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Escherichia coli (E. coli) is a prevalent pathogen that is frequently associated with the foodborne illness. It causes various infections and poses a significant threat to human health. A rapid and sensitive assay for detecting E. coli is essential for timely diagnosis. Herein, a simple and sensitive colorimetric analysis method for detecting E. coli was developed based on the formation of Au@Ag core-shell nanoparticles facilitated by p-benzoquinone (BQ). E. coli reduced p-benzoquinone to generate hydroquinone (HQ), which could reduce the added Tollens' reagent to silver elemental and grow on the surface of gold nanoparticles (AuNPs). As the E. coli concentration increased, the silver layer thickess on the AuNPs surface growed, resulting in a stronger silver absorption peak observed at 390 nm. The color of the solution changed from red to orange, which could be used to detect E. coli by the naked eye. As a result, E. coli was detected with a linear range from 1.0 × 101 to 1.0 × 107 CFU/mL based on the absorbance intensity. In addition, this method accurately detected E. coli in real milk sample, demonstrating promising applications in foodborne pathogen detection. With satisfactory accuracy, the proposed colorimetric method holds excellent prospects in detecting pathogens in actual food samples.

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The utilization of Hydroquinone (HQ) in over-the-counter skincare items is subject to restrictions. Consequently, Arbutin (AR) serves as a reliable alternative for addressing hyperpigmentation in non-prescription topical formulations. Nevertheless, AR undergoes decomposition into HQ and p-Benzoquinone (BZ) when exposed to temperature stress, ultraviolet light, or dilution in an acidic environment, all of which can induce skin toxicity. The intention of this paper is to investigate the effect of extraction procedure on the conversion of AR to HQ and or BZ and to evaluate kinetics of AR hydrolysis to HQ. Meanwhile this study aims to evaluate AR and BZ interference with the United States Pharmacopoeia (USP) identification and assessment method for HQ Hydrolytic stress during extraction conditions underwent optimization through systematic screening tests. Subsequent assessment of the residual drug and its degradation products were achieved by HPLC method. The resulting data were meticulously fitted to various kinetic models. To analyze the potential interference of AR in HQ measurement using USP method, the standard concentrations of AR and HQ were analyzed through UV-VIS spectrophotometry. For enhanced certainty, a validated HPLC method analysis was also conducted. Notably, the acid hydrolysis of AR exhibited independence from its initial concentration. So, the hydrolytic degradation of AR exhibited a Zero-order kinetic profile. Furthermore, the proven interference of AR in the UV-VIS spectrophotometry method was identified within the context of the USP method. This study successfully utilized an adopted HPLC method for the concurrent quantification of AR, HQ, and BZ. The potential interference of AR in the UV-VIS spectrophotometric assay for HQ may lead to false results especially for regulatory purposes.

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It is of great significance to establish an effective method for removing Cr(VI) from wastewater. Herein, Fe-doped g-C3N4 (namely Fe-g-C3N4-2) was synthesized and then employed as photocatalyst to conduct the test of Cr(VI) reduction. Notably, the embedding of Fe ion in g-C3N4 can offer the Fe2+/Fe3+ redox couples, so reducing the interfacial resistance of charge transfer and suppressing the recombination of photogenerated electrons and holes. The impurity energy levels will form in g-C3N4 after the introduction of Fe ion, thereby boosting the light absorption capacity of catalyst. Thus, Fe-g-C3N4-2 showed good performance in photocatalytic Cr(VI) reduction, and the reduction efficiency of Cr(VI) can reach 39.9% within 40 min. Different with many previous studies, current work unexpectedly found that the addition of p-benzoquinone (BQ) can promote the Cr(VI) reduction, and the reduction efficiency of Cr(VI) over Fe-g-C3N4-2 was as high as 93.2% in the presence of BQ (1.5 mM). Further analyses showed that BQ can be reduced to hydroquinone (HQ) by photogenerated electrons, and UV light can also directly induce BQ to generate HQ by using H2O as the hydrogen donor. The HQ with reducing ability can accelerate the Cr(VI) reduction. In short, current work shared some novel insights into photocatalytic Cr(VI) reduction in the presence of BQ. Future research should consider possible reactions between photogenerated electrons and BQ. For the UV-induced photocatalysis, the suitability of BQ as the scavenger of O2•‒ must be given carefully consideration.

