A green edge-hosted zinc single-site heterogeneous catalyst for superior Fenton-like activity.

Developing green heterogeneous catalysts with excellent Fenton-like activity is critical for water remediation technologies. However, current catalysts often rely on toxic transitional metals, and their catalytic performance is far from satisfactory as alternatives of homogeneous Fenton-like catalysts. In this study, a green catalyst based on Zn single-atom was prepared in an ammonium atmosphere using ZIF-8 as a precursor. Multiple characterization analyses provided evidence that abundant intrinsic defects due to the edge sites were created, leading to the formation of a thermally stable edge-hosted Zn-N4 single-atom catalyst (ZnN4-Edge). Density functional theory calculations revealed that the edge sites equipped the single-atom Zn with a super catalytic performance, which not only promoted decomposition of peroxide molecule (HSO5-) but also greatly lowered the activation barrier for •OH generation. Consequently, the as-prepared ZnN4-Edge exhibited extremely high Fenton-like performance in oxidation and mineralization of phenol as a representative organic contaminant in a wide range of pH, realizing its quick detoxification. The atom-utilization efficiency of the ZnN4-Edge was ~104 higher than an equivalent amount of the control sample without edge sites (ZnN4), and the turnover frequency was ~103 times of the typical benchmark of homogeneous catalyst (Co2+). This study opens up a revolutionary way to rationally design and optimize heterogeneous catalysts to homogeneous catalytic performance for Fenton-like application.

Screening Novel Per- and Polyfluoroalkyl Substances in Human Blood Based on Nontarget Analysis and Underestimated Potential Health Risks.

Nontarget analysis has gained prominence in screening novel perfluoroalkyl and polyfluoroalkyl substances (PFASs) in the environment, yet remaining limited in human biological matrices. In this study, 155 whole blood samples were collected from the general population in Shijiazhuang City, China. By nontarget analysis, 31 legacy and novel PFASs were assigned with the confidence level of 3 or above. For the first time, 11 PFASs were identified in human blood, including C1 and C3 perfluoroalkyl sulfonic acids (PFSAs), C4 ether PFSA, C8 ether perfluoroalkyl carboxylic acid (ether PFCA), C4-5 unsaturated perfluoroalkyl alcohols, C9-10 carboxylic acid-perfluoroalkyl sulfonamides (CA-PFSMs), and C1 perfluoroalkyl sulfonamide. It is surprising that the targeted PFASs were the highest in the suburban population which was impacted by industrial emission, while the novel PFASs identified by nontarget analysis, such as C1 PFSA and C9-11 CA-PFSMs, were the highest in the rural population who often drank contaminated groundwater. Combining the toxicity prediction results of the bioaccumulation potential, lethality to rats, and binding affinity to target proteins, C3 PFSA, C4 and C7 ether PFSAs, and C9-11 CA-PFSMs exhibit great health risks. These findings emphasize the necessity of broadening nontarget analysis in assessing the PFAS exposure risks, particularly in rural populations.

Physiologically based toxicokinetic modelling of Tri(2-chloroethyl) phosphate (TCEP) in mice accounting for multiple exposure routes.

Exposure routes are important for health risk assessment of chemical risks. The application of physiologically based toxicokinetic (PBTK) models to predict concentrations in vivo can determine the effects of harmful substances and tissue accumulation on the premise of saving experimental costs. In this study, Tri(2-chloroethyl) phosphate (TCEP), an organophosphate ester (OPE), was used as an example to study the PBTK model of mice exposed to different exposure doses by multiple routes. Different routes of exposure (gavage and intradermal injection) can cause differences in the concentration of chemicals in the organs. TCEP that enters the body through the mouth is mainly concentrated in the gastrointestinal tract and liver. However, the concentrations of chemicals that enter the skin into the mice are higher in skin, rest of body, and blood. In addition, TCEP was absorbed and accumulated very rapidly in mice, within half an hour after a single exposure. We have successfully established a mouse PBTK model of the TCEP accounting for multiple exposure Routes and obtained a series of kinetic parameters. The model includes blood, liver, kidney, stomach, intestine, skin, and rest of body compartments. Oral and dermal exposure route was considered for PBTK model. The PBTK model established in this study has a good predictive ability. More than 70% of the predicted values deviated from the measured values by less than 5-fold. In addition, we extrapolated the model to humans. A human PBTK model is built. We performed a health risk assessment for world populations based on human PBTK model. The risk of TCEP in dust is greater through mouth than through skin. The risk of TCEP in food of Chinese population is greater than dust.

