A critical review of biochar for the remediation of PFAS-contaminated soil and water.

Per- and polyfluoroalkyl substances (PFAS) present significant environmental and health hazards due to their inherent persistence, ubiquitous presence in the environment, and propensity for bioaccumulation. Consequently, the development of efficacious remediation strategies for soil and water contaminated with PFAS is imperative. Biochar, with its unique properties, has emerged as a cost-effective adsorbent for PFAS. Despite this, a comprehensive review of the factors influencing PFAS adsorption and immobilization by biochar is lacking. This narrative review examines recent findings indicating that the application of biochar can effectively immobilize PFAS, thereby mitigating their environmental transport and subsequent ecological impact. In addition, this paper reviewed the sorption mechanisms of biochar and the factors affecting its sorption efficiency. The high effectiveness of biochars in PFAS remediation has been attributed to their high porosity in the right pore size range (>1.5 nm) that can accommodate the relatively large PFAS molecules (>1.02-2.20 nm), leading to physical entrapment. Effective sorption requires attraction or bonding to the biochar framework. Binding is stronger for long-chain PFAS than for short-chain PFAS, as attractive forces between long hydrophobic CF2-tails more easily overcome the repulsion of the often-anionic head groups by net negatively charged biochars. This review summarizes case studies and field applications highlighting the effectiveness of biochar across various matrices, showcasing its strong binding with PFAS. We suggest that research should focus on improving the adsorption performance of biochar for short-chain PFAS compounds. Establishing the significance of biochar surface electrical charge in the adsorption process of PFAS is necessary, as well as quantifying the respective contributions of electrostatic forces and hydrophobic van der Waals forces to the adsorption of both short- and long-chain PFAS. There is an urgent need for validation of the effectiveness of the biochar effect in actual environmental conditions through prolonged outdoor testing.

Relief effect of biochar on continuous cropping of tobacco through the reduction of p-hydroxybenzoic acid in soil.

Biochar application to soil has proven to be an excellent approach for decreasing the concentration of auto-toxic compounds and promoting plant growth in continuous-cropping fields. However, the mechanisms underlying the action pathway among biochars, auto-toxic compounds and tobacco remain unknown. In this study, we conducted an experiment tracking the incidence rate of black rot and auto-toxic compounds for a 3-year continuous-cropping tobacco pot trial in response to biochar treatment intensity compared with that of non-biochar treatment. Biochar inhibited the incidence of black rot. Using ultra-high-performance liquid chromatography-mass spectrometry (UPLC‒MS/MS), we revealed that biochar can effectively decrease the concentration of p-hydroxybenzoic acid (PHA), which is associated with the incidence rate of black rot (R2 = 0.890, p < 0.05). The sorption kinetics and isotherm of PHA sorption on biochar indicate that the coexistence of heterogeneous and monolayer sorption plays an important role in the adsorption process. Using Molecular dynamics (MD), Density functional theory (DFT) and Independent gradient model (IGM) analyses, we provide evidence that van der Waals force (vdW), π-π bonds and H-bonds between biochar and PHAs are the dominant factors that affect adsorption capacity. Moreover, the molecular adsorption rate (Nbiochar: NPHAs = 1:4) was theoretically calculated. In contrast, biochar dramatically increased nutrient retention capacity and improved soil properties, further enhancing tobacco quality, including its agronomic and physiological traits. Therefore, we considered that biochar not only relieved continuous cropping but also improved soil properties suitable for tobacco growth. Together, we demonstrate that the action of biochar in continuously cropped soil improves soil traits and alleviates auto-toxic compound toxicity. These data contribute to the direction of modified biochar application to improve continuous-cropping soil.

TNFα regulates the expression of the CSE gene in HUVEC.

The hydrogen sulfide (H2S)/cystathionine γ-lyase (CSE) signaling pathway is involved in several inflammatory conditions, where tumor necrosis factor-α (TNFα) is one of the inflammatory cytokines activated during sepsis. Therefore, the present study investigated the role of the NF-κB transcription factor binding site in the transcriptional regulation of the CSE gene in 293T cells following treatment with TNFα using luciferase assays, as well as using western blotting and reverse transcription-quantitative PCR to examine the effect of TNFα on CSE expression in HUVECs. After transfected 293T cells were incubated with various concentrations of TNFα for 1, 3, and 6 h, the wild-type promoter of the CSE gene increased significantly at 1 h compared to 0 h. By contrast, after the transfected 293T cells were incubated with various concentrations of TNFα for 1 h, the mutant-type promoter activity of the CSE gene decreased significantly compared to the wild-type. These results revealed that the DNA sequence GGGACATTCC on the CSE gene promoter was directly associated with the transcriptional regulation of the CSE gene in Human cells (293T cells) that's were treated with TNFα. This suggests that TNFα affects CSE gene expression, such that vascular endothelial cells respond to TNFα in the blood by regulating CSE expression. The regulatory mechanisms associated with the effects of TNFα on the transcriptional regulation of the CSE gene in HUVECs and the NF-κB pathway warrant further investigation.