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A photoluminescent terbium (III)-based Metal Organic Framework (MOF) was synthesized at room temperature by layer diffusion method utilizing mixed carboxylate linkers (4,4'-oxybis(benzoic acid) and benzene-1,3,5 tricarboxylic acid). Synthesized MOF has crystalline nature and rod-shaped morphology and is thermally stable up to 455 °C. The fluorescence emission spectra and theoretical results revealed that carboxylate linkers functioned as sensitizers for Tb(III) photoluminescence which resulted in four distinct emission peaks at 495, 547, 584, and 621 nm corresponding to the transitions 5D4 → 7F6, 5D4 → 7F5, 5D4 → 7F4, and 5D4 → 7F3. Using synthesized MOF as fluorescent probe, hydroquinone was detected in aqueous medium with a detection limit of 0.048 µM, remarkable recovery (95.6-101.1%), and relative standard deviation less than 2.25%. The quenching phenomenon may be ascribed to electron transfer from synthesized probe to oxidized hydroquinone via carboxylic groups on the surface of MOF, which is further supported by photo-induced electron transfer mechanism. This study introduces a cheaper, faster, and more accurate method for hydroquinone detection.

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The detection of volatile amines is necessary due to the serious toxicity hazards they pose to human skin, respiratory systems, and nervous systems. However, traditional amines detection methods require bulky equipment, high costs, and complex measurements. Herein, we report a new simple, rapid, convenient, and visual method for the detection of volatile amines based on the gas-solid reactions of tetrachloro-p-benzoquinone (TCBQ) and volatile amines. The gas-solid reactions of TCBQ with a variety of volatile amines showed a visually distinct color in a time-dependent manner. Moreover, TCBQ can be easily fabricated into simple and flexible rapid test strips for detecting and distinguishing n-propylamine from other volatile amines, including ethylamine, n-butyamine, n-pentamine, n-butyamine and dimethylamine, in less than 3 s without any equipment assistance.

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Leucosceptrum canum nectar (LCN) emerges as a novel food resource, distinguished by its unique dark brown hue. This study delves into the composition and toxicity assessment of novel pigments within LCN. Through liquid chromatography-tandem mass spectrometry (LC-MS/MS) and chemical synthesis, seventeen 2,5-di-(N-(-)-prolyl)-para-benzoquinone (DPBQ) analogs in LCN were identified. These compounds are synthesized in LCN via the Michael addition reaction, utilizing p-benzoquinone (BQ), derived from phenol metabolism, and amino acids as substrates in an alkaline environment (pH = 8.47 ± 0.06) facilitated by dissolved ammonia and the presence of alkaloids. Analytical techniques, including principal component analysis (PCA), orthogonal partial least squares discrimination analysis (OPLS-DA), and volcano plot analysis, were employed to investigate DPBQ analog degradation within the nectar and honey's unique environments. Toxicity assays revealed that DPBQ analogs exhibited no toxicity, displaying a significant difference in toxicity compared to the precursor compound BQ at concentrations exceeding 25 µM.

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The toxicity of Polystyrene (PS) may be higher through co-exposure with other pollutants. Human can simultaneously face the challenges from the various pollutants. Nevertheless, little research has been done on the combined effects of PS and 2,6-dichloro-p-benzoquinone (DCBQ) disinfection byproduct. Considering the potential risk of PS and DCBQ, we aimed to illustrate the effects of PS in combination with DCBQ on the immune responses of mice. We found that cotreatment of DCBQ and PS may inhibit the activity of spleen CD4+ T cells and interfere with the normal function of the immune system. Further research found that DCBQ + PS resulted in increasing amount of the inflammatory cells in intestine via histopathological evaluation. The reason might be that DCBQ + PS has changed the composition of intestinal flora, abnormally activated intestinal macrophage, and inhibited the expression of immune-related genes, thus leading to intestinal immune disorders and triggering intestinal inflammation. In summary, PS may alter the cooperation mechanism of gut microbiota and immune system through co-exposure with DCBQ. Current results suggested that more attention should be paid to the combined toxic effects of environmental contaminants.