Insights into the Competitive Mechanisms of Per- and Polyfluoroalkyl Substances Partition in Liver and Blood.

Some per- and polyfluoroalkyl substances (PFASs) tend to be accumulated in liver and cause hepatotoxicity. However, the difficulty to directly measure liver concentrations of PFASs in humans hampers our understanding of their hepatotoxicity and mechanisms of action. We investigated the partitioning of 11 PFASs between liver and blood in male CD-1 mice. Although accumulation of the perfluoroalkanesulfonic acids (PFSAs) in mice serum was higher than their carboxylic acids (PFCAs) counterparts as expected, the liver-blood partition coefficients (RL/S) of PFSAs were lower than the PFCAs RL/S, implying a competition between liver and blood. The in vitro experiments further indicated that the partitioning was dominantly determined by their competitive binding between human liver fatty acid binding protein (hL-FABP) and serum albumin (HSA). The binding affinities (Kd) of PFASs to both proteins were measured. The correlations between the RL/S and log Kd (hL-FABP)/log Kd (HSA) were stronger than those with log Kd (hL-FABP) alone, magnifying that the partitioning was dominantly controlled by competitive binding between hL-FABP and HSA. Therefore, the liver concentrations of the selected PFASs in humans could be predicted from the available serum concentrations, which is important for assessing their hepatotoxicity.

Quantifying Indirect Contribution from Precursors to Human Body Burden of Legacy PFASs Based on Paired Blood and One-Week Duplicate Diet.

The restriction on legacy perfluoroalkyl substances (PFASs) has led to increasing application and contamination of their precursors and novel alternatives. However, the indirect contribution from precursors has not been well characterized. In this study, 24 PFASs were measured in the paired human blood and urine from general volunteers (n = 20), as well as their corresponding exposure matrices (7 day duplicate diet, drinking water and dust). Perfluorooctanoic acid (PFOA) was predominant, followed by 6:2 chlorinated polyfluoroalkyl ether sulfonate (6:2 Cl-PFESA), contributing 21.6-47.0 and 6.6-20.0% of the total concentrations, respectively. Total oxidable precursor (TOP) assay and isomeric analysis coupled with a toxicokinetic model suggested that around 19% of perfluorooctane sulfonate (PFOS) in human was contributed by its precursors. The strong correlation between the estimated daily intake (EDI) and human blood concentration for 6:2 Cl-PFESA suggested that it was mainly contributed by direct exposure. The bioavailability of 6:2 Cl-PFESA in the food matrices was estimated as 18.6% by comparing the estimated and measured blood concentrations, implying that human exposure might be overestimated if the bioavailability of PFASs in food was not considered. Assuming that they had a similar bioavailability, it was estimated that ca. 20% of PFOS body burden was from indirect exposure to its precursors, which was supported by TOP assay.

Structure-Activity Relationship Investigation on Reaction Mechanism between Chlorinated Quinoid Carcinogens and Clinically-Used Aldoxime Nerve-Agent Antidote under Physiological Condition.

