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.

Effects of digestate-encapsulated biochar on plant growth, soil microbiome and nitrogen leaching.

The increasing amount of food waste and the excessive use of mineral fertilizers have caused detrimental impacts on soil, water, and air quality. Though digestate derived from food waste has been reported to partially replace fertilizer, its efficiency requires further improvement. In this study, the effects of digestate-encapsulated biochar were comprehensively investigated based on growth of an ornamental plant, soil characteristics, nutrient leaching and soil microbiome. Results showed that except for biochar, the tested fertilizers and soil additives, i.e., digestate, compost, commercial fertilizer, digestate-encapsulated biochar had positive effects on plants. Especially, the digestate-encapsulated biochar had the best effectiveness as evidenced by 9-25% increase in chlorophyll content index, fresh weight, leaf area and blossom frequency. For the effects of fertilizers or soil additives on soil characteristics and nutrient retention, the digestate-encapsulated biochar leached least N-nutrients (<8%), while the compost, digestate and mineral fertilizer leached up to 25% N-nutrients. All the treatments had minimal effects on the soil properties of pH and electrical conductivity. According to the microbial analysis, the digestate-encapsulated biochar has the comparable role with compost in improving the soil immune system against pathogen infection. The metagenomics coupling with qPCR analysis suggested that digestate-encapsulated biochar boosted the nitrification process and inhibited the denitrification process. This study provides an extensive understanding into the impacts of the digestate-encapsulated biochar on an ornamental plant and offers practical implications for the choice of sustainable fertilizers or soil additives and food-waste digestate management.

Fluorine-doped BiVO4 photocatalyst: Preferential cleavage of C-N bond for green degradation of glyphosate.

With increasing concerns on the environment and human health, the degradation of glyphosate through the formation of less toxic intermediates is of great importance. Among the developed methods for the degradation of glyphosate, photodegradation is a clean and efficient strategy. In this work, we report a new photocatalyst by doping F ion on BiVO4 that can efficiently degrade glyphosate and reduce the toxic emissions of aminomethylphosphonic acid (AMPA) through the selective (P)-C-N cleavage in comparison of BiVO4 catalyst. The results demonstrate that the best suppression of AMPA formation was achieved by the catalyst of 0.3F@BiVO4 at pH = 9 (AMPA formation below 10%). In situ attenuated total reflectance Fourier transforms infrared (ATR-FTIR) spectroscopy indicates that the adsorption sites of glyphosate on BiVO4 and 0.3F@BiVO4 are altered due to the difference in electrostatic interactions. Such an absorption alteration leads to the preferential cleavage of the C-N bond on the N-C-P skeleton, thereby inhibiting the formation of toxic AMPA. These results improve our understanding of the photodegradation process of glyphosate catalyzed by BiVO4-based catalysts and pave a safe way for abiotic degradation of glyphosate.

CFD-assisted modeling of the hydrodynamic cavitation reactors for wastewater treatment - A review.

Hydrodynamic cavitation has been a promising method and technology in wastewater treatment, while the principles based on the design of cavitational reactors to optimize cavitation yield and performance remains lacking. Computational fluid dynamics (CFD), a supplementation of experimental optimization, has become an essential tool for this issue, owing to the merits of low investment and operating costs. Nevertheless, researchers with a non-engineering background or few CFD fundamentals used straightforward numerical strategies to treat cavitating flows, and this might result in many misinterpretations and consequently poor computations. This review paper presents the rationale behind hydrodynamic cavitation and application of cavitation modeling specific to the reactors in wastewater treatment. In particular, the mathematical models of multiphase flow simulation, including turbulence closures and cavitation models, are comprehensively described, whilst the advantages and shortcomings of each model are also identified and discussed. Examples and methods of the coupling of CFD technology, with experimental observations to investigate into the hydrodynamic behavior of cavitating devices that feature linear and swirling flows, are also critically summarized. Modeling issues, which remain unaddressed, i.e., the implementation strategies of numerical models, and the definition of cavitation numbers are identified and discussed. Finally, the advantages of CFD modeling are discussed and the future of CFD applications in this research area is also outlined. It is expected that the present paper would provide decision-making support for CFD beginners to efficiently perform CFD modeling and promote the advancement of cavitation simulation of reactors in the field of wastewater treatment.