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The Acetaminophen Detection Kit® (Kanto Chemical Company Co. Inc., Tokyo, Japan) is a colorimetric test based on an indophenol reaction. The test involves three reactions: deproteination of the sample, hydrolysis of acetaminophen to yield p-aminophenol, and coupling p-aminophenol with a derivative of phenol in alkali conditions to form a blue-colored indophenol dye. The kit was devised to accomplish these three reactions with only two reagents, allowing the prompt diagnosis of acetaminophen overdose in emergency medicine. In the user instructions included with the kit and in reports introducing the kit, the chemical composition of the two reagents was not disclosed. Details about the composition can be found in the Safety Data Sheet from the manufacturer; however, there is little explanation about the principle (mechanism) of the coupling reaction. This lack of information appears to have hampered the use of this kit in forensic medicine. In this report, we conducted the coupling reaction by successively adding the two reagents to a p-aminophenol (intermediate molecule) solution with the reaction vessel open to the air and under an anaerobic condition. Development of the blue color was inhibited in the absence of air but gradually developed when the reaction vessel was opened to air. Thus, the coupling reaction is an oxidation-reduction (redox) reaction that requires molecular oxygen (O2) dissolved from the air to act as an oxidant. This finding corroborates statements in previous reports and will hopefully facilitate the use of the kit for forensic purposes.

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During the COVID-19 pandemic, the release of toxic disinfection by-products (DBPs) has increased due to the intensive, large-scale use of disinfectants. Halogenated benzoquinones (HBQs) are among the most toxic DBPs, but there is no rapid, convenient, and economical detection method. In this study, a novel PDIL/BDD-modified electrode was prepared in a mixed solvent of dimethyl sulfoxide (DMSO) and acetonitrile (ACN) by electrochemical polymerization with a di-ionic ionic liquid containing alkenyl groups as the monomer. The electrochemical behavior of tetra-chloro-p-benzoquinone (TCBQ) on the modified electrode was studied. By studying the cyclic voltammetry behavior of TCBQ on the PDIL/BDD electrode, it was concluded that the electrode reactions of TCBQ included the reduction of TCBQ to TCBQH2 (C1) and the reduction of bis-quinhydrone imidazole π-π type charge transfer complex to TCBQH2 (C2). By studying the SWV responses of TCBQ in the concentration range of 1-100 ng/L on the PDIL/BDD electrode, it was found that the reduction peak current (Ipa) had a linear relationship with the concentration. The electrochemical SWV technique was used to detect the concentration of trace TCBQ in water and is expected to be used for the detection of other HBQs in drinking water and swimming pool water.

