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The role of tumor-resident microbiota in modulating tumor immunity remains unclear. Here, we discovered an abundance of intra-tumoral bacteria, such us E.coli, residing and resulting in Colorectal cancer liver metastasis (CRLM). E.coli enhanced lactate production, which mediated M2 macrophage polarization by suppressing nuclear factor-κB -gene binding (NF-κB) signaling through retinoic acid-inducible gene 1 (RIG-I) lactylation. Lactylation of RIG-I suppressed recruitment of NF-κB to the Nlrp3 promoter in macrophages, thereby reducing its transcription. This loss of Nlrp3 affected the immunosuppressive activities of regulatory T cells (Tregs) and the antitumor activities of and CD8+ T cells. Small-molecule compound screening identified a RIG-I lactylation inhibitor that suppressed M2 polarization and sensitized CRLM to 5-fluorouracil (5-FU). Our findings suggest that tumor-resident microbiota may be a potential target for preventing and treating CRLM.
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Neoplasias Colorretais , Neoplasias Hepáticas , NF-kappa B , Neoplasias Colorretais/patologia , Neoplasias Colorretais/microbiologia , Neoplasias Colorretais/imunologia , Neoplasias Hepáticas/secundário , Neoplasias Hepáticas/microbiologia , Neoplasias Hepáticas/imunologia , Neoplasias Hepáticas/patologia , Animais , Humanos , Camundongos , NF-kappa B/metabolismo , Microbiota/imunologia , Macrófagos/imunologia , Macrófagos/metabolismo , Escherichia coli , Linfócitos T Reguladores/imunologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Linhagem Celular Tumoral , Fluoruracila/farmacologia , Transdução de SinaisRESUMO
The mortality of hepatocellular carcinoma (HCC) is on the rise globally, particularly in the Western world, with etiology gradually shifting from virus-related liver diseases to metabolic disorders such as non-alcoholic fatty liver disease. Early detection of HCC is challenging, and effective prognostic indicators are currently lacking, urgently necessitating reliable markers to assist in treatment planning and clinical management. Here, we introduce hepatocellular carcinoma senescence genes (HSG) to assess cellular senescence in HCC and devise a hepatocellular carcinoma senescence score (HSS) for prognostic prediction. Higher HSS levels signify poorer prognosis and increased tumor proliferation activity. Additionally, we observe alterations in the tumor immune microenvironment with higher HSS levels, such as increased infiltration of Treg, potentially providing a basis for immunotherapy. Furthermore, we identify key genes, such as PTTG1, within the senescence gene set and demonstrate their regulatory roles in HCC cells and Treg through experimentation. In summary, we establish a scoring system based on hepatocellular carcinoma senescence genes for prognostic prediction in HCC, potentially offering guidance for clinical treatment planning.
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The role of hypoxia in the tumor microenvironment of intrahepatic cholangiocarcinoma (iCCA) remains unclear. Here, we generated a comprehensive atlas of the entire tumor microenvironment and delineated the multifaceted cell-cell interactions to decipher hypoxia-induced pro-tumor immune suppression. We discovered hypoxia is significantly associated with iCCA progression via the activation of HIF1A expression. Moreover, hypoxia-dependent PPARγ-mediated fatty acid oxidation in APOE+ TAMs promoted M2 macrophage polarization by activating the HIF1A-PPARG-CD36 axis. These polarized APOE+ TAMs recruited Treg cell infiltration via the CCL3-CCR5 pair to form an immunosuppressive microenvironment. APOE+ TAMs tended to co-localize spatially with Treg cells in the malignant tissue based on spatial transcriptome data and immunofluorescence analysis results. We identified tumor-reactive CXCL13+ CD8-PreTex with specific high expression of ENTPD1 and ITGAE, which acted as precursors of CD8-Tex and had higher cytotoxicity, lower exhaustion, and more vigorous proliferation. Consequently, CXCL13+ CD8-PreTex functioned as a positive regulator of antitumor immunity by expressing the pro-inflammatory cytokines IFNG and TNF, associated with a better survival outcome. Our study reveals the mechanisms involved in hypoxia-induced immunosuppression and suggests that targeting precursor-exhausted CXCL13+CD8+ T cells might provide a pratical immunotherapeutic approach.