Upregulation of autophagy in M2 macrophage by vitamin D alleviates crystalline silica-induced pulmonary inflammatory damage.

Crystalline silica (CS) is a universal environmental pollutant, which causes a typical inflammatory lung injury. Vitamin D shows huge potential against particles-induced lung injury, while little known about the molecular mechanism involved in macrophage autophagy. In this study, we aim to identify the protective effects of vitamin D on CS caused lung inflammatory injury and clarify the detail mechanism. After exposure to CS (3 mg/mice in 50 µl PBS), wildtype and Atg7flox/flox Lyz2-cre mice were treated with or without vitamin D3 (40,000 IU/kg). The results indicated that exposure to CS caused an obvious lung injury, manifesting as pathological structural changes, macrophage-dominated inflammatory cell infiltration and increased pro-inflammatory cytokines. Remarkably, these damages were more serious in Atg7flox/flox Lyz2-cre mice. Vitamin D was found to inverse CS-induced inflammatory cell infiltration and restored anti-inflammatory M2 macrophages by inducing autophagy, which attenuated lung injury, as determined by decreased levels of apoptosis and inflammatory response. While, this effects of vitamin D were slashed in Atg7flox/flox Lyz2-cre mice. This study reveals the adverse effect of CS on lung tissue and the protective mechanism of vitamin D involved in M2 macrophages autophagy, which attenuates CS-caused lung injury.

Protection of melatonin against long-term radon exposure-caused lung injury.

Radon is one of the major pathogenic factors worldwide. Recently, epidemiological studies have suggested that radon exposure plays an important role in lung injury, which could further cause cancer. However, the toxic effects and underlying mechanism on lung injury are still not clear. Here, we identified the detailed toxic effects of long-term radon exposure. Specifically, the manifestations were inflammatory response and cell apoptosis in dose- and time-dependent manners. In detail, it caused the mitochondrial dysfunction and oxidative stress as determined by the abnormal levels of mitochondrial DNA copy number, adenosine triphosphate, mitochondrial membrane potential, superoxide dismutase, and cycloxygenase-2. Furthermore, we found that melatonin treatment ameliorated mitochondrial dysfunction and attenuated the levels of oxidative stress caused by long-term radon exposure, which could further inhibit the lung tissue apoptosis as determined by the decreased levels of cleaved caspase 3. Our study would provide potential therapeutic application of melatonin on lung tissue injury caused by long-term radon exposure.

Silver nanoparticles: Correlating particle size and ionic Ag release with cytotoxicity, genotoxicity, and inflammatory responses in human cell lines.

The widespread use of silver nanoparticles (AgNPs), their many sources for human exposure, and the ability of AgNPs to enter organisms and induce general toxicological responses have raised concerns regarding their public health and environmental safety. To elucidate the differential toxic effects of polyvinylpyrrolidone-capped AgNPs with different primary particle sizes (i.e. 5, 50, and 75 nm), we performed a battery of cytotoxicity and genotoxicity assays and examined the inflammatory responses in two human cell lines (i.e. HepG2 and A549). Concentration-dependent decreases in cell proliferation and mitochondrial membrane potential and increases in cytokine (i.e. interleukin-6 and interleukin-8) excretion indicated disruption of mitochondrial function and inflammation as the main mediating factors of AgNPs-induced cytotoxicity. An incremental increase in genotoxicity with decreasing AgNPs diameter was noted in HepG2 cells, which was associated with S and G2/M accumulation and transcriptional activation of the GADD45α promoter as reflected by luciferase activity. Dose-related genetic damage, as indicated by Olive tail moment and micronucleus formation, was also observed in A549 cells, but these effects as well as the AgNPs-induced cytotoxicity were more associated with ionic Ag release from nanoparticles (NPs). In summary, the present study addressed different toxicity mechanisms of AgNPs, depending on the cell model, toxicological endpoint, particle size, and degree of Ag+ release from NPs. The results suggest that the GADD45α promoter-driven luciferase reporter cell system provided a rapid screening tool for the identification of genotoxic properties of NPs across a range of different sizes and concentrations.

