Boosted Photocatalytic Degradation of Atrazine Using Oxygen-Modified g-C3N4: Investigation of the Reactive Oxygen Species Interconversion.

Elaborating the specific reactive oxygen species (ROS) involved in the photocatalytic degradation of atrazine (ATZ) is of great significance for elucidating the underlying mechanism. This study provided conclusive evidence that hydroxyl radicals (·OH) were the primary ROS responsible for the efficient photocatalytic degradation of ATZ, thereby questioning the reliability of widely adopted radical quenching techniques in discerning authentic ROS species. As an illustration, oxygen-modified g-C3N4 (OCN) was prepared to counteract the limitations of pristine g-C3N4 (CN). Comparative assessments between CN and OCN revealed a remarkable 10.44-fold improvement in the photocatalytic degradation of ATZ by OCN. This enhancement was ascribed to the increased content of C-O functional groups on the surface of the OCN, which facilitated the conversion of superoxide radicals (·O2-) into hydrogen peroxide (H2O2), subsequently leading to the generation of ·OH. The increased production of ·OH contributed to the efficient dealkylation, dechlorination, and hydroxylation of ATZ. Furthermore, toxicity assessments revealed a significant reduction in ATZ toxicity following its photocatalytic degradation by OCN. This study sheds light on the intricate interconversion of ROS and offers valuable mechanistic insights into the photocatalytic degradation of ATZ.

Effect of hydrothermal-acid pretreatment on methane yield and microbial community in anaerobic digestion of rice straw.

Hydrothermal pretreatment has been proposed to enhance straw methane yield during anaerobic digestion recently. However, the combined effect of hydrothermal and organic acid pretreatment (HTOAP) needs further investigation. This study identified optimal pretreatment at 120 °C with 3 % acetic acid for 24 h by orthogonal design method. The HTOAP increased the reducing sugar content by destroying the lignocellulosic structure. A 79 % increment of methane production after HTOAP was observed compared to the untreated group. Microbial analysis showed that HTOAP enriched the relative abundance of lignocellulose-degraders, such as W5053, Thermanaerovibrio, Caldicoprobacter, as well as the syntrophic acetate oxidizing bacteria Syntrophaceticus. Moreover, Methanobacterium conducted hydrogenotrophic methanogenesis dominantly. Furthermore, the potential function analysis showed that HTOAP stimulated the expression of key enzymes in the hydrogenotrophic pathway, including carbon-monoxide dehydrogenase (EC 1.2.7.4) and coenzyme F420 hydrogenase (EC 1.12.98.1). This investigation illustrated the potential of HTOAP of rice straw to facilitate methane production.

FePO4/WB as an efficient heterogeneous Fenton-like catalyst for rapid removal of neonicotinoid insecticides: ROS quantification, mechanistic insights and degradation pathways.

Iron-based catalysts for peroxymonosulfate (PMS) activation hold considerable potential in water treatment. However, the slow conversion of Fe(III) to Fe(II) restricts its large-scale application. Herein, an iron phosphate tungsten boride composite (FePO4/WB) was synthesized by a simple hydrothermal method to facilitate the Fe(III)/Fe(II) redox cycle and realize the efficient degradation of neonicotinoid insecticides (NEOs). Based on electron paramagnetic resonance (EPR) characterization, scavenging experiments, chemical probe approaches, and quantitative tests, both radicals (HO• and SO4⋅-) and non-radicals (1O2 and Fe(IV)) were produced in the FePO4/WB-PMS system, with relative contributions of 3.02 %, 3.58 %, 6.24 %, and 87.16 % to the degradation of imidacloprid (IMI), respectively. Mechanistic studies revealed that tungsten boride (WB) promoted the reduction of FePO4, and the generated Fe(II) dominantly activated PMS through a two-electron transfer to form Fe(IV), while a minority of Fe(II) engaged in a one-electron transfer with PMS to produce SO4⋅-, HO•, and 1O2. In addition, four degradation pathways of NEOs were proposed by analyzing the byproducts using UPLC-Q-TOF-MS/MS. Besides, seed germination experiments revealed the biotoxicity of NEOs was significantly reduced after degradation via the FePO4/WB-PMS system. Meanwhile, the recycling experiments and continuous flow reactor experiments showed that FePO4/WB exhibited high stability. Overall, this study provided a new perspective on water remediation by Fenton-like reaction. ENVIRONMENTAL IMPLICATION: Neonicotinoids (NEOs) are a type of insecticide used widely around the world. They've been found in many aquatic environments, raising concerns about their possible negative effects on the environment and health. Iron-based catalysts for peroxymonosulfate (PMS) activation hold great promise for water purification. However, the slow conversion of Fe(III) to Fe(II) restricts its large-scale application. Herein, iron phosphate tungsten boride composite (FePO4/WB) was synthesized by a simple hydrothermal method to facilitate the Fe(III)/Fe(II) redox cycle and realize the efficient degradation of NEOs. The excellent stability and reusability provided a great prospect for water remediation.

Investigation of singlet oxygen and superoxide radical produced from vortex-based hydrodynamic cavitation: Mechanism and its relation to cavitation intensity.