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Neoplasias dos Ductos Biliares , Colangiocarcinoma , Análise de Célula Única , Microambiente Tumoral , Colangiocarcinoma/imunologia , Colangiocarcinoma/patologia , Colangiocarcinoma/metabolismo , Microambiente Tumoral/imunologia , Humanos , Neoplasias dos Ductos Biliares/patologia , Neoplasias dos Ductos Biliares/imunologia , Neoplasias dos Ductos Biliares/metabolismo , Animais , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Linfócitos T Reguladores/imunologia , Linfócitos T Reguladores/metabolismo , Camundongos , Linhagem Celular Tumoral , Macrófagos Associados a Tumor/imunologia , Macrófagos Associados a Tumor/metabolismo , Macrófagos Associados a Tumor/patologiaRESUMO
BACKGROUND/AIMS: Metabolic dysfunction-associated steatohepatitis (MASH) is an unmet clinical challenge due to the rapid increased occurrence but lacking approved drugs. Autophagy-related protein 16-like 1 (ATG16L1) plays an important role in the process of autophagy, which is indispensable for proper biogenesis of the autophagosome, but its role in modulating macrophage-related inflammation and metabolism during MASH has not been documented. Here, we aimed to elucidate the role of ATG16L1 in the progression of MASH. METHODS: Expression analysis was performed with liver samples from human and mice. MASH models were induced in myeloid-specific Atg16l1-deficient and myeloid-specific Atg16l1-overexpressed mice by high-fat and high-cholesterol diet or methionine- and choline-deficient diet to explore the function and mechanism of macrophage ATG16L1 in MASH. RESULTS: Macrophage-specific Atg16l1 knockout exacerbated MASH and inhibited energy expenditure, whereas macrophage-specific Atg16l1 transgenic overexpression attenuated MASH and promotes energy expenditure. Mechanistically, Atg16l1 knockout inhibited macrophage lipophagy, thereby suppressing macrophage ß-oxidation and decreasing the production of 4-hydroxynonenal, which further inhibited stimulator of interferon genes(STING) carbonylation. STING palmitoylation was enhanced, STING trafficking from the endoplasmic reticulum to the Golgi was promoted, and downstream STING signaling was activated, promoting proinflammatory and profibrotic cytokines secretion, resulting in hepatic steatosis and hepatic stellate cells activation. Moreover, Atg16l1-deficiency enhanced macrophage phagosome ability but inhibited lysosome formation, engulfing mtDNA released by pyroptotic hepatocytes. Increased mtDNA promoted cGAS/STING signaling activation. Moreover, pharmacological promotion of ATG16L1 substantially blocked MASH progression. CONCLUSION: ATG16L1 suppresses MASH progression by maintaining macrophage lipophagy, restraining liver inflammation, and may be a promising therapeutic target for MASH management.
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Proteínas Relacionadas à Autofagia , Autofagia , Macrófagos , Proteínas de Membrana , Animais , Camundongos , Proteínas Relacionadas à Autofagia/metabolismo , Proteínas Relacionadas à Autofagia/genética , Humanos , Macrófagos/metabolismo , Proteínas de Membrana/metabolismo , Proteínas de Membrana/genética , Masculino , Progressão da Doença , Camundongos Knockout , Modelos Animais de Doenças , Fígado Gorduroso/metabolismo , Fígado Gorduroso/patologia , Fígado Gorduroso/genética , Dieta Hiperlipídica/efeitos adversos , Metabolismo Energético , Fígado/metabolismo , Fígado/patologia , Transdução de Sinais , Camundongos Endogâmicos C57BLRESUMO
Plasma cell mastitis (PCM) is a sterile inflammatory condition primarily characterized by periductal inflammation and ductal ectasia. Currently, there is a lack of non-invasive or minimally invasive treatment option other than surgical intervention. The NLRP3 inflammasome has been implicated in the pathogenesis and progression of various inflammatory diseases, however, its involvement in PCM has not yet been reported. In this study, we initially observed the pronounced upregulation of NLRP3 in both human and mouse PCM tissue and elucidated the mechanism underlying the attenuation of PCM through inhibition of NLRP3. We established the PCM murine model and collected samples on day 14, when inflammation reached its peak, for subsequent research purposes. MCC950, an NLRP3 inhibitor, was utilized to effectively ameliorate PCM by significantly reducing plasma cell infiltration in mammary tissue, as well as attenuate the expression of pro-inflammatory cytokines including IL-1ß, TNF-α, IL-2, and IL-6. Mechanistically, we observed that MCC950 augmented the function of myeloid-derived suppressor cells (MDSCs), which in turn inhibited the infiltration of plasma cells. Furthermore, it was noted that depleting MDSCs greatly compromised the therapeutic efficacy of MCC950. Collectively, our findings suggest that the administration of MCC950 has the potential to impede the progression of PCM by augmenting MDSCs both numerically and functionally, ultimately treating PCM effectively. This study provides valuable insights into the utilization of pharmacological agents for PCM treatment.
