Effects of carbon sources and operation modes on the performances of aerobic denitrification process and its microbial community shifts.

Carbon source, operation mode and microbial species have great effects on the synthesis of poly-ß-hydroxybutyrate (PHB) which has been identified as the key issue for aerobic denitrification process. In this study, an aerobic denitrification SBR was operated under anoxic/oxic mode and completely oxic mode with the carbon source of CH3COONa and CH3CH2CH2COONa, respectively. Total nitrogen (TN) removal efficiencies, PHB content in activated sludge, production of nitric oxide (NO) and nitrous oxide (N2O) of the process were investigated in great detail. The main results obtained from the trial were: (1) the average TN removal was in the range of 86.11%-90.05%; (2) the maximum TN removal efficiency and the maximum PHB content of the process being achieved when the carbon source of CH3CH2CH2COONa was applied under anoxic/oxic mode; (3) in case of CH3COONa as the carbon source, the concentrations of NO and N2O in the bulk liquid were ∼0.4 mg/L and ∼0.02 mg/L, respectively, while in case of CH3CH2CH2COONa, N2O of ∼0.2 mg/L and NO of ∼2.5 mg/L were recorded and the latter was decreased to ∼1.0 mg/L at the end of the cycle; (4) no obvious dominant genus in case of using CH3COONa, while Plasticicumulans sp. being the major microbial community when using CH3CH2CH2COONa. Overall, the effect of carbon source on microbial community is obvious. Nevertheless, operation mode affects the PHB synthesis, while PHB plays an important role in aerobic denitrification process for achieving a relatively high TN nitrogen removal efficiency. CH3COONa is a better carbon source for aerobic denitrification compared with CH3CH2CH2COONa.

Europium-doped Gd2O3 nanotubes cause the necrosis of primary mouse bone marrow stromal cells through lysosome and mitochondrion damage.

With the wide applications of europium-doped Gd2O3 nanoparticles (Gd2O3:Eu(3+) NPs) in biomedical fields, it will inevitably increase the chance of human exposure. It was reported that Gd2O3:Eu(3+) NPs could accumulate in bone. However, there have been few reports about the potential effect of Gd2O3:Eu(3+) NPs on bone marrow stromal cells (BMSCs). In this study, the Gd2O3:Eu(3+) nanotubes were prepared and characterized by powder X-ray diffraction (XRD), photoluminescence (PL) excitation and emission spectra, scanning electron microscope (SEM), and transmission electron microscopy (TEM). The cytotoxicity of Gd2O3:Eu(3+) nanotubes on BMSCs and the associated mechanisms were further studied. The results indicated that they could be uptaken into BMSCs by an energy-dependent and macropinocytosis-mediated endocytosis process, and primarily localized in lysosome. Gd2O3:Eu(3+) nanotubes effectively inhibited the viability of BMSCs in concentration and time-dependent manners. A significant increase in the percentage of late apoptotic/necrotic cells, lactate dehydrogenase (LDH) leakage and the number of PI-stained cells was found after BMSCs were treated by 10, 20, and 40µg/mL of Gd2O3:Eu(3+) nanotubes for 12h. No obvious DNA ladders were detected, but a dispersed band was observed. The above results revealed that Gd2O3:Eu(3+) nanotubes could trigger cell death by necrosis instead of apoptosis. Two mechanisms were involved in Gd2O3:Eu(3+) nanotube-induced BMSCs necrosis: lysosomal rupture and release of cathepsins B; and the overproduction of reactive oxygen species (ROS) injury to the mitochondria and DNA. The study provides novel evidence to elucidate the toxicity mechanisms and may be beneficial to more rational applications of these nanomaterials in the future.

Biocompatibility of defect-related luminescent nanostructured and microstructured hydroxyapatite.

Three defect-related luminescent hydroxyapatite (HAP) particles, S1, S2, and S3, with different morphologies (the samples S1 and S2 are nanorods with diameters of 25 nm and lengths of 30 and 100 nm, respectively; sample S3 is bur-like microspheres with diameters of 5-6 µm) were synthesized, and their biocompatibility was investigated by MTT, reactive oxygen species (ROS), interleukin-6 (IL-6), comet, and hemolysis assays. The results indicated that all samples were stable in cell culture medium and did not induce the synthesis of proinflammatory cytokine IL-6 or result in hemolysis. It was found that samples S1 and S3 inhibited osteoblast (OB) viability at concentrations of 5, 10, 20, 40, and 80 µg/mL for 24, 48, and 72 h. Sample S2 had no effect on the viability of OB at all tested concentrations for 24 and 48 h, but the viability of OB was increased at concentrations of 20, 40, and 80 µg/mL for 72 h. Samples S1 and S3 could increase the level of cellular ROS; sample S2 had no effect on the level of cellular ROS at a concentration of 20 µg/mL for 48 h. Although samples S1 and S3 induced significant DNA damage, sample S2 could not cause significant DNA damage at a concentration of 20 µg/mL for 72 h. The results suggest that longer nanorod HAP can show excellent biocompatibility and therefore may find potential applications in biomedical fields.

Size-dependent cytotoxicity of europium doped NaYF 4 nanoparticles in endothelial cells.

Lanthanide-doped sodium yttrium fluoride (NaYF4) nanoparticles exhibit novel optical properties which make them be widely used in various fields. The extensive applications increase the chance of human exposure to these nanoparticles and thus raise deep concerns regarding their riskiness. In the present study, we have synthesized europium doped NaYF4 (NaYF4:Eu(3+)) nanoparticles with three diameters and used endothelial cells (ECs) as a cell model to explore the potential toxic effect. The cell viability, cytomembrane integrity, cellular uptake, intracellular localization, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), apoptosis detection, caspase-3 activity and expression of inflammatory gene were studied. The results indicated that these nanoparticles could be uptaken into ECs and decrease the cell viability, induce the intracellular lactate dehydrogenase (LDH) release, increase the ROS level, and decrease the cell MMP in a size-dependent manner. Besides that, the cells were suffered to apoptosis with the caspase-3 activation, and the inflammation specific gene expressions (ICAM1 and VCAM1) were also increased. Our results suggest that the damage pathway may be related to the ROS generation and mitochondrial damage. The results provide novel evidence to elucidate their toxicity mechanisms and may be helpful for more rational applications of these compounds in the future.

Thulium ion promotes apoptosis of primary mouse bone marrow stromal cells.

Bone is one of the main target organs for the lanthanides (Ln). Biodistribution studies of Tm-based compounds in vivo showed that bone had significant uptake. But the effect of Tm(3+) on primary mouse bone marrow stromal cells (BMSCs) has not been reported. So we investigated the effect and underlying mechanisms of Tm(3+) on BMSCs. Cell viability, cell apoptosis, reactive oxygen species (ROS) level, lactate dehydrogenase (LDH) activity and mitochondrial membrane potential (MMP) were studied. The results indicated that Tm(3+) increased the viability of BMSCs at concentrations of 1×10(−7), 1×10(−6), 1×10(−5), and 1×10(−4) mol/L in a dose-dependent manner, turned to decrease the viability of BMSCs at the highest concentration of 1×10(−3) mol/L for 24, 48, and 72 h. Tm(3+) at 1×10(−3) mol/L promoted apoptosis of BMSCs, increased the ROS and LDH levels, and decreased MMP in BMSCs. Taken together, we demonstrated that Tm(3+) + at 1×10(−3) mol/L might induce cellular apoptosis through mitochondrial pathway. These resultsmay be helpful for more rational application of Tm-based compounds in the future.