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Background & Aims: Acetaminophen (APAP)-induced acute liver injury (AILI) is a leading cause of acute liver failure (ALF). N-acetylcysteine (NAC) is only effective within 24 h after APAP intoxication, raising an urgent need for alternative approaches to treat this disease. This study aimed to test whether cathelicidin (Camp), which is a protective factor in chronic liver diseases, protects mice against APAP-induced liver injury and ALF. Methods: A clinically relevant AILI model and an APAP-induced ALF model were generated in mice. Genetic and pharmacological approaches were used to interfere with the levels of cathelicidin in vivo. Results: An increase in hepatic pro-CRAMP/CRAMP (the precursor and mature forms of mouse cathelicidin) was observed in APAP-intoxicated mice. Upregulated cathelicidin was derived from liver-infiltrating neutrophils. Compared with wild-type littermates, Camp knockout had no effect on hepatic injury but dampened hepatic repair in AILI and reduced survival in APAP-induced ALF. CRAMP administration reversed impaired liver recovery observed in APAP-challenged Camp knockout mice. Delayed CRAMP, CRAMP(1-39) (the extended form of CRAMP), or LL-37 (the mature form of human cathelicidin) treatment exhibited a therapeutic benefit for AILI. Co-treatment of cathelicidin and NAC in AILI displayed a stronger hepatoprotective effect than NAC alone. A similar additive effect of CRAMP(1-39)/LL-37 and NAC was observed in APAP-induced ALF. The pro-reparative role of cathelicidin in the APAP-damaged liver was attributed to an accelerated resolution of inflammation at the onset of liver repair, possibly through enhanced neutrophil phagocytosis of necrotic cell debris in an autocrine manner. Conclusions: Cathelicidin reduces APAP-induced liver injury and ALF in mice by promoting liver recovery via facilitating inflammation resolution, suggesting a therapeutic potential for late-presenting patients with AILI with or without ALF. Impact and implications: Acetaminophen-induced acute liver injury is a leading cause of acute liver failure. The efficacy of N-acetylcysteine, the only clinically approved drug against acetaminophen-induced acute liver injury, is significantly reduced for late-presenting patients. We found that cathelicidin exhibits a great therapeutic potential in mice with acetaminophen-induced liver injury or acute liver failure, which makes up for the limitation of N-acetylcysteine therapy by specifically promoting liver repair after acetaminophen intoxication. The pro-reparative role of cathelicidin, as a key effector molecule of neutrophils, in the APAP-injured liver is attributed to an accelerated resolution of inflammation at the onset of liver repair, possibly through enhanced phagocytic function of neutrophils in an autocrine manner.

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P-benzoquinone (PBQ) is toxic and harmful for health. The development of portable sensor to realize the detection of PBQ is of great significance. Herein, a novel covalent organic framework (COFML-TFPB) with intramolecular charge transfer and aggregation induced emission properties was proposed via condensation reaction of melem (ML) and 1,3,5-tris (4-formylphenyl) benzene (TFPB). COFML-TFPB shows strong fluorescence in both solution and solid state and can be used for the fluorescence detection of PBQ. Due to the internal filtration effect and photoinduced electron transfer effect, PBQ can quench the fluorescence of COFML-TFPB. The developed COFML-TFPB fluorescent sensor displayed a wide linear range for PBQ from 0.138 ng mL-1 - 35 µg mL-1, and the detection limit was 0.046 ng mL-1. In addition, fluorescent test paper for rapid and portable detection of PBQ was also developed by depositing COFML-TFPB on filter paper directly. It reduces the cost and time of detection and realizes the semiquantitative detection of PBQ. Moreover, the fluorescence color was converted into digital RGB value to calculate the concentration of PBQ accurately by a smartphone. This method realizes the portable qualitative and semiquantitative determination of PBQ.

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In this work, a colorimetric biosensor based on the rapid color change of Escherichia coli DH 5α (E. coli) and p-benzoquinone (BQ) was introduced to evaluate water toxicity. Here, dark brown quinhydroquinone (QHQ) was obtained from the reaction between E. coli and BQ. The inhibition ratios were calculated by RGB (red, green, blue) values of samples or oxidation current of hydroquinone (HQ). Here, RGB technology was used for biotoxicity assessment for the first time. The results suggested that the biosensor-based RGB has an obvious dose-dependent response. The IC20 values of Hg2+ and Cu2+ obtained based on RGB values were 1.0 and 1.5 mg L-1, respectively. This biosensor can be used to detect quickly toxicity of the Cu2+ and Hg2+ in water without complicated operation steps. Therefore, the biosensor has potential application value in the field of water toxicity detection.