Presently, the hydroxyl radical oxidation mechanism is widely acknowledged for the degradation of organic pollutants based on hydrodynamic cavitation technology. The presence and production mechanism of other potential reactive oxygen species (ROS) in the cavitation systems are still unclear. In this paper, singlet oxygen (1O2) and superoxide radical (·O2-) were selected as the target ROS, and their generation rules and mechanism in vortex-based hydrodynamic cavitation (VBHC) were analyzed. Computational fluid dynamics (CFD) were used to simulate and analyze the intensity characteristics of VBHC, and the relationship between the generation of ROS and cavitation intensity was thoroughly revealed. The results show that the operating conditions of the device have a significant and complicated influence on the generation of 1O2 and ·O2-. When the inlet pressure reaches to 4.5 bar, it is more favorable for the generation of 1O2 and ·O2- comparing with those lower pressure. However, higher temperature (45 °C) and aeration rate (15 (L/min)/L) do not always have positive effect on the 1O2 and ·O2- productions, and their optimal parameters need to be analyzed in combination with the inlet pressure. Through quenching experiments, it is found that 1O2 is completely transformed from ·O2-, and ·O2- comes from the transformation of hydroxyl radicals and dissolved oxygen. Higher cavitation intensity is captured and shown more disperse in the vortex cavitation region, which is consistent with the larger production and stronger diffusion of 1O2 and ·O2-. This paper shed light to the generation mechanism of 1O2 and ·O2- in VBHC reactors and the relationship with cavitation intensity. The conclusion provides new ideas for the research of effective ROS in hydrodynamic cavitation process.

Hepatotoxicity induced in rats by chronic exposure to F-53B, an emerging replacement of perfluorooctane sulfonate (PFOS).

A plethora of studies have shown the prominent hepatotoxicity caused by perfluorooctane sulfonate (PFOS), yet the research on the causality of F-53 B (an alternative for PFOS) exposure and liver toxicity, especially in mammals, is largely limited. To investigate the effects that chronic exposure to F-53 B exert on livers, in the present study, male SD rats were administrated with F-53 B in a certain dose range (0, 1, 10, 100, 1000 µg/L, eight rats per group) for 6 months via drinking water and the hepatotoxicity resulted in was explored. We reported that chronic exposure to 100 and 1000 µg/L F-53 B induced remarkable histopathological changes in liver tissues such as distinct swollen cells and portal vein congestion. In addition, the increase of cytokines IL-6, IL-2, and IL-8 upon long-term administration of F-53 B demonstrated the high level of inflammation. Moreover, F-53 B exposure was revealed to disrupt the lipid metabolism in the rat livers, mainly manifesting as the upregulation of some proteins involved in lipid synthesis and degradation, including ACC, FASN, SREBP-1c as well as ACOX1. These findings provided new evidence for the adverse effects caused by chronic exposure to F-53 B in rodents. It is crucial for industries, regulatory agencies as well as the public to remain vigilant about the adverse health effects associated with the emerging PFOS substitutes such as F-53 B. Implementation of regular monitoring and risk assessments is of great importance to alleviate environmental concerns towards PFOS alternatives exposure, and furthermore, to minimize the latent health risks to the public health.

Repeated radon exposure induced epithelial-mesenchymal transition-like transformation via disruption of p53-dependent mitochondrial function.

Backgrouds: As a human carcinogen, radon and its progeny are the second most important risk factor for lung cancer after smoking. The tumor suppressor gene, p53, is reported to play an important role in the maintenance of mitochondrial function. In this work, we investigated the association between p53 and p53-responsive signaling pathways and radon-induced carcinogenesis. Methods: After repeated radon exposure, the malignant characteristics, cell cycle arrest, cell apoptotic rate, adenosine triphosphate (ATP) content, reactive oxygen species (ROS) level, mitochondrial DNA (mtDNA) copy number as well as indicative biomarkers involved in mitochondrial energy metabolism were evaluated in BEAS-2B cells or BALB-c mouse lung tissue. Results: Radon exposure induced epithelial-mesenchymal transition (EMT)-like transformation in BEAS-2B cells, as indicated by increased cell proliferation and migration. Additional mitochondrial alterations, including decreased ATP content, increased ROS levels, mtDNA copy numbers, cell apoptosis, and G2/M cell cycle arrest were observed. Radon exposure caused an energy generation shift from aerobic respiration to glycolysis as reflected by increased expression of TIGAR and p53R2 proteins and decreased expression of SCO2 protein in BEAS-2B cells, and increased expression of p53, SCO2 and TIGAR proteins in mouse lung tissue, respectively. The effects of p53 deficiency on the prevention of mitochondrial dysfunction suggested a protective role of p53 in radon-induced malignant-like features in BEAS-2B cells. Conclusions: Repeated radon exposure induced EMT-like transformation in BEAS-2B cells via disruption of mitochondrial function. Activation of p53 and p53-responsive signaling pathways in BEAS-2B cells and BALB-c mice may confer a protective mechanism for radon-induced lung injury.