The emission quenching of upconversion nanoparticles coated with amorphous silica by fluorescence resonance energy transfer: A mercury-sensing nanosensor excited by near-infrared radiation.

In this paper, a rhodamine derivative was synthesized as a probe for Hg(II) detection. Its spectral response and sensing mechanism towards Hg(II) were discussed carefully. It was found that its absorption and emission were increased by Hg(II), via a direct bonding stoichiometry of 1:1. Its association constant was determined with absorption titration as 2.59 × 105 M-1, which suggested a coordination procedure between Hg(II) and this rhodamine probe. It showed good selectivity towards Hg(II) over competing metal cations, no increased emission or absorption was observed in the presence of interfering metal cations. It was then covalently grafted onto silica (SiO2)-encapsulated upconversion nanoparticles (UCNPs). Upon near-infrared (NIR) excitation (980 nm), RHO accepted energy from these UCNPs through a FRET (fluorescence resonance energy transfer) procedure, quenching their upconversion emission. A sensing response towards Hg(II) was thus constructed. Good linearity and selectivity were still preserved in this composite sample. On the other hand, this work found a different phenomenon from literature cases, which was the emission absence of rhodamine emission in this composite structure. Detailed analysis suggested that rhodamine emission absence was caused by its self-quenching effect.

Analysis of cardiovascular disease-related NF-κB-regulated genes and microRNAs in TNFα-treated primary mouse vascular endothelial cells.

Activated nuclear factor-κB (NF-κB) plays an important role in the development of cardiovascular disease (CVD) through its regulated genes and microRNAs (miRNAs). However, the gene regulation profile remains unclear. In this study, primary mouse vascular endothelial cells (pMVECs) were employed to detect CVD-related NF-κB-regulated genes and miRNAs. Genechip assay identified 77 NF-κB-regulated genes, including 45 upregulated and 32 downregulated genes, in tumor necrosis factor α (TNFα)-treated pMVECs. Ten of these genes were also found to be regulated by NF-κB in TNFα-treated HeLa cells. Quantitative real-time PCR (qRT-PCR) assay confirmed the up-regulation of Egr1, Tnf, and Btg2 by NF-κB in the TNFα-treated pMVECs. The functional annotation revealed that many NF-κB-regulated genes identified in pMVECs were clustered into classical NF-κB-involved biological processes. Genechip assay also identified 26 NF-κB-regulated miRNAs, of which 21 were upregulated and 5 downregulated, in the TNFα-treated pMVECs. Further analysis showed that nine of the identified genes are regulated by seven of these miRNAs. Finally, among the identified NF-κB-regulated genes and miRNAs, 5 genes and 12 miRNAs were associated with CVD by miRWalk and genetic association database analysis. Taken together, these findings show an intricate gene regulation network raised by NF-κB in TNFα-treated pMVECs. The network provides new insights for understanding the molecular mechanism underlying the progression of CVD.

The binding site for the transcription factor, NF-κB, on the cystathionine γ-lyase promoter is critical for LPS-induced cystathionine γ-lyase expression.

Hydrogen sulfide (H2S) is regarded as the third endogenous gaseous signaling molecule. Cystathioine γ-lyase (CSE), one of the three enzymes in the transsulfuration pathway, is responsible for the production of endogenous H2S. The H2S/CSE signaling pathway is involved in the inflammation induced by lipopolysaccharides (LPS). Therefore, in this study, we investigated the effects of the binding site (on the CSE promoter) for the transcription factor, nuclear factor (NF)-κB, on the transcriptional regulation of the CSE gene in mammalian cells treated with LPS. For this purpose, HEK-293 and COS-7 cells were transfected with 5 µg pGL4.12-KM1478 or 5 µg pGL4.12-KM1478m (mutant) together with the pRL-CMV control vector (0.032 µg for the HEK-293 cells, 0.0032 µg for the COS-7 cells). Subsequently, the cells were treated with LPS for 6 h. The expression of CSE was measured by RT-qPCR. cDNA pooled from J774.1A and RAW264.7 cells treated with LPS for 6 h was used to estimate the quantity of the transcripts. Our results revealed that LPS markedly increased the mRNA and protein expression levels of the CSE gene in the J774.1A and RAW264.7 cells following treatment with LPS for 6 h. In addition, we found that the GGGACATTCC DNA sequence on the promoter of the CSE gene was closely associated with the transcriptional regulation of the CSE gene in the HEK-293 and COS-7 cells treated with LPS. Taken together, our data suggest that the NF-κB binding site on CSE promoter is critical for LPS-induced CSE expression in mammalian cells.