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In previous studies, propofol has shown immunomodulatory abilities on various in vitro models. As this anesthetic molecule is extensively used in intensive care units, its anti-inflammatory properties present a great interest for the treatment of inflammatory disorders like the systemic inflammatory response syndrome. In addition to its inhibition abilities on important neutrophils mechanisms (chemotaxis, reactive oxygen species (ROS) production, Neutrophil Extracellular Traps (NETs) formation, …), our group has shown that propofol is also a reversible inhibitor of the oxidant myeloperoxidase (MPO) activity. Propofol being subject to rapid metabolism, its derivatives could contribute to its anti-inflammatory action. First, propofol-ß-glucuronide (PPFG), 2,6-diisopropyl-1,4-p-benzoquinone (PPFQ) and 3,5,3',5'-tetraisopropyl-(4,4')-diphenoquinone (PPFDQ) were compared on their superoxide (O2.-) scavenging properties and more importantly on their inhibitory action on the O2.- release by activated neutrophils using EPR spectroscopy and chemiluminescence assays. PPFQ and PPFDQ are potent superoxide scavengers and also inhibit the release of ROS by neutrophils. An Enzyme-Linked Immunosorbent Assay (ELISA) has also highlighted the ability of both molecules to significantly decrease the MPO degranulation process of neutrophils. Fluorescence enzymatic assays helped to investigate the action of the propofol derivatives on the peroxidase and chlorination activities of MPO. In addition, using SIEFED (Specific Immunological Extraction Followed by Enzyme Detection) assays and docking, we demonstrated the concentration-dependent inhibitory action of PPFQ and its ability to bind to the enzyme active site while PPFG presented a much weaker inhibitory action. Overall, the oxidation derivatives and metabolites PPFQ and PPFDQ can, at physiological concentrations, perpetuate the immunomodulatory action of propofol by acting on the oxidant response of PMN and MPO.

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Background & Aims: Acetaminophen (APAP)-induced acute liver injury (ALI) is a global health issue characterised by an incomplete understanding of its pathogenesis and unsatisfactory therapies. NEK7 plays critical roles in both cell cycle regulation and inflammation. In the present study, we investigated the role and mechanism of NEK7 in APAP-induced ALI. Methods: In mice with NEK7 overexpression (hydrodynamic tail vein injection of NEK7 plasmids), hepatocyte-specific NEK7 knockout (cKO), and inducible NEK7 knockout (iKO), an overdose of APAP was administered to induce ALI. Liver injury was determined by an analysis of serum liver enzymes, pathological changes, inflammatory cytokines, and metabonomic profiles. In vitro, hepatocyte damage was evaluated by an analysis of cell viability, the reactive oxygen species levels, and mitochondrial function in different cell lines. Hepatocyte proliferation and the cell cycle status were determined by Ki-67 staining, EdU staining, and the cyclin levels. Results: NEK7 was markedly downregulated in APAP-induced injured liver and damaged hepatocytes. NEK7 overexpression in the liver significantly alleviated APAP-induced liver injury, as shown by the restored liver function, reduced pathological injury, and decreased inflammation and oxidative stress, which was confirmed in a hepatocyte cell line. Moreover, both NEK7 cKO and iKO mice exhibited exacerbation of APAP-induced ALI. Finally, we determined that cyclin B1-mediated cell cycle progression could mediate the protective effect of NEK7 against APAP-induced ALI. Conclusions: Reduced NEK7 contributes to APAP-induced ALI, possibly by dysregulating cyclins and disturbing cell cycle progression. Lay summary: Acetaminophen-induced acute liver injury is one of the major global health issues, owing to its high incidence, potential severity, and limited therapeutic options. Our current understanding of its pathogenesis is incomplete. Herein, we have shown that reduced NEK7 (a protein with a key role in the cell cycle) exacerbates acetaminophen-induced acute liver injury. Hence, NEK7 could be a possible therapeutic target for the prevention or treatment of this condition.