Pyridinium aldoximes are best-known therapeutic antidotes used for clinical treatment of poisonings by organophosphorus nerve-agents and pesticides. Recently, we found that pralidoxime (2-PAM, a currently clinically used nerve-agent antidote) could also detoxify tetrachloro-1,4-benzoquinone (TCBQ), which is a carcinogenic quinoid metabolite of the widely used wood preservative pentachlorophenol under normal physiological conditions, via an unusually mild and facile Beckmann fragmentation mechanism accompanied by radical homolysis. However, it is not clear whether the less-chlorinated benzoquinones (CnBQs, n ≤ 3) act similarly; if so, what is the structure-activity relationship? In this study, we found that (1) The stability of reaction intermediates produced by different CnBQs and 2-PAM was dependent not only on the position but also the degree of Cl-substitution on CnBQs, which can be divided into TCBQ- and DCBQ (dichloro-1,4-benzoquinone)-subgroup; (2) The pKa value of hydroxlated quinones (Cn-1BQ-OHs, the hydrolysis products of CnBQs), determined the stability of corresponding intermediates, that is, the decomposition rate of the intermediates depended on the acidity of Cn-1BQ-OHs; (3) The pKa value of the corresponding Cn-1BQ-OHs could also determine the reaction ratio of Beckmann fragmentation to radical homolysis in CnBQs/2-PAM. These new findings on the structure-activity relationship of the halogenated quinoid carcinogens detoxified by pyridinium aldoxime therapeutic agents via Beckmann fragmentation and radical homolysis reaction may have broad implications on future biomedical and environmental research.

Probing Mechanisms for the Tissue-Specific Distribution and Biotransformation of Perfluoroalkyl Phosphinic Acids in Common Carp (Cyprinus carpio).

This study investigated the tissue-specific accumulation and biotransformation of 6:6 and 8:8 perfluoroalkyl phosphinic acids (PFPiA) in common carp (Cyprinus carpio) during 90 d exposure and 30 d depuration in water in the laboratory. Both 6:6 and 8:8 PFPiAs could quickly accumulate in the carp, and 6:6 PFPiA displayed higher bioaccumulation potential than 8:8 PFPiA. The highest concentrations of PFPiAs were observed in the blood, while the lowest were found in the muscle. The equilibrium dialysis experiment indicated that both PFPiAs had higher binding affinities with the proteins in the fish serum than in liver, which was supported by the molecular docking analysis. The results also indicated that 6:6 PFPiA had higher binding affinities with the serum and liver proteins than 8:8 PFPiA. These results suggested that the tissue-specific distribution of PFPiAs was highly dependent on the binding affinities with the specific proteins. Both in vivo and in vitro experiments consistently indicated that PFPiAs experienced biotransformation and produced perfluoroalkyl phosphonic acids (PFPAs), and biotransformation of 8:8 PFPiA was more active than 6:6 PFPiA. It was worth noting that perfluorohexanonate and perfluorooctanoic acids were identified in fish as metabolites after long-term exposure to PFPiAs for the first time.

Estimation of internal human daily intakes of organophosphate esters using one-compartment toxicokinetic model in the whole blood from Hebei Province, China.

To evaluate the human health risks attributed by organophosphate ester (OPE) exposure, it is very important to estimate the daily intakes (DIs) of OPEs in human. In this study, the DIs of OPEs were estimated using a simplified one-compartment toxicokinetic model based on their total clearance rates in human and their whole blood concentrations. Thirty paired human whole blood and plasma samples were collected from participants in Hengshui, Hebei Province, China. The detection frequencies of most OPEs in the whole blood were lower than 50.0%. Thus, the OPE levels in whole blood were converted from the corresponding plasma levels using the fractions of OPEs in plasma (Fp), which were estimated from an in vitro partition assay and the values were in the range of 0.52-0.98. The measured whole blood concentrations of triphenyl phosphate (TPHP) and tris(chloroethyl) phosphate (TCEP) were comparable to those converted from the plasma concentrations, suggesting that the conversion method was reliable. The estimated total DIs of TPHP, TCEP, and tris(2-chloroisopropyl) phosphate were 1-30 times of those derived by the external exposure method, which usually excluded many exposure sources. The estimated human health risks based on the DIs indicated that the carcinogenic and non-carcinogenic effects of OPEs for the participants in Hengshui, Hebei Province, China, were negligible. This study recommended a more reliable and simpler method to estimate the human health risks attributed to the exposure of OPEs.