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Indenos , Mastite , Células Supressoras Mieloides , Feminino , Humanos , Animais , Camundongos , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Células Supressoras Mieloides/metabolismo , Plasmócitos/metabolismo , Sulfonas/farmacologia , Sulfonamidas/uso terapêutico , Sulfonamidas/farmacologia , Inflamassomos/metabolismo , Inflamação/tratamento farmacológico , Mastite/tratamento farmacológico , Furanos/uso terapêutico , Furanos/farmacologiaRESUMO
Soil, the largest terrestrial carbon reservoir, is central to climate change and relevant feedback to environmental health. Minerals are the essential components that contribute to over 60% of soil carbon storage. However, how the interactions between minerals and organic carbon shape the carbon transformation and stability remains poorly understood. Herein, we critically review the primary interactions between organic carbon and soil minerals and the relevant mechanisms, including sorption, redox reaction, co-precipitation, dissolution, polymerization, and catalytic reaction. These interactions, highly complex with the combination of multiple processes, greatly affect the stability of organic carbon through the following processes: (1) formation or deconstruction of the mineral-organic carbon association; (2) oxidative transformation of the organic carbon with minerals; (3) catalytic polymerization of organic carbon with minerals; and (4) varying association stability of organic carbon according to the mineral transformation. Several pieces of evidence related to the carbon turnover and stability during the interaction with soil minerals in the real eco-environment are then demonstrated. We also highlight the current research gaps and outline research priorities, which may map future directions for a deeper mechanisms-based understanding of the soil carbon storage capacity considering its interactions with minerals.
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The objective of the study was to evaluate the contribution of insulin resistance and ß cell dysfunction to gestational diabetes mellitus (GDM) in Chinese women stratified by pre-pregnant body mass index (BMI). A total of 847 pregnant women were enrolled. They were divided into low BMI and high BMI groups according to the median of pre-pregnancy BMI. The homeostasis model assessment of insulin resistance (HOMA-IR) and ß cell function (HOMA-ß), Matsuda index, and 60-min insulinogenic index (IGI60) were used to evaluate insulin resistance and ß cell function. In all the participants, 150 (17.71%) were diagnosed with GDM. ROC analyses showed that in the low BMI group, the association of ß cell dysfunction (IGI60 or HOMA-ß) with GDM was stronger than that of insulin resistance (Matsuda index or HOMA-IR), while in the high BMI group, the association of ß cell dysfunction with GDM was weaker than that of insulin resistance (all P < 0.05). Among all GDM patients, 47.33% demonstrated predominant insulin resistance (Matsuda index < 25th percentile), and 46% had predominant ß cell defect (IGI60 < 25th percentile). In the low BMI group, 15.09% of GDM patients demonstrated predominant insulin resistance, and 62.26% of GDM patients had predominant ß cell defect, whereas in the high BMI group, 64.95% of GDM patients demonstrated mainly insulin resistance and 36.08% of GDM patients had mainly ß cell defect. In women with low BMI, ß cell dysfunction is the major etiologic factor, whereas, in women with high BMI, insulin resistance is the predominant etiologic factor in the development of GDM.