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In this work, a systematical investigation on the role of hydrogen sulfide (H2S) on the transformation of tetrachloro-p-benzoquinone (TCBQ) under ultraviolet (UV) irradiation (at 253.7 nm) in aqueous solution has been conducted through quantum chemical calculations. Under the UV irradiation, with the forward energy barrier (Ea,f, 11.7 kcal mol-1) much lower than the reverse one (Ea,r, 22.3 kcal mol-1), the first triplet state of TCBQ was kinetically feasible to react with bisulfide anion (HS-) via the Michael addition, and the addition of HS- could promote the release of Cl- and the formation of primary dechlorination product (HS-TriCBQ). During the UV photolysis of the primary dechlorination products (HO-TriCBQ and HS-TriCBQ) in the presence of H2O and H2S, the addition of nucleophile (OH- or HS-) to the ortho-position of the hydroxyl or thiol group might be the most efficient pathway for the dechlorination, and their respective Ea,f were 9.2 kcal mol-1 (for HS--hydroxyl), 1.1 kcal mol-1 (for OH--thiol) and 8.9 kcal mol-1 (for HS--thiol). Moreover, the electron transfer from HS- to the first triplet states could generate hydrosulfide radical for the dechlorination of TCBQ. The findings in the present study may provide some important theoretical foundation for the dehalogenation of TCBQ as well as other halobenzoquinones.

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An infusion from the aerial parts of Justicia spicigera Schltdl., an herb commonly used to treat diabetes, inhibited the activity of protein tyrosine phosphatase 1B (PTP1B). Two undescribed compounds, 2-N-(p-coumaroyl)-3H-phenoxazin-3-one, and 3″-O-acetyl-kaempferitrin, along with kaempferitrin, kaempferol 7-O-α-L-rhamnopyranoside, perisbivalvine B and 2,5-dimethoxy-p-benzoquinone were isolated from the active extract. Their structures were elucidated by a combination of spectroscopic and spectrometric methods. The isolates were evaluated for their inhibitory activity against PTP1B; the most active compounds were 2-N-(p-coumaroyl)-3H-phenoxazin-3-one, and perisbivalvine B with IC50 values of 159.1 ± 0.02 µM and 106.6 ± 0.01 µM, respectively. However, perisbivalvine B was unstable. Kinetic analysis of 2-N-(p-coumaroyl)-3H-phenoxazin-3-one and 2,5-dimethoxy-p-benzoquinone (obtained in good amounts) indicated that both compounds behaved as parabolic competitive inhibitors and bind to the enzyme forming complexes with 1:1 and 1:2 stoichiometry. Docking of 2-N-(p-coumaroyl)-3H-phenoxazin-3-one and 2,5-dimethoxy-p-benzoquinone to PTP1B1-400 predicted a good affinity of these compounds for PTP1B catalytic site and demonstrated that the binding of a second ligand is sterically possible. The 1:2 complex was also supported by the second docking analysis, which predicted an important contribution of π-stacking interactions to the stability of these 1:2 complexes. Finally, an UHPLC-MS method was developed and validated to quantify the content of kaempferitrin in the infusion of the plant.

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The toxic oxidation intermediate p-benzoquinone exists in aqueous environments at dilute concentrations above the fish-toxicity limit of 0.045 mg/L, affecting aquatic life. The reduction of this compound to the concentrations required to achieve safe discharge limits is challenging. In this study, the adsorptive removal of p-benzoquinone by a biosolid-based activated carbon (SBAC) was systematically investigated in batch experiments. The adsorption rate was rapid, and the bulk of p-benzoquinone adsorption occurred within 30 min. The maximum adsorption capacity of SBAC was estimated at 19.6 mg/g using the Langmuir isotherm model. Its adsorptivity was independent of temperature from 6 to 40 °C. The presence of 6 g/L of chloride and 500 mg/L of sulphate did not affect the removal of 1 mg/L p-benzoquinone, whereas 15 mg/L of humic acid media slightly decreased the p-benzoquinone removal from 87.0% to 83.2%. Diffusion, hydrophilic, and electrostatic interactions (i.e., dipole-dipole) govern the adsorption of p-benzoquinone and are influenced by the SBAC surface chemistry. Biosolid-based activated carbon can lower the residual p-benzoquinone to below the fish-toxicity limit of 0.045 mg/L within 1 h of sequential adsorption. Thus, biosolid-based activated carbon can effectively remove p-benzoquinone from aqueous environments; this is a waste-to-resource approach that addresses sustainability (waste disposal) and environmental protection (pollutant removal).

