determination of biogenic amines in seafood using fluorescence or eye-vision
A new optical sensing microplate was developed for rapid screening for the presence of biogenic amines (BAs) in seafood samples with high sensitivity. The deposition of a sensing spot (containing a chameleon dye (Py-1) in a polymeric cocktail) on the bottom of the wells of a standard microplate renders the plate a new sensing tool for a rapid and parallel detection of up to 96 (real) samples. This sensing microplate enables (1) a semi-quantitative readout of analyte concentration by eye-vision, (2) a rapid fluorescence readout of 96 samples with standard instrumentation in less than two minutes (unlike chromatographic and electrophoretic methods), (3) a statistically robust data evaluation (with 8–12 replicates) and (4) a rapid parallel sample preparation with standard 8 or 12-channel micropipettes. On reaction with biogenic amines, the dye shows a significant visible color change from blue over green to red color. The appearance of red color favorably coincides with the concentration of BAs that can induce symptoms of poisoning. The linear ranges of fluorescence calibration data for six biogenic amines cover the clinical toxicological relevant range of BAs that is too low to be detected by the human nose. The LODs range from 0.16 to 0.56 μg mL−1, with correlation coefficients (r2) between 0.985 and 0.999. Finally, the evolution of spoilage of four fish samples (monitored by determination of their BA status) and the increase of their total amine content were found to agree well with previous data on time-dependent evolution of BAs in fish
Sestrin2 suppression aggravates oxidative stress and apoptosis in endothelial cells subjected to pharmacologically induced endoplasmic reticulum stress
Endoplasmic reticulum (ER) stress is an inflammatory response that contributes to endothelial dysfunction, a hallmark of cardiovascular diseases, in close interplay with oxidative stress. Recently, Sestrin2 (SESN2) emerged as a novel stress-inducible protein protecting cells from oxidative stress. We investigated here, for the first time, the impact of SESN2 suppression on oxidative stress and cell survival in human endothelial cells subjected to pharmacologically (thapsigargin)-induced ER stress and studied the underlying cellular pathways. We found that SESN2 silencing, though did not specifically induce ER stress, it aggravated the effects of thapsigargin-induced ER stress on oxidative stress and cell survival. This was associated with a dysregulation of Nrf-2, AMPK and mTORC1 signaling pathways. Furthermore, SESN2 silencing aggravated, in an additive manner, apoptosis caused by thapsigargin. Importantly, SESN2 silencing, unlike thapsigargin, caused a dramatic decrease in protein expression and phosphorylation of Akt, a critical pro-survival hub and component of the AMPK/Akt/mTORC1 axis. Our findings suggest that patients with conditions characterized by ER stress activation, such as diabetes, may be at higher risk for cardiovascular complications if their endogenous ability to stimulate and/or maintain expression levels of SESN2 is disturbed or impaired. Therefore, identifying novel or repurposing existing pharmacotherapies to enhance and/or maintain SESN2 expression levels would be beneficial in these conditions
Hydrothermal synthesis of calcium silicate hydrates in the presence of <em>3d-</em>ferromagnetic cations
1098-1101The effect of-transition metal cations, Fe3+ , Co2+ and Ni2+ on the formation of calcium silicate hydrates CaO·SiO2·H2O in the reaction system has been studied. The hydrothermal reaction products have been examined by X-ray diffraction, infrared spectroscopy and atomic absorption spectrophotometric techniques. The results indicate the presence of different shifts in the main interlayer d-spacing of calcium silicate hydrate hydrothermal products, especially 11 Å-tobermorites: 5CaO·6SiO25H2O. Calcium silicate hydrate phases formed are affected by ionic radii, acidic radical, concentration of the concerned cations and the reaction time. The mechanism of the reaction and incorporation (or substitution) of these cations in the crystal lattice of calcium silicate hydrate phases is also discussed
Ultrasonic Measurements of the Elastic Constants and their Temperature Dependence for Nearly Perfect Single Crystals of Potassium Tetrachlorozincate (K<sub>2</sub>ZnCl<sub>4</sub>)
Hydrothermal synthesis of calcium silicate hydrates in the presence of <em>3d-</em>ferromagnetic cations
1098-1101The effect of-transition metal cations, Fe3+ , Co2+ and Ni2+ on the formation of calcium silicate hydrates CaO·SiO2·H2O in the reaction system has been studied. The hydrothermal reaction products have been examined by X-ray diffraction, infrared spectroscopy and atomic absorption spectrophotometric techniques. The results indicate the presence of different shifts in the main interlayer d-spacing of calcium silicate hydrate hydrothermal products, especially 11 Å-tobermorites: 5CaO·6SiO25H2O. Calcium silicate hydrate phases formed are affected by ionic radii, acidic radical, concentration of the concerned cations and the reaction time. The mechanism of the reaction and incorporation (or substitution) of these cations in the crystal lattice of calcium silicate hydrate phases is also discussed
Ultrasonic Measurements of the Elastic Constants and their Temperature Dependence for Nearly Perfect Single Crystals of Potassium Tetrachlorozincate (K<sub>2</sub>ZnCl<sub>4</sub>)
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