Glass fiber supported BiOI thin-film fixed-bed photocatalytic reactor for water decontamination under solar light irradiation.

BiOI powder has been proved to be an efficient photocatalyst, but the difficulty in removing it from water after reaction limits its application in real water treatment. To solve this problem, a thin-film fixed-bed reactor (TFFBR) was set-up by developing a BiOI thin film on glass fiber cloth (GFC). The composition and structure of the as-prepared films were characterized with X-ray diffraction, X-ray photoelectron spectroscopy, field emission microscopy, transmission electron microscopy and Fourier transform infrared spectroscopy. The BiOI thin film was made by painting a silica sol containing BiOI on GFC, which could be tailored to desired sizes to accommodate the TFFBR. The mass of BiOI on the GFC increased with the number of iterations of the painting process. SiO2 sol glued the BiOI particles tightly onto the GFC, making the thin film strong enough to resist fluid flushing in the TFFBR. The photocatalytic activity of the BiOI thin film was investigated by degrading bisphenol A (BPA) under simulated sunlight. Ninety eight percent of BPA (20 mg/L in 2 L) was degraded by the BiOI thin film sample of seven layers (GFC-7) on the TFFBR within 8 hr irradiation. The GFC-7 displayed good photocatalytic ability toward artificial sewage containing BPA in a wide pH range (5-9), and also demonstrated excellent durability and reusability. The working conditions were optimized and it was found that the thickness of the fluid film and residence time over the thin film were key factors affecting the photocatalytic efficiency.

Perfluoroalkyl Acids Including Isomers in Tree Barks from a Chinese Fluorochemical Manufacturing Park: Implication for Airborne Transportation.

Measurement of airborne perfluoroalkyl acids (PFAAs) is challenging, but important for understanding their atmospheric transport. Tree bark is good media for monitoring semivolatile compounds in the atmosphere. Whether it could work as an indicator of airborne PFAAs was first examined in this study. Bark and leaf samples collected around a Chinese fluorochemical manufacturing park (FMP) were analyzed for PFAAs and their branched isomers. Total PFAA concentrations (∑PFAAs) in the bark (mean, 279 ng/g dw) and leaf (250 ng/g dw) samples were comparable. ∑PFAAs in the barks collected within the boundaries of the FMP were significantly (p < 0.05) higher than those outside the FMP, and displayed a decreasing spatial trend as the distance from the FMP increased. However, such spatial difference and trend were not observed for the leaves. PFAA compositional profiles in most of the tree barks were consistent with each other, but different from those in tree leaves. These results indicated that tree barks mainly accumulated airborne PFAAs, while uptake from soil and translocation could make partial contribution to those in leaves. Perfluorooctanoate and perfluorooctanesulfonate in barks had strictly consistent isomeric compositions with their electrochemical fluorination products. Overall, these results indicated that the bark could be a good indicator of airborne PFAAs with respect to their occurrence, isomeric signature, and atmospheric transport.

Molecular mechanism of metal-independent decomposition of organic hydroperoxides by halogenated quinoid carcinogens and the potential biological implications.

