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Hydroquinone (HQ) is extensively utilized in various industrial applications and as a dermatological agent; however, its metabolic processes and toxicological effects, particularly in the liver, remain insufficiently understood. This study aimed to investigate the impact of different doses of HQ on liver injury and lipid metabolism in C57BL/6 mice, with a specific focus on the SCD1/AMPK signaling pathway. We administered HQ at doses of 0, 12.5, 25.0, and 50.0 mg/kg over a period of 13 weeks, followed by biochemical analyses, RNA sequencing, and Western blotting to elucidate the underlying mechanisms. Our findings indicated that lower doses of HQ (12.5 and 25.0 mg/kg) led to lipid accumulation in the liver, accompanied by increased liver TG and serum TC. In contrast, the highest dose (50.0 mg/kg) resulted in elevated liver enzyme levels, indicative of liver damage, while lipid levels decreased. Notably, the mRNA or protein levels of SCD1 were upregulated in response to the lower doses of HQ (12.5 and 25.0 mg/kg), whereas AMPK activation and enhanced autophagy were observed in the 50.0 mg/kg HQ-treated group, reflecting an energy stress response. These findings suggest that lipid dysregulation may serve as an early indicator of HQ-induced liver injury, and that the SCD1/AMPK pathway may play a protective role against chemically induced hepatotoxicity. This study offers new insights into the toxicological effects of HQ on the liver and underscores the necessity for further exploration of the protective mechanisms of SCD1 and AMPK in mitigating HQ-induced hepatotoxicity.

Mesenchymal stem cell - originated exosomes (MSC-exo) are promising non-cellular treatment agents for various diseases. The present study aimed to explore whether human umbilical cord MSC - originated exosomes (HUC-MSC-exo) have the function of protecting human cells (16HBE) against the damage caused by HQ and the related mechanism. HUC-MSC-exo was isolated with differential gradient ultracentrifugation method and characterized by using transmission electron microscope (TEM). 16HBE cells were used as the tool cells and co-cultured with HUC-MSC-exo. Confocal laser scanning microscope was employed to confirm the ingestion of HUC-MSC-exo by 16HBE. Cell proliferation, migration, oxidative stress, DNA and chromosome damages of 16HBE were analyzed under HQ stress, and the role of miR-221/PTEN axis was investigated. Our data showed that under HQ stress, different groups of cells exhibited significantly decreased proliferation and migration abilities, and significant oxidative stress, DNA and chromosome damage effects. HUC-MSC-exo could alleviate the cytotoxic, oxidative stress and genotoxic damage effects of HQ on 16HBE cells. Mechanistically, HQ exposure up-regulated the level of miR-221 and down-regulated PTEN, while HUC-MSC-exo could significantly reduce the level of miR-221 and promote PTEN expression, which was involved in alleviating the toxic effects of HQ on 16HBE cells. Our data indicates that HUC-MSC-exo can alleviate the oxidative stress, cytotoxic and genotoxic effects of HQ on 16HBE cells via miR-221/PTEN pathway, and it may be a promising agent for protecting against the toxicity of HQ.

The nuclear factor erythroid 2-related factor 2 (Nrf2) is overexpressed in multiple tumor cells. Nevertheless, the role of Nrf2 in malignant transformation induced by hydroquinone (HQ) is unknown. Here, we hypothesized that Nrf2 might participate in HQ-induced malignant transformation of TK6 cells, a line of normal human lymphoblastoid cells, by accelerating cell proliferation and regulating cell cycle progression. The data indicated that TK6 cells chronically exposed to HQ continuously activated Nrf2-Keap1 signaling pathway. Furthermore, we found that defects in Nrf2 inhibited cell proliferation and prevented cells from entering S phase from G1 phase. Mechanistically, Nrf2 is involved in cell cycle abnormalities induced by prolonged exposure to HQ by binding to p16, thereby activating the p16/Rb signaling pathway. Taken together, Nrf2 might be a potential driver of carcinogenesis that promotes malignant cell proliferation and affects cell cycle distribution.