Regulation of cystathionine γ-lyase in mammalian cells by hypoxia.

Hydrogen sulfide (H2S), an endogenous signaling molecule in mammalian cells, shows a variety of biological effects. Cystathionine γ-lyase (CSE) is a key enzyme in the trans-sulfuration pathway responsible for the production of endogenous H2S. Whether CSE expression is regulated by hypoxia in mammalian cells remains largely unknown. This study revealed that these regulatory effects changed with time at transcriptional and post-transcriptional levels. Hypoxia regulated CSE expression in mammalian cells in a complex manner; CSE transcription went through a down-regulation and recovery period, while CSE mRNA and protein levels increased during hypoxia. Taken together, the results suggest that CSE can respond to hypoxia through transcriptional and post-transcriptional regulation, and CSE expression can be up-regulated by hypoxia to a certain extent. Therefore, the up-regulation of CSE expression during hypoxia may be useful for increasing the production and concentration of H2S in mammalian cells and indirectly protecting cells from hypoxia.

The effect of certain conditions in the regulation of cystathionine γ-lyase by exogenous hydrogen sulfide in mammalian cells.

Cystathionine γ-lyase (CSE), one of three enzymes in the trans-sulfuration pathway, is responsible for the production of endogenous hydrogen sulfide (H2S) using L-cysteine or L-homocysteine as a substrate. The regulatory mechanism of CSE by exogenous H2S remains unknown. The transcription and expression of the CSE gene regulated by exogenous H2S at approximately physiologic concentrations was investigated using luciferase assay, Western blotting, and quantitative RT-PCR. The results revealed that exogenous H2S down-regulates the transcription and expression of CSE in mammalian cells at 10-80 µM. Exogenous H2S at 120 µM increases the transcription and expression of CSE significantly. At a concentration of exogenous H2S over 160 µM, the transcription and expression of CSE are inhibited completely. These findings suggest that CSE expression has not only a feedback to the enzyme itself at lower concentrations of exogenous H2S but also can be up-regulated at higher concentrations, and H2S may become toxic at higher levels.

Cystathionine gamma-lyase expression is regulated by exogenous hydrogen peroxide in the mammalian cells.

Hydrogen sulfide (H2S), as an endogenous signaling molecule in mammals, shows a variety of biological effects. Cystathionine gamma-lyase (CSE)/H2S pathway has been implicated in scavenging reactive oxygen species (ROS) in the mammalian cells. Therefore, we first investigated the regulatory effects of exogenously applied hydrogen peroxide (H2O2) on CSE expression in the mammalian cells. African green monkey kidney fibroblastlike cells (COS-7 cells) or human embryonic kidney 293 cells (HEK 293 cells) were transfected with CSE promoter-luciferase reporter constructs and treated with H2O2 of 1, 5, and 10 microM for 0.5 and 1.5 h at 37 degrees C. The transfected cells were assayed for firefly luciferase activities normalized by Renilla luciferase activity. Human lung adenocarcinoma cells (A549 cells) or human liver cancer cells (SMMC-7721 cells) were treated with H2O2 of 1, 5, and 10 microM for 0.5 and 1.5 h at 37 degrees C, and were then harvested and analyzed by Western blotting and quantitative RT-PCR. Our results showed that the treatment of a medium concentration (5 microM) of H2O2 at a longer time (1.5 h) upregulated CSE expression in the mammalian cells at the levels of the promoter, message RNA, and protein. Collectively, exogenously applied H2O2 can not only markedly affect CSE mRNA and protein expression, but also can affect the CSE promoter activity in the mammalian cells. Our observations indicate that that exogenous H2O2 can upregulate the expression of the CSE gene in the mammalian cells, which will provide the possibility of the scavenging effect of the CSE gene indirectly on ROS in the mammalian cells. However, the regulatory mechanism involved in the effects of exogenously applied H2O2 on CSE expression in the mammalian cells need be further studied.