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Diabetes Gestacional , Resistência à Insulina , Feminino , Humanos , Gravidez , Diabetes Gestacional/diagnóstico , Índice de Massa Corporal , Insulina , Glicemia/análiseRESUMO
Non-alcoholic fatty liver disease (NAFLD) has emerged as the primary risk factor for hepatocellular carcinoma (HCC), owing to improved vaccination rates of Hepatitis B and the increasing prevalence of metabolic syndrome related to obesity. Although the importance of innate and adaptive immune cells has been emphasized, the malignant transformation of hepatocytes and their intricate cellular network with the immune system remain unclear. The study incorporated four single-cell transcriptomic datasets of liver tissues covering healthy and NAFLD-related disease status. To identify the subsets and functions of hepatocytes and macrophages, we employed differential composition analysis, functional enrichment analysis, pseudotime analysis, and scenic analysis. Furthermore, an experimental mouse model for the transformation of nonalcoholic steatohepatitis into hepatocellular carcinoma was established for validation purposes. We defined CYP7A1+ hepatocytes enriched in precancerous lesions as 'Transitional Cells' in the progression from NAFLD to HCC. CYP7A1+ hepatocytes upregulated genes associated with stress response, inflammation and cancer-associated pathways and downregulated the normal hepatocyte signature. We observed that hypoxia activation accompanied the entire process of inflammation-cancer transformation. Hepatocyte-derived HIF1A was gradually activated during the progression of NAFLD disease to adapt to the hypoxic microenvironment and hepatocytes under hypoxic environment led to changes in the metabolism, proliferation and angiogenesis, promoting the occurrence of tumours. Meanwhile, hypoxia induced the polarization of RACK1+ macrophages that enriched in the liver tissues of NASH towards immunosuppressed TREM2+ macrophages. Moreover, immunosuppressive TREM2+ macrophages were recruited by tumour cells through the CCL15-CCR1 axis to enhance immunosuppressive microenvironment and promote NAFLD-related HCC progression. The study provides a deep understanding of the development mechanism of NAFLD-related HCC and offers theoretical support and experimental basis for biological targets, drug research, and clinical application.
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Carcinoma Hepatocelular , Neoplasias Hepáticas , Hepatopatia Gordurosa não Alcoólica , Animais , Camundongos , Carcinoma Hepatocelular/patologia , Hepatopatia Gordurosa não Alcoólica/genética , Hepatopatia Gordurosa não Alcoólica/metabolismo , Neoplasias Hepáticas/patologia , Inflamação/genética , Transformação Celular Neoplásica/genética , Perfilação da Expressão Gênica , Microambiente TumoralRESUMO
To customize biochar suitable for efficient adsorption of benzene derivatives, this study presents programmed microwave pyrolysis to produce hydrophobic porous biochar with low-dose ferric chloride. Designated control of the ramping rates in the carbonization stage and the temperatures in the activation stage were conducive to enlarging the specific surface area. Iron species, including amorphous iron minerals, could create small-scale hotspots during microwave pyrolysis to promote microporous structure development. Compared with conventional pyrolysis, programmed microwave pyrolysis could increase the specific surface area from 288.6 m2 g-1 to 455.9 m2 g-1 with a short heating time (15 min vs. 2 h) under 650 °C. Engineered biochar exhibited higher adsorption capacity for benzene and toluene (136.6 and 94.6 mg g-1), and lower adsorption capacity for water vapour (6.2 mg g-1). These findings provide an innovative design of engineered biochar for the adsorption of volatile organic compounds in the environment.