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Acetaminophen (APAP)-induced liver injury (AILI) is the most common cause of acute liver failure. Although the mechanisms that trigger AILI are well known, it is less understood how to halt AILI progression and facilitate liver recovery. Therefore, it is necessary to understand the pathophysiology of APAP hepatotoxicity in patients and to examine predictive/preventive markers. In a clinical study, we had a case in which aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels increased in a patient with a low ratio of APAP glucuronide concentration (AP-G)/APAP plasma concentration. Then a reverse translational study was conducted for clarifying this clinical question. The relationship between plasma AP-G/APAP concentration ratio and the levels of AST and ALT was examined by in vivo and in vitro experiments. In in vivo experiments, 10-week-old rats showed lower UGT activity, lower AP-G/APAP concentration ratios, and higher AST and ALT levels than 5-week-old rats. This suggests an inverse correlation between the AP-G/APAP concentration ratio and the AST, ALT levels in APAP-treated rats. Furthermore, as a result of the in vitro experiment, it was confirmed that the cell viability decreased when the AP-G/APAP concentration ratio in the culture medium decreased. Since the decrease in the plasma AP-G/APAP concentration ratio appears earlier than the increase of AST and ALT levels, the ratio might be a presymptomatic marker of AILI. When APAP is used for a long time, it is recommended to perform therapeutic drug monitoring of the AP-G/APAP concentration ratio, which is a predictive/preventive marker of AILI.

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To create both greener and high-power metal-ion batteries, it is of prime importance to invent an unprecedented electrode material that will be able to store a colossal amount of charge carriers by a redox mechanism. Employing periodic DFT calculations, we modeled a new metal-organic framework, which displays energy density exceeding that of conventional inorganic and organic electrodes, such as Li- and Na-rich oxides and anthraquinones. The designed MOF has a rhombohedral unit cell in which an Ni(II) node is coordinated by 2,5-dicyano-p-benzoquinone linkers in such a way that all components participate in the redox reaction upon lithiation, sodiation and magnesiation. The spatial and electronic changes occurring in the MOF after the interaction with Li, Na and Mg are discussed on the basis of calculated electrode potentials versus Li0/Li+, Na0/Na+ and Mg0/Mg2+, respectively. In addition, the specific capacities and energy densities are calculated and used as a measure for the electrode applicability of the designed material. Although the highest capacity and energy density are predicted for Li storage, the greater structural robustness toward Na and Mg uptake suggests a higher cycling stability in addition to lower cost. The theoretical results indicate that the MOF is a promising choice for a green electrode material (with <10% heavy metal content) and is well worth experimental testing.

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A method for a sensitive fluorescence detection of glutathione was established. Glutathione-stabilized copper nanoclusters (CuNCs) were synthesized via a facile process. These CuNCs showed blue fluorescence with a peak around 450 nm. In the presence of p-benzoquinone (PBQ), the electron transfer from the copper nanoclusters to PBQ quenched the fluorescence of the CuNCs. Glutathione (GSH), as a reducing agent, formed a complex with PBQ. This formation inhibited the quenching from PBQ, and a restored fluorescence was obtained. This interaction provided a fluorescence enhancement for the measurement of GSH. Under the optimal condition, linear responses were obtained toward GSH in the ranges of 0.06-6.0 µM, with a limit of detection at 20 nM. This developed assay was easy in operation with high sensitivity and selectivity. The applicability was approved with successful glutathione measurements in real samples.

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