Leukemia caused by environmental chemical pollutants has attracted great attention, the malignant leukemic transformation model of TK6 cells induced by hydroquinone (HQ) has been previously found in our team. However, the type of leukemia corresponding to this malignant transformed cell line model needs further study and interpretation. Furthermore, the molecular mechanism of malignant proliferation of leukemic cells induced by HQ remains unclear. This study is the first to reveal the expression of aberrant genes in leukemic cells of HQ-induced malignant transformation, which may correspond to chronic lymphocytic leukemia (CLL). The expression of Linc01588, a long non-coding RNA (lncRNA), was significantly up-regulated in CLL patients and leukemic cell line model which previously described. After gain-of-function assays and loss-of-function assays, feeble cell viability, severe apoptotic phenotype and the increased secretion of TNF-α were easily observed in malignant leukemic TK6 cells with Linc01588 deletion after HQ intervention. The tumors derived from malignant TK6 cells with Linc01588 deletion inoculated subcutaneously in nude mice were smaller than controls. In CLL and its cell line model, the expression of Linc01588 and miR-9–5p, miR-9–5p and SIRT1 were negative correlation respectively in CLL and cell line model, while the expression of Linc01588 and SIRT1 were positive correlation. The dual-luciferase reporter assay showed that Linc01588 & miR-9–5p, miR-9–5p & SIRT1 could bind directly, respectively. Furthermore, knockdown of miR-9–5p successfully rescued the severe apoptotic phenotype and the increased secretion of TNF-α caused by the Linc01588 deletion, the deletion of Linc01588 in human CLL cell line MEC-2 could also inhibit malignant biological characteristics, and the phenotype caused by the deletion of Linc01588 could also be rescued after overexpression of SIRT1. Moreover, the regulation of SIRT1 expression in HQ19 cells by Linc01588 and miR-9–5 P may be related to the Akt/NF-κB pathway. In brief, Linc01588 deletion inhibits the malignant biological characteristics of HQ-induced leukemic cells via miR-9–5p/SIRT1, and it is a novel and hopeful clue for the clinical targeted therapy of CLL.

The primary objective of this research endeavor is to develop a highly sensitive and selective electrochemical sensor for the accurate detection of hydroquinone (HQ), a prevalent environmental contaminant. To achieve this, we employed a novel nanocomposite consisting of Ga2O3-doped ZnO (Ga2O3.ZnO) as the active nanomaterial for fabricating a glassy carbon electrode (GCE). The structure and morphology of the Ga2O3.ZnO nanocomposite were rigorously analyzed using a diverse range of techniques to ensure its suitability as the sensing nanomaterial. This innovative sensor exhibits remarkable capabilities, enabling the detection of HQ across a broad concentration range, spanning from 1 to 11070 µM, in a neutral phosphate buffer solution. It boasts an exceptionally high sensitivity of 1.0229 µA µM−1 cm−2 and an impressive detection limit of 0.063 µM. Thanks to its exceptional sensitivity and specificity, this sensor can precisely quantify HQ levels in real-world samples. Moreover, its outstanding reproducibility, repeatability, and stability establish it as a dependable and resilient choice for HQ determination.

Bisphenol A (BPA) is a commonly utilized phenolic contaminant in several manufacturing processes, contributing to environmental pollution. Therefore, the detection of BPA holds significant importance for monitoring water quality. In this work, we report a robust electrochemical detection method for BPA utilizing cobalt−nickel bimetal phosphide nanoparticles (CoNiP) supported on reduced graphene oxide (rGO). The CoNiP@rGO-modified glassy carbon electrode exhibits remarkable electrochemical activity in BPA detection. The detection mechanism is controlled by adsorption-mediated electron transfer, showcasing a low limit of detection (LOD) at 0.38 nM and a high sensitivity of 96.4 A M−1 cm−2 within the linear range of 0.001–8 μM. Furthermore, our developed sensor demonstrates good reproducibility and successfully detected BPA in actual water samples. The electrochemical activity of CoNiP@rGO was also characterized for hydroquinone (HQ) detected through a diffusion-controlled mechanism, displaying an excellent sensitivity of 36.4 A M−1 cm−2 across a broad linear range. These findings underscore the promising potential of CoNiP@rGO as a candidate for electrochemical detection of phenolic contaminants, especially in the sensing of BPA in environmental water samples. This efficacy is attributed to the modulation of its electronic properties, combined with its large electroactive surface area and low electron-transfer resistance.

Bimetallic cobalt–nickel supported on carbon fiber (Co-Ni@CF) was synthesized by a straightforward homogeneous co-precipitation approach. Electrochemical results demonstrated that the modified Co-Ni@CF electrode demonstrated excellent electrooxidation activity toward dopamine (DA) and hydroquinone (HQ) without any other activating treatments, which could be modified as an electrochemical biosensor for DA and HQ detection simultaneously. The as-proposed biosensor was developed for simultaneous detection of DA and HQ, featuring low detection limits (LODs) of 0.4698 μM for DA and 0.2388 mM for HQ, respectively. The sensor also offers broad linear ranges for DA (5.0–30 μM), and HQ (0.5–5.0 mM). Along with these attractive features, the Co-Ni@CF electrode also performed good long-term stability and reproducibility, making it a promising candidate for electrochemical biosensing of DA and HQ.

