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[Display omitted] • S-nZVI/PAA system could effectively degrade CIP in 60 min. • S doping promotes Fe(II)/Fe(III) cycling and improves the degradation efficiency of CIP. • Reactive oxygen species (ROS) and Fe(IV) contributed to CIP elimination. • S-nZVI/PAA system was effective at mitigating the toxicity of CIP. As commonly observed water pollutants, antibiotics can induce antibiotic-resistance genes and pose significant risks to ecosystems and human health. Consequently, eliminating antibiotics from water environments is essential. We used the sulfidated nano zero-valent iron (S-nZVI) to activate peracetic acid (PAA) system to facilitate ciprofloxacin (CIP) degradation. S-nZVI was fabricated using the liquid-phase method, yielding particles with a predominantly spherical morphology and an average size range of 70–110 nm. Under optimized conditions, the S-nZVI/PAA system had a remarkable CIP removal efficiency of 95.61 % in 60 min. The reactive oxygen species (ROS) and Fe species (Fe(IV)) generated in the S-nZVI/PAA system were fundamental in facilitating the degradation of CIP. The reaction products of CIP were identified, and the toxicity was reduced after degradation. Additionally, an investigation was conducted to explore the practical application potential of the S-nZVI/PAA system. The work provides a promising strategy for the removal of antibiotics in water, and gives new insights into the mechanism of S-nZVI activating PAA to remove antibiotics. [ABSTRACT FROM AUTHOR]

Aggregation‐induced emission luminogens (AIEgens) as a new class of optical probes for two‐photon imaging (2PI) have attracted extensive attention in the research community. However, their non‐radiative energy dissipation plays a non‐negligible role in energy consumption, thereby weakening their performance in 2PI. Exploration of a facile and general approach to control the energy relaxation pathways is thus a fascinating yet significantly challenging task. To address this concern, an organic doping method is proposed herein by using TPE‐Br as the doping AIEgen and MeOTTMN as the functional AIEgen. With increased amount of doping molecules, a steadily strengthened brightness (up to 29‐fold of quantum yield) is observed at the expense of reactive oxygen species production. Remarkably, an ultradeep imaging depth of 1000 µm in a mouse brain is realized via 2PI using the heavily organic‐doped AIEgen(ODA) nanoparticles (NPs). Such result is far superior to the imaging depth of 156 µm enabled by MeOTTMN NPs. The safe use of ODA NPs is further evaluated by in vitro and in vivo toxicity assessment. This study thus provides an attractive paradigm to control the energy relaxation of AIEgen NPs and maximize their performance in 2PI while circumventing the difficulties in molecular engineering. [ABSTRACT FROM AUTHOR]

Background: Drug-induced liver damage is a severe medical issue that affects people all over the world. Sorafenib has some side effects that cause liver injury. A dietary medicinal plant called Penthorum chinense Pursh. (PCP) has hepatoprotective properties. There are currently few reports on PCP's protective impact and mechanism against sorafenib-induced liver injury. Methods: To create a liver injury model, sorafenib was administered to BRL-3A cells. Cell viability assays, immunofluorescence tests, Western blotting, real-time quantitative PCR, and high-content imaging systems were utilized to examine PCP's effect and mechanism. Results: In this study, PCP treatment mitigated the liver damage caused by sorafenib by enhancing cell survival, lowering lipid reactive oxygen species and malondialdehyde levels, and elevating glutathione levels. In addition, PCP can enhance the protein expression of cystine/glutamate transporter xCT and glutathione peroxidase 4, reduce iron content and alleviate mitochondrial toxicity. Further mechanism studies revealed that PCP inhibited ferroptosis by promoting the production of nuclear factor E2-related factor 2 nuclear translocation and subsequently affecting target genes (HO-1 and NQO1). Conclusion: Together, PCP regulates the nuclear factor E2-related factor 2 pathway, which helps to lessen ferroptosis brought on by sorafenib. [ABSTRACT FROM AUTHOR]