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Micro-Ondas , Pirólise , Adsorção , Porosidade , Carvão Vegetal/química , FerroRESUMO
Ca-biochar is an efficient material for As(III)-containing acid mine drainage (AMD) decontamination, while it is challenging to fabricate Ca-biochar with oyster shell waste as the Ca source due to its complex structure. Herein, a mechanochemical method was proposed to activate oyster shell waste and wood waste for Ca-biochar design and production, and its efficacy and relevant mechanisms for AMD detoxification were evaluated. The smaller size Ca-biochar produced by the medium-speed ball milling showed a higher As(III) removal (74.0 %) compared to high-speed ball milling (60.9 %), attributed to the formation of finer Ca(OH)2 while avoiding particle aggregation, which could release more Ca (89.0 mg/g) and alkalinity for the co-precipitation of As. Meanwhile, wood-based biochar substrate served as a platform for co-precipitation, and its surface functionality supported the oxidative immobilization of As. This study presents a promising route for upcycling food and wood waste to produce Ca-biochar for AMD decontamination.
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Arsênio , Cálcio , Descontaminação , Carvão Vegetal/química , AdsorçãoRESUMO
The dense surface passivation layer on zero-valent iron (ZVI) restricts its efficiency for water decontamination, causing a poor economy and waste of resources. Herein, we found that the ZVI on Fe-Mn biochar could afford a high electron-donating efficiency for the Cr(VI) reduction and immobilization. Over 78.0% of Fe in the Fe-Mn biochar was used for the Cr(VI) reduction and immobilization, i.e., 56.2 - 161.7 times higher than the commercial ZVI (0.5%) and modified ZVI (0.9 -1.3%), indicating that the unique ZVI species in Fe-Mn biochar offered an outstanding Fe utilization efficiency. We proposed that oxygen atoms in the FeO in the FeMnO2 precursor were removed during pyrolysis with biochar while the MnO skeleton was preserved, forming the embedded ZVI clusters within Fe-Mn oxide. The unique structure inhibited the formation of the Fe-Cr complex on Fe(0), which would facilitate the electron transfer between core Fe(0) and Cr(VI). Moreover, the surface FeMnO2 inhibited the diffusion of Fe and facilitated its affinity with pollutants, thus supporting higher efficiency for pollutant immobilization. The preserved performance of Fe-Mn biochar was proved in industrial wastewater and after long-term oxidation process, and the economic benefit was evaluated. This work provides a new approach for developing active ZVI-based materials with high Fe utilization efficiency and economics for water pollution control.
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Background & Aims: Oxidative stress-mediated ferroptosis and macrophage-related inflammation play an important role in various liver diseases. Here, we explored if and how hepatocyte ferroptosis regulates macrophage stimulator of interferon genes (STING) activation in the development of spontaneous liver damage, fibrosis, and tumorigenesis. Methods: We used a transforming growth factor-beta-activated kinase 1 (TAK1) deficiency-induced model of spontaneous liver damage, fibrosis, and tumorigenesis to investigate hepatocyte ferroptosis and its impact on macrophage STING signalling. Primary hepatocytes and macrophages were used for in vitro experiments. Results: Significant liver injury and increased numbers of intrahepatic M1 macrophages were found in hepatocyte-specific TAK1-deficient (TAK1ΔHEP) mice, peaking at 4 weeks and gradually decreasing at 8 and 12 weeks. Meanwhile, activation of STING signalling was observed in livers from TAK1ΔHEP mice at 4 weeks and had decreased at 8 and 12 weeks. Treatment with a STING inhibitor promoted macrophage M2 polarisation and alleviated liver injury, fibrosis, and tumour burden. TAK1 deficiency exacerbated liver iron metabolism in mice with a high-iron diet. Moreover, consistent with the results from single-cell RNA-Seq dataset, TAK1ΔHEP mice demonstrated an increased oxidative response and hepatocellular ferroptosis, which could be inhibited by reactive oxygen species scavenging. Suppression of ferroptosis by ferrostatin-1 inhibited the activation of macrophage STING signalling, leading to attenuated liver injury and fibrosis and a reduced tumour burden. Mechanistically, increased intrahepatic and serum levels of 8-hydroxydeoxyguanosine were detected in TAK1ΔHEP mice, which was suppressed by ferroptosis inhibition. Treatment with 8-hydroxydeoxyguanosine antibody inhibited macrophage STING activation in TAK1ΔHEP mice. Conclusions: Hepatocellular ferroptosis-derived oxidative DNA damage promotes macrophage STING activation to facilitate the development of liver injury, fibrosis, and tumorigenesis. Inhibition of macrophage STING may represent a novel therapeutic approach for the prevention of chronic liver disease. Impact and implications: The precise mechanism by which hepatocyte ferroptosis regulates macrophage STING activation in the progression of liver damage, fibrosis, and tumorigenesis remains unclear. Herein, we show that deletion of TAK1 in hepatocytes caused oxidative stress-mediated ferroptosis and macrophage-related inflammation in the development of spontaneous liver injury, fibrosis, and hepatocellular carcinoma.