Halogenated quinones (XQ) are a class of carcinogenic intermediates and newly identified chlorination disinfection byproducts in drinking water. Organic hydroperoxides (ROOH) can be produced both by free radical reactions and enzymatic oxidation of polyunsaturated fatty acids. ROOH have been shown to decompose to alkoxyl radicals via catalysis by transition metal ions, which may initiate lipid peroxidation or transform further to the reactive aldehydes. However, it is not clear whether XQ react with ROOH in a similar manner to generate alkoxyl radicals metal-independently. By complementary applications of ESR spin-trapping, HPLC/high resolution mass spectrometric and other analytical methods, we found that 2,5-dichloro-1,4-benzoquinone (DCBQ) could significantly enhance the decomposition of a model ROOH tert-butylhydroperoxide, resulting in the formation of t-butoxyl radicals independent of transition metals. On the basis of the above findings, we detected and identified, for the first time, an unprecedented C-centered quinone ketoxy radical. Then, we extended our study to the more physiologically relevant endogenous ROOH 13-hydroperoxy-9,11-octadecadienoic acid and found that DCBQ could also markedly enhance its decomposition to generate the reactive lipid alkyl radicals and the genotoxic 4-hydroxy-2-nonenal (HNE). Similar results were observed with other XQ. In summary, these findings demonstrated that XQ can facilitate ROOH decomposition to produce reactive alkoxyl, quinone ketoxy, lipid alkyl radicals, and genotoxic HNE via a novel metal-independent mechanism, which may explain partly their potential genotoxicity and carcinogenicity.

A combined experimental and computational investigation on the unusual molecular mechanism of the Lossen rearrangement reaction activated by carcinogenic halogenated quinones.

The classic Lossen rearrangement is a well-known reaction describing the transformation of an O-activated hydroxamic acid into the corresponding isocyanate. In this study, we found that chlorinated benzoquinones (CnBQ) serve as a new class of agents for the activation of benzohydroxamic acid (BHA), leading to Lossen rearrangement. Compared to the classic one, this new kind of CnBQ-activated Lossen rearrangement has the following unique characteristics: (1) The stability of CnBQ-activated BHA intermediates was found to depend not only on the degree but also on the position of Cl-substitution on CnBQs, which can be divided into two subgroups. (2) It is the relative energy of the anionic CnBQ-BHA intermediates that determine the rate of this CnBQ-activated rearrangement, which is the rate-limiting step, and the Cl or H ortho to the reaction site at CnBQ is crucial for the stability of the anionic intermediates. (3) A pKa-activation energy correlation was observed, which can explain why the correlation exists between the rate of the rearrangement and the acidity of the conjugate acid of the anionic leaving group, the hydroxlated quinones. These findings may have broad implications for future research on halogenated quinoid carcinogens and hydroxamate biomedical agents.

UBE2L3 Promotes Oxidative Stress-regulated Necroptosis to Accelerate Osteosarcoma Progression.