Green and efficient degradation of cefoperazone sodium by Bi4O5Br2 leading to the production of non-toxic products: Performance and degradation pathway.

Photocatalytic process represents a promising approach to overcome the pollution challenge associated with the antibiotics-containing wastewater. This study provides a green, efficient and novel approach to remove cephalosporins, particularly cefoperazone sodium (CFP). Bi4O5Br2 was chosen for the first time to systematically study its degradation for CFP, including the analysis of material structure, degradation performance, the structure and toxicity of the transformation products, etc. The degradation rate results indicated that Bi4O5Br2 had an excellent catalytic activity leading to 78% CFP removal compared with the pure BiOBr (38%) within 120 min of visible light irradiation. In addition, the Bi4O5Br2 presents high stability and good organic carbon removal efficiency. The effects of the solution pH (3.12 - 8.75) on catalytic activity revealed that CFP was mainly photocatalyzed under acidic conditions and hydrolyzed under alkaline conditions. Combined with active species and degradation product identification, the photocatalytic degradation pathways of CFP by Bi4O5Br2 was proposed, including hydrolysis, oxidation, reduction and decarboxylation. Most importantly, the identified products were all hydrolysis rather than oxidation byproducts transformed from the intermediate of ß-lactam bond cleavage in CFP molecule, quite different from the mostly previous studies. Furthermore, the final products were demonstrated to be less toxic through the toxicity analysis. Overall, this study illustrates the detailed mechanism of CFP degradation by Bi4O5Br2 and confirms Bi4O5Br2 to be a promising material for the photodegradation of CFP.

Insights into Ammonia Adaptation and Methanogenic Precursor Oxidation by Genome-Centric Analysis.

Ammonia released from the degradation of protein and/or urea usually leads to suboptimal anaerobic digestion (AD) when N-rich organic waste is used. However, the insights behind the differential ammonia tolerance of anaerobic microbiomes remain an enigma. In this study, the cultivation in synthetic medium with different carbon sources (acetate, methanol, formate, and H2/CO2) shaped a common initial inoculum into four unique ammonia-tolerant syntrophic populations. Specifically, various levels of ammonia tolerance were observed: consortia fed with methanol and H2/CO2 could grow at ammonia levels up to 7.25 g NH+-N/L, whereas the other two groups (formate and acetate) only thrived at 5.25 and 4.25 g NH+-N/L, respectively. Metabolic reconstruction highlighted that this divergent microbiome might be achieved by complementary metabolisms to maximize biomethane recovery from carbon sources, thus indicating the importance of the syntrophic community in the AD of N-rich substrates. Besides, sodium/proton antiporter operon, osmoprotectant/K+ regulator, and osmoprotectant synthesis operon may function as the main drivers of adaptation to the ammonia stress. Moreover, energy from the substrate-level phosphorylation and multiple energy-converting hydrogenases (e.g., Ech and Eha) could aid methanogens to balance the energy request for anabolic activities and contribute to thriving when exposed to high ammonia levels.

Expression profiles of long non-coding RNA in mouse lung tissue exposed to radon.

Long non-coding RNAs (lncRNA) exert biological functions by interacting with RNAs, proteins, and DNA. Although lung damage associated with radon exposure was attributed to disturbances in microRNA and protein expression, the influence of radon on lncRNA is at present not known. The aim of this study was to (1) examine the effect of radon on lncRNA-mediated expression of transcription factors in mRNA in mouse lung tissue and (2) determine potential function and targets. Female BALB/c mice were divided into two groups: control and radon exposure to approximately 100,000 Bq/m3 (equivalent up to 60 working level month, WLM).RNA was extracted from lung tissue and used for high through-put lncRNA microarray analysis. A total of 1256 lncRNA transcripts were differentially expressed between the two groups of mice. Among these, the top 200 lncRNA-mRNA sets, with fold change of >2 and p-value <.05, were selected for KEGG analysis. Functional analysis via bioinformatics prediction in this study also suggested involvement of ErbB and Notch pathways in radon-induced mouse pulmonary injury. The results from immunohistochemical and Western blot analysis indicated that EbB2 and k-Ras protein expressions were significantly increased. In conclusion, approximately 1,000 dysregulated lncRNA transcripts were found in radon-exposed mice and these lncRNA may play an important role in lung damage following radon exposure. The observations in this study also suggested that ErbB2 and Notch pathways are activated and may be involved in radon-induced pulmonary toxicity.