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Selective and highly efficient extraction technologies for the recovery of critical metals including lithium, nickel, cobalt, and manganese from spent lithium-ion battery (LIB) cathode materials are essential in driving circularity. The tailored deep eutectic solvent (DES) choline chloride-formic acid (ChCl-FA) demonstrated a high selectivity and efficiency in extracting critical metals from mixed cathode materials (LiFePO4:Li(NiCoMn)1/3O2 mass ratio of 1:1) under mild conditions (80 °C, 120 min) with a solid-liquid mass ratio of 1:200. The leaching performance of critical metals could be further enhanced by mechanochemical processing because of particle size reduction, grain refinement, and internal energy storage. Furthermore, mechanochemical reactions effectively inhibited undesirable leaching of nontarget elements (iron and phosphorus), thus promoting the selectivity and leaching efficiency of critical metals. This was achieved through the preoxidation of Fe and the enhanced stability of iron phosphate framework, which significantly increased the separation factor of critical metals to nontarget elements from 56.9 to 1475. The proposed combination of ChCl-FA extraction and the mechanochemical reaction can achieve a highly selective extraction of critical metals from multisource spent LIBs under mild conditions.
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Lítio , Reciclagem , Metais , Cobalto , Fontes de Energia Elétrica , FerroRESUMO
Oxidative extraction has become an economically viable option for recycling lithium (Li) from spent lithium iron phosphate (LiFePO4) batteries. In this study, the releases behaviour of Li from spent LiFePO4 batteries under different oxidizing conditions was investigated with sodium hypochlorite (NaClO) as the solid oxidant. We revealed that, due to the intervention of graphitic carbon, the generated species of Li in mechanochemical oxidation (NaClO:LiFePO4 at a molar ratio of 2:1, 5 min, and 600 rpm) was lithium carbonate (Li2CO3). The graphite layer provided a channel for the conversion of Li species released by mechanochemical oxidation. While in hydrometallurgical oxidation (NaClO:LiFePO4 at a molar ratio of 2:1 and 12.5 min), the presence of hydrogen species led to the formation of lithium chloride (LiCl). Moreover, life cycle assessment (LCA) demonstrated that for recycling 1.0 kg of spent LiFePO4 batteries, mechanochemical and hydrometallurgical oxidation could reduce carbon footprints by 2.81 kg CO2 eq and 2.88 kg CO2 eq, respectively. Our results indicate that the oxidative environment determines the release pathway of Li from the spent LiFePO4 cathode material, thereby regulating the product forms of Li and environmental impacts. This study can provide key technical guidance for Li recycling from spent LiFePO4 batteries.
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Background: Programmed cell death-1 (PD-1) immune checkpoint inhibitors are not effective in treating all patients with hepatocellular carcinoma (HCC), and regulatory T cells (Tregs) may determine the resistance to anti-PD-1 therapy. Methods: Patients were divided into two groups based on the clinical efficacy of anti-PD-1 therapy. Flow cytometry was used to determine the phenotype of CD4+, CD8+, and Tregs in peripheral blood mononuclear cells (PBMCs). CD4+CD45RA+T cells were sorted to analyze Treg differentiation and function. Results: No significant differences were found between resistant and sensitive patients in the percentage of CD4+ T cells and Tregs in PBMCs or the differentiation and function of induced Tregs (iTregs). However, iTregs from resistant patients presented higher monocarboxylate transporter (MCT) expression. Lactate induced more iTregs and improved OXPHOS levels in the resistant group. MCT1 and MCT2 were highly expressed in tumor-infiltrating Tregs, and patients with higher MCT1 expression had worse clinical outcomes. Combinatorial therapy with MCT antibody and anti-PD-1 therapy effectively inhibited tumor growth. Conclusion: MCT and its downstream lactate signal in Tregs can confer anti-PD-1 resistance and may be a marker of poor prognosis in HCC.