Resumen: El melasma corresponde a un trastorno pigmentario crónico que se caracteriza por máculas hiperpigmentadas que se localizan principalmente en la cara. Afecta con mayor frecuencia a mujeres en edad fértil y de fototipos oscuros. Se asocia a un importante deterioro de la calidad de vida debido a su ubicación, cronicidad y alto porcentaje de recidiva. Los tratamientos clásicos incluyen agentes tópicos, peelings, láser y tratamientos basados en luz, o una combinación de ellos. Los tratamientos combinados han demostrado ser la mejor solución sea de forma doble o triple. La terapia triple combinada (hidroquinona, tretinoína y corticoides) actualmente muestra ser el tratamiento más efectivo.Dentro de los nuevos tratamientos publicados hasta la fecha, el ácido tranexámico oral ha mostrado resultados favorables en el melasma moderado, severo, recurrente y/o refractario, por lo que se debería considerar como una nueva estrategia terapéutica. Abstract: Melasma is a chronic pigmentary disorder, characterized by hyper-pigmented macules in photo-exposed areas that are located mainly on the face. It more frequently affects women in childbearing age and with darker skin phototypes. It is associated with a significant impact in quality of life because of its location, chronicity and high percentage of relapse.Classical treatments include topical agents, peelings, laser and light based therapies, or a combination of these. Combined treatments have proven to be the best solution, whether double or triple. Hydroquinone alone or a triple combination cream (hydroquinone, tretinoin and corticosteroid) currently have the greatest evidence of efficacy in the treatment of melasma.Among the new treatments published to date, oral tranexamic acid has shown favorable results in moderate, severe, recurrent and/or refractory melasma, and should be considered as a new therapeutic strategy.

Long non-coding RNAs (lncRNAs) have been shown to play a critical role in the damage caused to the body by environmental exogenous chemicals; however, few studies have explored their effects during exposure to benzene and its metabolite, hydroquinone (HQ). An emerging lncRNA, LINC01480, was found to be associated with the immune microenvironment of some cancers, but its specific function remains unknown. Therefore, this study aimed to investigate the role of LINC01480 in HQ-induced apoptosis. The biological function of LINC01480 was investigated through gain-of-function and loss-of-function experiments. Mechanically, nuclear-cytoplasmic fractionation experiment, chromatin immunoprecipitation (ChIP), dual-luciferase reporter assay, and rescue experiments were performed. In this study, when TK6 cells were treated with HQ (0, 5, 10, and 20 μM) for 12, 24, 48, and 72 h, the expression of LINC01480 was increased in a dose-dependent manner. Meanwhile, the phosphorylation levels of PI3K and AKT decreased, and apoptosis increased. As compared to the control group, HQ-induced apoptosis was significantly reduced, and the relative survival rate of TK6 cells increased after silencing LINC01480, while overexpression of LINC01480 further sensitized TK6 cells to HQ-induced apoptotic cell death. LINC01480 negatively regulated the PI3K/AKT pathway in TK6 cells, and the apoptosis-inhibiting effect of LINC01480 silencing was reversed after inhibition of the PI3K/AKT pathway. In addition, ChIP and the dual-luciferase reporter assays showed that the transcription factor Foxo3a promoted LINC01480 transcription by directly binding to the promoter regions − 149 to − 138 of LINC01480. Moreover, short-term HQ exposure promoted the expression of Foxo3a. From these findings, we can conclude that LINC01480 is activated by Foxo3a, and promotes HQ-induced apoptosis by inhibiting the PI3K/AKT pathway, suggesting that LINC01480 might become a possible target for therapeutic intervention of HQ-induced toxicity.

Hydroquinone (HQ) is a prevalent pollutant in aquatic environments, posing significant risks to ecosystems and human health. Practical methods for the simultaneous detection and degradation of HQ are essential. To address this requirement, a dual-mode detection and degradation strategy has been developed utilizing designed nanozymes (DM) consisting of a porous SiO 2 core and MnO 2 shell. Due to the catalytic activity of DM nanozymes, the three types of reactive oxygen species (ROS), singlet oxygen ( 1 O 2 ), superoxide anion (O 2 •- ), and hydroxyl radical (•OH), were generated to induce the color transferring of 3,3',5,5'-tetramethylbenzidine (TMB) from colorless to blue form (oxTMB). During the reductive HQ-mediated oxTMB fading, the DM has significant selectivity towards HQ from isomers (catechol and resorcinol) due to the differing reductive reaction rates, with an excellent linear range of 0.2-45 μM with a detection limit as low as 0.11 μM. In addition, according to the color parameter changes in the sensing process, colorimeters and smartphones are utilized to achieve on-site and convenient HQ detection. Besides, the DM nanozyme can oxidatively decompose HQ without auxiliary equipment. We believe this research provides a powerful tool for detecting and removing HQ precisely., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2025. Published by Elsevier B.V.)