Vitamin D protects against particles-caused lung injury through induction of autophagy in an Nrf2-dependent manner.

Fine particulate matter is a well-known air pollutant threatening public health. Studies have confirmed long-term exposure to the particles could decrease the pulmonary function, induce asthma exacerbation, and chronic obstructive pulmonary disease, as well as increase the incidence and mortality of lung cancer. A clinical study has explored that the prevalence and risks of vitamin D (VD) deficiency in various chronic disease and toxins induced tissue damage. Our current study aimed to explore the mechanism and further therapeutic potential of VD administration to ameliorate fine particles exposure induced pulmonary damage in vivo and in vitro. To elucidate the effects and mechanisms of VD in particles-induced pulmonary damage, a murine model was established with fine particles intratracheal instillation along with VD intramuscular injection. Our study demonstrated that treatment with VD attenuated particles-induced pulmonary damage and promoted tissue repair by repressing of TGFß1 signaling pathway and upregulation of MMP9 expression. VD treatment could also regulate the autophagy-related signals along with activation of Nrf2 transcription factor. Furthermore, the results from the in vitro study demonstrated that VD protected against particles-induced cells' damage through the induction of autophagy in an Nrf2-dependent manner. VD treatment caused the degradation of P62 and its bound Keap1, which decreased the Nrf2 ubiquitination and increasing its protein stability. Our work explored a novel potential mechanism in the protection of VD in particles-induced pulmonary injury and tissue repair, and could further bring insights into exploring antifine particles exposure caused inflammation among other natural products and contributes to inflammation disease medical therapies.

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.

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.

Startup performance and microbial communities of a decentralized anaerobic digestion of food waste.

The aim of this work was to evaluate the feasibility of treating food waste generated from a hawker centre in a pilot-scale anaerobic digester operating on site in an urban area of Singapore. For this purpose, a 10.4 m3 digester was housed within two 20 feet containerized systems and sited adjacent to the hawker centre. The system reported in this work was during the startup phase, for over 71 days of real and varying food wastes loading rate. The results demonstrated that the decentralized system had an average specific methane yield of 0.55 ± 0.04 m3CH4/kgVS, with methane concentrations of 56.6 ± 2.3%. For the power generation output, the energy assessment revealed an average of 2.05 ± 0.57 m3/kW h consumption rate. Accordingly, on the last day of startup phase, the inoculum of the digester was richer in organisms from the phylum Thermoplasmatota, i.e., genera Candidatus_Methanogranum and Candidatus_Methanoplasma, alongside with other dominant abundance from phyla Bacteroidota, Firmicutes, Synergistota, and Verrucomicrobiota. This study provides new insights into pilot scale decentralized anaerobic digestion with varying food waste relate to the characterizations of digester microbial communities, as well as turning in a typical integrated anaerobic digestion of food waste-to-energy system a reality.

A closed loop case study of decentralized food waste management: System performance and life cycle carbon emission assessment.

Food waste (FW) has become a worldwide issue, while anaerobic digestion (AD) has appeared as a widely adopted technology to recover energy and resources from FW. Compared to many existing case studies of centralized AD system, the comprehensive study of decentralized micro-AD system from both system energy efficiency and carbon emission perspective is still scanty, particularly system operated under ambient temperature conditions. In this study, an actual decentralized micro-AD system with treating capacity of 300 kg FW/d for a local hawker center in Singapore was reported and evaluated. The results showed that 1894.5 kg of FW was treated and 173 m3 biogas with methane content of 53 % was produced during the experimental period of 75 days. The methane yield results showed a high FW degradation efficiency (87.87 %). However, net energy consumption and net carbon emission were observed during the experimental period. Nevertheless, energy self-efficiency and carbon neutrality, even net energy output and carbon reduction, can be achieved by increasing daily FW loading and biogas engine efficiency. Specifically, the FW loading for system energy self-efficiency was identified as 159 kg/d for engine efficiency of 35 % at a high kitchen waste/table waste ratio (63 %/37 %, with covid-19 dine-in restrictions); while they were 112 and 58 kg/d for engine efficiency of 25 % and 35 %, respective, at a low kitchen waste/table waste ratio (31 %/69 %, without covid-19 dine-in restrictions). The carbon emission ranged from 156.08 kg CO2-eq/t FW to -77.35 kg CO2-eq/t FW depending on the FW loading quantity and engine efficiency. Moreover, the sensitivity analysis also showed that the used electricity source for substitution influenced the carbon emission performance significantly. The obtained results imply that the decentralized micro-AD system could be a feasible FW management solution for energy generation and carbon reduction when the FW loading and engine electrical efficiency are carefully addressed.