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Biochar has been demonstrated as an efficient amendment for immobilizing contaminants. However, a certain number of micro/nano-scale particles are inevitably present in the fresh or aged biochar, which may facilitate the downward transport of contaminants along the soil profile, posing a detrimental impact on the groundwater. Herein, the effects of biochar colloids derived from wood chip and wheat straw at two temperatures (350 °C and 500 °C) on the transport and transformation of Cr(VI) in soil were investigated. All biochar colloids facilitated the transport of Cr(VI) in a loam clay Ultisol, which was attributed to the competition between biochar colloids and Cr(VI) for the available sorption sites on the soil surface. Wheat straw biochar colloids caused more transport of Cr(VI) than wood chip ones due to the more negative charge and higher polarity, which resulted in stronger electrostatic repulsion and competition with Cr(VI). It is soluble Cr(VI) that dominated the transport of Cr in the effluent solution, however, the particulate Cr(VI) could be reduced into Cr(III) before being carried by biochar colloids for co-transport. The 350 °C biochar colloids had higher electron donating capacities than 500 °C ones, resulting in more reduction of Cr(VI) and more co-transport as biochar colloids-associated Cr(III) in the effluent. Moreover, the more negatively charged 350 °C biochar colloids could also attach more soil Fe oxides, further facilitating the cotransport of Cr via the formation of a binary or ternary complex. Modeling showed the experimental-consistently results that biochar colloids caused 0.5-7.0 times faster transport of Cr(VI) than no biochar colloids in the long-term period. Our findings demonstrate that biochar colloids can enhance transport and transformation of Cr(VI) in soils, which arouse migration risk concern about in-situ remediation of Cr(VI)-contaminated soils by biochar.
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Poluentes do Solo , Solo , Adsorção , Domínio Catalítico , Carvão Vegetal/química , Cromo/química , Argila , Coloides , Óxidos , Solo/química , Poluentes do Solo/químicaRESUMO
The process water (PW) from acid-catalyzed hydrothermal carbonization (HTC) is still an environmental burden due to the enriched organics, nutrients, and salts. This study proposed a novel strategy to valorize food waste digestate into multifunctional hydrochar by recirculating the PW in the HCl-catalyzed HTC process. The produced multifunctional hydrochar could be utilized as a high-quality solid fuel with HHV of 27.9 MJ kg-1 (hydrochar without PW recirculation) and a slow-release fertilizer by converting the complex Ca and P compounds from the food waste digestate into a Ca-P deposit (hydroxyapatite) with more than a 93 % P recovery rate (hydrochar with PW recirculation). Adding fresh HCl in the HTC PW recirculation system only displayed a marginal catalytic impact on the hydrochar properties after two cycles of recirculation. This study demonstrated the importance of inherent Ca in the feedstocks and the dual role of HCl in the HTC with PW recirculation.