BACKGROUND: Osteosarcoma is a highly invasive bone marrow stromal tumor with limited treatment options. Oxidative stress plays a crucial role in the development and progression of tumors, but the underlying regulatory mechanisms are not fully understood. Recent studies have revealed the significant involvement of UBE2L3 in oxidative stress, but its specific role in osteosarcoma remains poorly investigated. OBJECTIVE: This study aimed to explore the molecular mechanisms by which UBE2L3 promotes oxidative stress-regulated necroptosis to accelerate the progression of osteosarcoma using in vitro cell experiments. METHODS: Human osteoblast hFOB1.19 cells and various human osteosarcoma cell lines (MG-63, U2OS, SJSA-1, HOS, and 143B) were cultured in vitro. Plasmids silencing UBE2L3 and negative control plasmids were transfected into U2OS and HOS cells. The cells were divided into the following groups: U2OS cell group, HOS cell group, si-NC-U2OS cell group, si-UBE2L3-U2OS cell group, si-NC-HOS cell group, and si-UBE2L3-HOS cell group. Cell viability and proliferation capacity were measured using the Tunnel method and clonogenic assay. Cell migration and invasion abilities were assessed by Transwell and scratch assays. Cell apoptosis was analyzed by flow cytometry, and ROS levels were detected using immunofluorescence. The oxidative stress levels in various cell groups and the expression changes of necroptosis-related proteins were assessed by PCR and WB. Through these experiments, we aim to evaluate the impact of oxidative stress on necroptosis and uncover the specific mechanisms by which targeted regulation of oxidative stress promotes tumor cell necroptosis as a potential therapeutic strategy for osteosarcoma. RESULTS: The mRNA expression levels of UBE2L3 in human osteosarcoma cell lines were significantly higher than those in human osteoblast hFOB1.19 cells (p <0.01). UBE2L3 expression was significantly decreased in U2OS and HOS cells transfected with si-UBE2L3, indicating the successful construction of stable cell lines with depleted UBE2L3. Tunnel assay results showed a significant increase in the number of red fluorescent-labeled cells in si-UBE2L3 groups compared to si-NC groups in both cell lines, suggesting a pronounced inhibition of cell viability. Transwell assay demonstrated a significant reduction in invasion and migration capabilities of si-UBE2L3 groups in osteosarcoma cells. The clonogenic assay revealed significant suppression of proliferation and clonogenic ability in both U2OS and HOS cells upon UBE2L3 knockdown. Flow cytometry confirmed that UBE2L3 knockdown significantly enhanced apoptosis in U2OS and HOS cells. Immunofluorescence results showed that UBE2L3 silencing promoted oxidative stress levels in osteosarcoma cells and facilitated tumor cell death. WB analysis indicated a significant increase in phosphorylation levels of necroptosis-related proteins, RIP1, RIP3, and MLKL, in both osteosarcoma cell lines after UBE2L3 knockdown. In addition, the expression of necrosis-associated proteins was inhibited by the addition of the antioxidant N-acetylcysteine (NAC). CONCLUSION: UBE2L3 is upregulated in osteosarcoma cells, and silencing of UBE2L3 promotes oxidative stress in these cells, leading to enhanced necroptosis and delayed progression of osteosarcoma.

Detoxifying carcinogenic polyhalogenated quinones by hydroxamic acids via an unusual double Lossen rearrangement mechanism.

Hydroxamic acids, which are best-known for their metal-chelating properties in biomedical research, have been found to effectively detoxify the carcinogenic polyhalogenated quinoid metabolites of pentachlorophenol and other persistent organic pollutants. However, the chemical mechanism underlying such detoxication is unclear. Here we show that benzohydroxamic acid (BHA) could dramatically accelerate the conversion of the highly toxic tetrachloro-1, 4-benzoquinone (p-chloranil) to the much less toxic 2,5-dichloro-3, 6-dihydroxy-1, 4-benzoquonine (chloranilic acid), with rate accelerations of up to 150,000-fold. In contrast, no enhancing effect was observed with O-methyl BHA. The major reaction product of BHA was isolated and identified as O-phenylcarbamyl benzohydroxamate. On the basis of these data and oxygen-18 isotope-labeling studies, we proposed that suicidal nucleophilic attack coupled with an unexpected double Lossen rearrangement reaction was responsible for this remarkable acceleration of the detoxication reaction. This is the first report of an unusually mild and facile Lossen-type rearrangement, which could take place under normal physiological conditions in two consecutive steps. Our findings may have broad biological and environmental implications for future research on hydroxamic acids and polyhalogenated quinoid carcinogens, which are two important classes of compounds of major biomedical and environmental interest.

Electro-intensified simultaneous decontamination of coexisting pollutants in wastewater.

The treatment of wastewater has become increasingly challenging as a result of its growing complexity. To achieve synergistic removal of coexisting pollutants in wastewater, one promising approach involves the integration of electric fields. We conducted a comprehensive literature review to explore the potential of integrating electric fields and developing efficient electro-intensified simultaneous decontamination systems for wastewater containing coexisting pollutants. The review focused on comprehending the applications and mechanisms of these systems, with a particular emphasis on the deliberate utilization of positive and negative charges. After analyzing the advantages, disadvantages, and application efficacy of these systems, we observed electro-intensified systems exhibit flexible potential through their rational combination, allowing for an expanded range of applications in addressing simultaneous decontamination challenges. Unlike the reviews focusing on single elimination, this work aims to provide guidance in addressing the environmental problems resulting from the coexistence of hazardous contaminants.