Life cycle assessment and cost-benefit analysis of small-scale anaerobic digestion system treating food waste onsite under different operational conditions.

This study employed life cycle assessment and cost-benefit analysis to evaluate the environmental and economic profile of a real decentralized small-scale anaerobic digestion (AD) system treating food waste (FW). Different operational conditions, including temperature, biochar addition, biogas engine efficiency, and FW loading, were compared via scenario analysis. Biochar addition could potentially obtain carbon reduction and save fossil fuel. Moreover, at high FW loading and biogas engine efficiency, biochar addition achieved 1-3190% better performance than the system without biochar in all the nine impact categories. The system under mesophilic conditions performed worse than ambient conditions due to high energy demand. All the current scenarios resulted in a monetary loss at US$ 480 k-681 k, while profit was possible if the capital cost and operator salary decreased significantly. Overall, operating the small-scale AD system under ambient temperature with biochar addition was preferred due to its potential environmental benefits and economic profits.

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.

Repeated radon exposure induced lung damage via oxidative stress-mediated mitophagy in human bronchial epithelial cells and mice.

This study aimed to investigate the potential molecular mechanism underlying radon-induced lung damage. Our results showed that long-term radon exposure induced mitochondrial damage and redox imbalance in BEAS-2B cells and a time-dependent lung pathological injury in mice. The activation of Nrf-2 and its down-stream antioxidants, and the gene expression of the indicated markers at different stages of autophagy were found to be induced with the increasing of radon exposure time. Changes in the gene expression of PINK-1, Parkin, and p62 induced by radon showed differences in mechanisms of mitophagy activation and profiles of autophagic flux between BEAS-2B cells and mice. Our findings not only demonstrated that long-term radon exposure induced damages to bronchial epithelial cells and the mice lung through increasing oxidative stress, decreasing mitochondrial function and activating mitophagy with different profiles of autophagic flux, but also revealed Nrf-2 as a central regulator of mitochondrial homeostasis and lung damage.

Vitamin D protects silica particles induced lung injury by promoting macrophage polarization in a KLF4-STAT6 manner.

Silicosis is one of the severest occupational diseases worldwide, manifesting as infiltration of inflammatory cells, excessive secretion of pro-inflammatory mediators and pulmonary diffuse fibrosis. Macrophages polarization to M2 is one of the major strategies that attenuates inflammatory response. Our previous study found that vitamin D could protect against silica-induced lung injury by damping the secretion of pro-inflammatory cytokines. Here we further identified that vitamin D attenuated silica particles-induced lung inflammation by regulating macrophage polarization in a KLF4-STAT6 manner. Myeloid-specific Stat6 knockout (cKO) mice were generated for in vivo studies. Primary macrophages purified from bronchoalveolar lavage fluid (BALF) of wildtype or Stat6 cKO mice and differentiated THP-1 cells were used for in vitro studies. Vitamin D was found to promote alveolar macrophage polarizing to M2 phenotype through the STAT6 signaling pathway, as demonstrated by worse lung inflammation and ablated protection of vitamin D in silica particles-instilled Stat6 cKO mice. Mechanismly, vitamin D upregulated KLF4 expression in the alveolar macrophage, which synergistically activated STAT6. Additionally, KLF4 was found to upregulate macrophages autophagy, which protected them from silica particles-induced oxidative stress and cell apoptosis. The protective effects of vitamin D were dismissed by silencing KLF4. Our study demonstrates the potential mechanism of vitamin D-mediated macrophage polarization and reveals the therapeutic application of vitamin D in inflammatory disease.