Biochar is an environmentally friendly material with potential applications in water purification. In this study, herb residue nitrogen-doped biochar (N-BC) was fabricated and used to activate peroxymonosulfate (PMS). Characterization and density-functional theory (DFT) studies were conducted to explore the influence of nitrogen doping. Radical scavenging activity and electron paramagnetic resonance (EPR) spectroscopy revealed that non-radical singlet oxygen (1O 2) is the main reactive oxidative species. Additionally, pyridinic-N was shown to play a pivotal role in the 1O 2 -dominated pathway. Three possible degradation pathways were proposed based on the identified degradation intermediates. Batch experiments confirmed that N-BC showed excellent catalytic performance and reusability. The best condition for tetracycline (TC) degradation efficiency (>99%) in 60 min was obtained when the dosage of N-BC was 1 g/L and the concentration of PMS was 5 mM. Furthermore, N-BC showed approximately 65.5% degradation efficiency within 4 cycles. Furthermore, the toxicity of degradation intermediates was examined using ECOSAR and T.E.S.T procedures. This study brings forth a feasible strategy to synthesize biochar. Furthermore, the proposed approach will facilitate the use of biochar in water purification. [Display omitted] • Nitrogen doped biochar was an efficient catalyst for peroxymonosulfate activation. • Non-radical singlet oxygen was the dominant reactive oxidative species. • Nitrogen doped biochar maintained catalytic effect after four cycles. • The toxicity of TC degradation intermediates was evaluated using T.E.S.T and ECOSAR. [ABSTRACT FROM AUTHOR]

Oxidative stress is important in carcinogenesis and metastasis. Salidroside, a phenylpropanoid glycoside isolated from Rhodiola rosea L., shows potent antioxidant properties. The aim of the present study was to investigate the roles of salidroside in cell proliferation, the cell cycle, apoptosis, invasion and epithelial-mesenchymal transition (EMT) in A549 cells. The human alveolar adenocarcinoma cell line, A549, was incubated with various concentrations of salidroside (0, 1, 5, 10 and 20 µg/ml) and cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Propidium iodide (PI) staining was used to determine the cell cycle by low cytometry. Cell apoptosis was detected by Annexin V-fluorescein isothiocyanate and PI double-staining, and tumor invasion was detected by Boyden chamber invasion assay. Western blot analysis was performed to detect the expression of EMT markers, Snail and phospho-p38. The results showed that salidroside significantly reduced the proliferation of A549 cells, inhibited cell cycle arrest in the G0/G1 phase and induced apoptosis. Salidroside inhibited transforming growth factor-ß-induced tumor invasion and suppressed the protein expression of Snail. As an antioxidant, salidroside inhibited the intracellular reactive oxygen species (ROS) formation in a dose-dependent manner in A549 cells, and depletion of intracellular ROS by vitamin C suppressed apoptosis by salidroside treatment. Salidroside was also found to inhibit the expression of phospho-p38 in A549 cells. In conclusion, salidroside inhibits cell proliferation, the cell cycle and metastasis and induces apoptosis, which may be due to its interference in the intracellular ROS generation, thereby, downregulating the ROS-phospho-p38 signaling pathway. [ABSTRACT FROM AUTHOR]

Mobile phones are widely used globally. However, the biological effects due to exposure to electromagnetic fields (EMF) produced by mobile phones are largely unknown. Environmental and occupational exposure of humans to γ-rays is a biologically relevant phenomenon. Consequently studies were undertaken to examine the interactions between γ-rays and EMF on human health. In this study, exposure to 900-MHz EMF expanded γ-ray damage to SHG44 cells. Preexposure EMF enhanced the decrease in cell proliferation induced by γ-ray irradiation and the rate of apoptosis. The combination of EMF and γ-ray exposure resulted in a synergistic effect by triggering stress response, which increased reactive oxygen species, but the expression of hsp70 at both mRNA and protein levels remained unaltered. Data indicate that the adverse effects of γ-rays on cellular functions are strengthened by EMF. [ABSTRACT FROM AUTHOR]