This study introduces an innovative approach for quantifying isomeric pollutants utilizing an amperometric sensor. The determination of the isomers hydroquinone and catechol is based on the use of a glassy carbon electrode modified with Cu@PtPd/C nanoparticles (Cu@PtPd/C/GCE) in core-shell form, showing significant electrocatalytic activity in the oxidation of the later compounds. The determination was carried out at two different potentials: one at which where only hydroquinone is oxidized, and another in which where both hydroquinone and catechol are oxidized. Using these potentials, two calibration curves were built, one for the quantification of hydroquinone and the other for both isomers. Subsequently, the quantification of catechol was performed using a strategy based on the calculation of a difference using the information collected in the first step. The experiments using hydrogen peroxide as a redox probe demonstrate a clear synergistic effect in the catalytic reduction of hydrogen peroxide at -0.100 V, when Pt, Pd and Cu are incorporated into the core-shell nanostructure. The best performance was achieved with Cu@PtPd/C/GCE 1.00 mg mL -1 . For the selected sensor, the analytical parameters are very competitive compared to similar devices reported in recent years for hydroquinone and catechol, with comparable linearity ranges of 0.010-0.200 mmol L -1 (hydroquinone) and 0.005-0.500 mmol L -1 (catechol), low limits of detection (LODs) of 14.0 nmol L -1 (S/N = 3.3) and 1.75 nmol L -1 (S/N = 3.3) for hydroquinone and catechol. The resulting sensor platform has been successfully applied for the quantification of hydroquinone and catechol in river and tap water and could be a promising candidate for environmental monitoring and drinking water safety., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Inspired by the iron porphyrin structure of natural horseradish peroxidase (HRP), an efficient carbon-based nanozyme was fabricated using nitrogen-doped graphene quantum dots (NGQDs) and iron ion (Fe 3+ ) nanocomposite, enabling selective distinguishment of hydroquinone (HQ) from its isomers. NGQDs with good dispersibility and uniform size were synthesized via a one-step hydrothermal process. NGQDs lacked peroxidase-like activity but the formed nanocomposite (Fe 3+ -NGQDs) upon Fe 3+ addition possessed high peroxidase-like activity. Fe 3+ -NGQDs nanocomposite exhibited shuttle-shaped structure (∼30 nm), the lattice structure of NGQDs and electron transfer between Fe 3+ and NGQDs. The Fe 3+ -NGQDs nanocomposite can catalyze the production of superoxide radicals (•O 2 - ) from H 2 O 2 . The Michaelis constant (K m ) of Fe 3+ -NGQDs (0.115 mM) was lower than that of natural HRP (0.434 mM) with 3,3',5,5'-tetramethylbenzidine (TMB) as the substrate and the maximum initial reaction rate (V max , 16.47 × 10 -8  M/s) was nearly 4 times higher than that of HRP using H 2 O 2 substrate. HQ, unlike its isomers catechol (CC) and resorcinol (RE), could consume •O 2 - generated from the decomposition of H 2 O 2 catalyzed by Fe 3+ -NGQDs nanocomposite, reducing the oxidation of TMB. This principle enabled selective colorimetric determination of HQ ranged from 1 μM to 70 μM and a limit of detection (LOD) of 0.2 μM. Successful determination of HQ in pond water was also realized., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

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 × 10 1 to 1.0 × 10 7  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., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Hydroquinone (HQ), a well-known carcinogenic agent, induces oxidative stress, cell cycle arrest, apoptosis, and malignant transformation. As an antioxidant actor, the nuclear factor erythroid 2-related factor 2 (Nrf2) drives adaptive cellular protection in response to oxidative stress. The human lymphoblastoid cell line (TK6 cells) is widely used as a model for leukemia researches. In the present study, we focused on exploring whether Nrf2 regulatory cell cycle in TK6 cells upon HQ treatment and the underlying mechanisms. The results showed that the cell cycle arrest in TK6 cells induced by hydroquinone was accompanied by activation of the Nrf2 signaling pathway. We further clarified that Nrf2 loss accelerated cell cycle progression from G0/G1 to S and G2/M phases and promoted ROS production by downregulating the expression of SOD and GSH. Western blotting analysis indicated that Nrf2 regulated cell cycle progression via p16/pRb signaling pathways. Therefore, we conclude that Nrf2 is engaged in HQ-induced cell cycle arrest as well through p16/pRb and antioxidant enzymes.