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Eliminação de Resíduos , Água , Anaerobiose , Carbono , Catálise , Alimentos , Nutrientes , TemperaturaRESUMO
Electroactive Fe-biochar has attracted significant attention for As(III)/Cr(VI) immobilization through redox reactions, and its performance essentially lies in the regulation of various Fe/C moieties for desired redox performance. Here, a series of Fe-biochar with distinct Fe/C speciation were rationally produced via two-step pyrolysis of iron minerals and biomass waste at 400-850 °C (BCX-Fe-Y, X and Y represented the first- and second-step pyrolysis temperature, respectively). The redox transformation of Cr(VI) and As(III) by Fe-biochar was evaluated in simulated wastewater under oxic or anoxic conditions. Results showed that more effective Cr(VI) reduction could be achieved by BCX-Fe-400, while a higher amount of As (III) was oxidized by BCX-Fe-850 under the anoxic environment. Besides, BCX-Fe-400 could generate more reactive oxygen species (e.g.,â¢OH) by reducing the O2, which enhanced the redox-related transformation of pollutants under the oxic situation. The evolving redox performance of Fe-biochar was governed by the transition of the redox state from reductive to oxidative related to the Fe/C speciation. The small-sized amorphous/low-crystalline ferrous minerals contributed to a higher electron-donating capacity (0.43-1.28 mmol g-1) of BCX-Fe-400. In contrast, the oxidative surface oxygen-functionalities (i.e., carboxyl and quinoid) on BCX-Fe-850 endowed a stronger electron-accepting capacity (0.71-1.39 mmol g-1). Moreover, the graphitic crystallites with edge-type defects and porous structure facilitated the electron transfer, leading to a higher electron efficiency of BCX-Fe-850. Overall, we unveiled the roles of both Fe and C speciation in maneuvering the redox reactivity of Fe-biochar, which can advance our rational design of electroactive Fe-biochar for redox-related environmental remediation.
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Arsênio , Cromo , Carbono , Carvão Vegetal/química , Cromo/química , Ferro/química , Minerais , OxirreduçãoRESUMO
Heteroatom doping is a promising technique to enhance biochar for effective environmental remediation. However, development of electroactive heteroatom-doped biochars, e.g., sulfur-doped biochar, has been hindered due to complex nature of non-stoichiometric biomass-derived carbon and changeable electrochemical state of dopants. Herein, we produced a series of wood waste-derived biochars with customized levels of minerals and redox-active moieties, aiming to unravel the crucial factors for sulfur doping. Calcium (Ca) in biochar was found to preferentially coordinate with sulfur to form inactive inorganic sulfur minerals (i.e., CaSO4 and CaS) with inferior catalytic reactivity. After diminishing the inherent Ca minerals beforehand, we could introduce surface phenoxyl-type radicals (C-Oâ¢) and vacancy defects on the biochar to develop an electrophilic C-S-O bonding configuration, which guaranteed a high affinity towards peroxymonosulfate (PMS, 2.08 mM g-1, 30 min) and efficient removal of bisphenol A (BPA, 91.1%, 30 min). Scavenging experiments and in-situ Raman analyses indicated that the epoxide-like C-S-O structure induced nucleophilic addition of PMS to generate surface-bound singlet oxygen (1O2, major) and hydroxyl radicals (â¢OH, minor) through a preservative and stoichiometric interfacial reaction. Overall, the proposed approach overcomes the major hurdles in science-informed fabrication of sulfur-doped biochar and advances its development for environmental remediation.
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Recuperação e Remediação Ambiental , Compostos de Epóxi , Carvão Vegetal , EnxofreRESUMO
Electron transfer mediated by iron minerals is considered as a critical redox step for the dynamics of pollutants in soil. Herein, we explored the reduction process of Cr(VI) with different crystalline ferric oxyhydroxides in the presence of pyrogenic carbon (biochar). Both low- and high-crystallinity ferric oxyhydroxides induced Cr(VI) immobilization mainly via the sorption process, with a limited reduction process. However, the Cr(VI) reduction immobilization was inspired by the copresence of biochar. Low-crystallinity ferric oxyhydroxide had an intense chemical combination with biochar and strong sorption for Cr(VI) via inner-sphere complexation, leading to the indirect electron transfer route for Cr(VI) reduction, that is, the electron first transferred from biochar to iron mineral through C-O-Fe binding and then to Cr(VI) with Fe(III)/Fe(II) transformation on ferric oxyhydroxides. With increasing crystallinity of ferric oxyhydroxides, the direct electron transfer between biochar and Cr(VI) became the main electron transfer avenue for Cr(VI) reduction. The indirect electron transfer was suppressed in the high-crystallinity ferric oxyhydroxides due to less sorption of Cr(VI), limited combination with biochar, and higher iron stability. This study demonstrates that electron transfer mechanisms involving iron minerals change with the mineral crystallization process, which would affect the geochemical process of contaminants with pyrogenic carbon.