Occurrence of perfluoroalkyl substances in the environment compartments near a mega fluorochemical industry: Implication of specific behaviors and emission estimation.

With the stringent restrictions on long-chain per- and polyfluoroalkyl substances (PFASs), ether-PFASs are being widely used as alternatives. We estimated that the mega fluorochemical industrial park (FIP) in Shandong, China, had emitted a maximum of 5040 kg and 1026 kg of hexafluoropropylene oxides (HFPOs), and 7560 kg and 1890 kg of perfluorooctanoic acid (PFOA) to water and air during 2021. In the surface water, groundwater, outdoor dust, soil, tree leaf and bark collected in the vicinity of the FIP, PFOA was predominant, followed by HFPOs. The much higher percentage of HFPO dimer acid (HFPO-DA) in groundwater than in surface water verified that this compound was more mobile in porous media. The strong correlations between the main PFASs in outdoor dust and surface soil suggested that the soil PFASs were mainly derived from air deposition, particularly for HFPO trimer acid (HFPO-TA), which has a stronger binding affinity with particles than PFOA. High percentage of the hydroxylated product of 6:2 polyfluorinated ether sulfonic acid was observed in groundwater, implying reductive dechlorination might occur in groundwater. Strong correlations between PFASs in outdoor dust and those in tree leaf and bark magnified that tree could serve as a sampler to effectively monitor airborne PFASs. This study provides the first line of information about the discharge, transport, and fate of novel ether-PFASs in the multiple environmental media near a point source.

Novel insights into the mediating roles of cluster of differentiation 36 in transmembrane transport and tissue partition of per- and polyfluoroalkyl substances in mice.

Transmembrane transport is important for bioaccumulation of per- and polyfluoroalkyl substances (PFASs) in organisms, but has not yet been well understood. Here, the roles of cluster of differentiation 36 (CD36) in accumulation of PFASs were investigated. CD36 was overexpressed in Escherichia coli to get CD36-BL21 strain, and the binding affinities of 20 PFASs with CD36 were determined by microscale thermophoresis, which grew up to 17.5 µM with increasing carbon chain length. Consequently, the accumulation of most PFASs was remarkably promoted in CD36-BL21 in comparison to the wild strain, and the enhancement was proportional to their binding affinities with CD36 (r = -0.96). However, this effect was depressed greatly as CD36 was inhibited by sulfo-N-succinimidyl oleate (SSO). Additionally, as the mice received SSO pretreatment before they were exposed to perfluorododecanoic acid, its accumulation in the tissues rich in CD36, such as liver, was suppressed, but increased by 1.1 times in the serum. These indicated that CD36 played critical roles in the transmembrane transport and tissue partition of PFASs in organisms. The developed relationship between liver-blood partition of PFASs and their binding affinities with intracellular proteins was distinctly improved by incorporating that with CD36 (r = -0.97).

Photocatalytic degradation efficiency and mechanism of microcystin-RR by mesoporous Bi2WO6 under near ultraviolet light.

Microcystin-RR (MC-RR) is one of the most common cyanotoxin microcystins in fresh water and is of great concern due to its potential hepatotoxicity. In the present study, Bi(2)WO(6) was synthesized with a hydrothermal method by varying the pH of the reaction solution in the range of 1-11. The surface area of the catalysts decreased, but the crystallinity and crystal size increased with the pH. The adsorption and degradation capacities of the catalysts decreased with increasing the preparation solution pH. The Bi(2)WO(6) prepared at pH 1 (Bi(2)WO(6)-pH1) displayed the highest adsorption and degradation capacity to MC-RR even though it consisted of randomly aggregated particles. Nearly 100% of MC-RR at 10 mg L(-1) was removed after 30 min of irradiation of near-ultraviolet light (300-400 nm) in a solution with Bi(2)WO(6) concentration of 0.2 g L(-1). The photodegradation efficiency of Bi(2)WO(6)-pH1 was greater in acid medium than in basic solutions. Several intermediate products were observed and identified by liquid chromatography/mass spectrometry/mass spectrometry, and a unique photodegradation pathway was proposed. It was assumed that a photo-Kolbe process happened at the site carboxyl acid group of the d-Glu residue by the photogenerated holes, producing a hydroperoxyl product at m/z 513.8. This intermediate could be further decomposed to an alcohol product at m/z 505.8 and a ketone product at m/z 504.8. The aromatic ring and diene bond of the Adda chain could also be attacked by the holes and form phenol and diol products.

