Efficient adsorption of phosphorus by macroscopic MOF/chitosan composites and preliminary investigation of subsequent phosphorus recovery through electrochemically-driven struvite precipitation.

The proper management of phosphorus (P) from wastewater is crucial for sustainable development consideration. Herein, we developed a strategy which combines adsorption via tailored adsorbents and electrochemically-driven struvite precipitation (ESP) for P recovery. Novel polydopamine-modified Ce-MOF/chitosan composite beads (PDA@Ce-MOF-CS) were prepared by a facile in situ growth of Ce-MOF crystals incorporated natural polymers and PDA coating. The physicochemical properties of PDA@Ce-MOF-CS were characterized. Both batch and fixed-bed column experiments were conducted to evaluate its adsorption performances. Representatively, PDA@Ce-MOF-CS performed good selectivity for P removal and exhibited a maximum adsorption capacity of 161.13 mg P/g at pH 3 and 318 K. Meanwhile, the developed adsorbent showed great reusability after ten regeneration cycles as well as good adsorption stability. The dominant mechanism for efficient P adsorption included electrostatic attraction, surface precipitation and ligand exchange. Interestingly, PDA@Ce-MOF-CS exhibited a remarkable adsorption capacity of 92.86 mg P/g by treating real P-rich electroplating wastewater, and the desorbed P in the eluate could be effectively recovered and converted into a solid fertilizer as struvite via ESP. Overall, this work provided a new research direction for P recovery from wastewater as struvite by combined technologies with the help of macroscopic MOF architectures.

Community succession during the preventive control of cyanobacterial bloom by hydrogen peroxide in an aquatic microcosm.

Hydrogen peroxide (H2O2) is an environmentally friendly algaecide with good prospects for cyanobacterial bloom control. In this study, 0.2-1.5 mg L-1 of H2O2 was applied to an aquatic microcosm containing cyanobacteria, bacteria, and eukaryotic phytoplankton at the early cyanobacterial growth stage·H2O2 generated hormesis in cyanobacteria at 0.2 mg L-1; significantly (p < 0.05) inhibited cyanobacterial growth, cyanobacterial photosynthesis, and microcystin production at 0.5-1.5 mg L-1; and effectively prevented the formation of cyanobacterial bloom without generating adverse effects on eukaryotic phytoplankton at 1.0 and 1.5 mg L-1. Application of 0.5-1.5 mg L-1 H2O2 directly inhibited the abundance of five typical bloom-forming cyanobacterial genera (Microcystis, Anabeana, Synechococcus, Nostoc, and Oscillatoria), which were negatively correlated with four bacterial genera (Actinotalea, Flavobacterium, Fluviicola, and Exiguobacterium) and five eukaryotic phytoplankton genera (Cyclotella, Desmodesmus, Dinobryon, Fragilaria, and Mychonastes) and positively correlated with six proteobacterial genera (Brevundimonas, Devosia, Limnohabitans, Porphyrobacter, Pseudomonas, and Rhodobacter). After application of 1.0 and 1.5 mg L-1 H2O2 for 15 days, H2O2-treated groups showed significantly (p < 0.05) different prokaryotic community structures from that of the control group at the bloom stage (15th day), while eukaryotic community structures in H2O2-treated groups remained stable and showed high similarity with that of the control group at a non-bloom stage (5th day). Application of low-dose H2O2 during the early cyanobacterial growth stage could effectively prevent the formation of cyanobacterial blooms without disrupting non-target organisms.

Involvement of the Nrf2 pathway in the regulation of pterostilbene-induced apoptosis in HeLa cells via ER stress.

Among the various cancer cell lines, HeLa cells were found to be sensitive to pterostilbene (Pte), a compound that is enriched in small fruits such as grapes and berries. However, the mechanism involved in the cytotoxicity of Pte has not been fully characterized. Using biochemical and free radical biological experiments in vitro, we identified the pro-apoptotic profiles of Pte and evaluated the level of redox stress-triggered ER stress during HeLa cell apoptosis. The data showed a strong dose-response relationship between Pte exposure and the characteristics of HeLa apoptosis in terms of changes in apoptotic morphology, DNA fragmentation, and activated caspases in the intrinsic apoptotic pathway. During drug exposure, alterations in the intracellular redox homeostasis that favor oxidation were necessary to cause ER stress-related apoptosis, as demonstrated by enzymatic and non-enzymatic redox modulators. A statistically significant and dose-dependent increase (P < 0.05) was found with regard to the unique expression levels of Nrf2/ARE downstream target genes in HeLa cells undergoing late apoptosis, levels that were restored with anti-oxidant application with the Pte treatment. Our research demonstrated that Pte trigged ER stress by redox homeostasis imbalance, which was negatively regulated by a following activation of Nrf2.