Metal-independent decomposition of hydroperoxides by halogenated quinones: detection and identification of a quinone ketoxy radical.

We have shown recently that halogenated quinones could enhance the decomposition of hydroperoxides and formation of alkoxyl/hydroxyl radicals through a metal-independent mechanism. However, neither the proposed quinone enoxy radical intermediate, nor the major reaction products were unambiguously identified. In the present study, one of the major reaction products between 2,5-dichloro-1,4-benzoquinone (DCBQ) and t-butylhydroperoxide (t-BuOOH) was isolated and purified by semipreparative HPLC, and identified as 2-hydroxy-3-t-butoxy-5-chloro-1,4-benzoquinone [CBQ(OH)-O-t-Bu], which is the rearranged isomer of the postulated quinone-peroxide reaction intermediate. The formation of CBQ(OH)-O-t-Bu was found to be inhibited by the spin trapping agent 5,5-dimethyl-1-pyrroline N-oxide (DMPO), and concurrently, a new DMPO adduct with 1-chlorine isotope peak clusters at m/z 268 was observed. Further electron spin resonance (ESR) spin-trapping, (1)H-NMR and HPLC/Fourier transform ion cyclotron resonance (FTICR) mass spectrometric studies with oxygen-17-labeled and unlabeled hydrogen peroxide strongly suggest that the radical trapped by DMPO is a carbon-centered quinone ketoxy radical, which is the spin isomer of the proposed oxygen-centered quinone enoxy radical. Analogous results were observed when DCBQ was substituted by other halogenated quinones. This study represents the first detection and identification of an unusual carbon-centered quinone ketoxy radical, which provides direct experimental evidence to further support and expand our previously proposed mechanism for metal-independent decomposition of hydroperoxides by halogenated quinones.

Precolumn Derivatization High-Performance Liquid Chromatography for Determination of Perfluorocarboxylic Acids in Catalytic Degradation Solutions.

Perfluoroalkyl carboxylic acids (PFCAs), a series of ubiquitous contaminants in the global environment, attracted much attention due to their potential for high bioaccumulation and toxicity to various organisms. There are a lot of measurement requests in currently increasing degradation studies of PFCAs, which usually rely on expensive liquid chromatography-mass spectrometry (LC-MS). The degradation solutions containing high-concentration PFCAs can easily cause the pipeline pollution of the LC/MS instrument, which is usually used for trace analysis of environmental samples. In this study, a simple and reliable precolumn derivatization LC method coupled with an ultraviolet detector (UV) was developed for the determination of the main PFCAs (C4-9) of environmental concern. These PFCAs in degradation solutions were crosslinked to UV-responsive 3, 4-diphenylamine (DCA) by a carbodiimidization method, followed by a simple solid-phase extraction (SPE) cleanup, and quantitatively measured using a conventional LC-UV instrument. Compared to previously reported precolumn derivatization methods, this new derivatization approach has the advantages such as mild reaction conditions, easy operation, enhanced stability of derivatives, and low cost. The instrumental limits of detection (ILDs) for the targeted PFCAs in organic and aqueous mediums were 0.2-0.5 and 0.6-1.5 mg/L, respectively. The method has been successfully applied to the determination of PFCAs in catalytic degradation solutions and recommended for use in other assays involving relatively high-concentration PFCAs.