We propose the manufacture and optimization of a flexible electrochemical sensor composed of graphite and the polymer poly (butylene adipate-co-terephthalate) (PBAT). The characterization was performed by cyclic voltammetry (CV), electrochemical impedance spectroscopy (EIS), contact angle, Raman spectroscopy, mechanical tensile tests, and scanning electron microscopy (SEM). The electrochemical composite material shows a high electroactive area (0.52 cm²), with an electron transfer rate constant (k0) of 4.55 × 10−3 cm s−1 for potassium ferricyanide and good reproducibility (relative standard deviation (RSD) of 4.5%). As proof of potentiality, the composite sensor was applied for hydroquinone (HQ) detection using the Differential Pulse Voltammetry (DPV) technique. Under optimized manufacturing and instrumental parameters, a linear concentration ranging from 0.1 to 1.4 mmol L−1 HQ with a LOD of 1.01 × 10−6 mol L−1 and LOQ 3.4 × 10−6 mol L−1 were obtained using the flexible composite sensor. In addition, the proposed method was applied to the detection of HQ in the pharmaceutical ointment sample with good agreement between the labelled value and found by the proposed method. Besides, recovery values ranging from 91.85 to 101.37% were obtained, highlighting the adequate accuracy of the method. The sensors described here have the advantage of being flexible, disposable, reproducible (RSD = 4.5%), and of low manufacturing cost ($0.17 per device), which makes them attractive for portable analysis.

Reprogramming of cellular metabolism is a vital event during tumorigenesis. The role of glycolysis in malignant progression promoted by hydroquinone (HQ), one of the metabolic products of benzene, remains to be understood. Recently, we reported the overexpression of sirtuin 1 (SIRT1) in HQ-enhanced malignant progression of TK6 cells and hypothesized that SIRT1 might contribute to glycolysis and favor tumorigenesis. Our data showed that acute exposure of TK6 cells to HQ for 48 h inhibited glycolysis, as indicated by reduction in glucose consumption, lactate production, hexokinase activity, and the expression of SIRT1 and glycolytic enzymes, including HIF-1α, hexokinase-2 (HK-2), ENO-1, glucose transporter 1 (Glut-1), and lactic dehydrogenase A (LDHA). Knockdown of SIRT1 or inhibition of glycolysis using the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) downregulated the levels of SIRT1 and glycolytic enzymes and significantly enhanced HQ-induced cell apoptosis, although knockdown of SIRT1 or 2-DG alone had little effect on apoptosis. Furthermore, immunofluorescence and Co-IP assays demonstrated that SIRT1 regulated the expression of HK-2, and HQ treatment caused a decrease in SIRT1 and HK-2 binding to mitochondria. Importantly, we found that glycolysis was promoted with increasing HQ treatment weeks. Long-term HQ exposure increased the expression of SIRT1 and several glycolytic enzymes and promoted malignant cell progression. Moreover, compared with the PBS group, glucose consumption and lactate production increased after 10 weeks of HQ exposure, and the protein levels of SIRT1 and HK-2 were increased after 15 weeks of HQ exposure, while those of Glut-1, ENO-1, and LDHA were elevated. In addition, SIRT1 knockdown HQ 19 cells exhibited decreased lactate production, glucose consumption, glycolytic enzymes expression, cell growth, and tumor formation in nude mice. Our findings identify the high expression of SIRT1 as a strong oncogenic driver that positively regulates HK-2 and promotes glycolysis in HQ-accelerated malignant progression of TK6 cells.

Cardiac troponin I (cTnI) has been widely used in clinical diagnosis of acute myocardial infarction (AMI). Herein, a sensitive electrochemical biosensor for cTnI analysis was designed, in which the simple synthesized Pd@PdPtCo mesoporous nanopolyhedras (MNPs) were utilized as signal amplifiers. The mesoporous polyhedral structure of Pd@PdPtCo MNPs endows them with more specific surface area and more active sites, as well as the synergistic effect between multiple metal elements, all of which increase the electrocatalytic performance of Pd@PdPtCo MNPs in efficiently oxidizing hydroquinone (HQ) to benzoquinone (BQ). Experimental results showed that Pd@PdPtCo MNPs had better performance in oxidation of HQ to BQ compared with their corresponding monometallic and bimetallic nanomaterials. With the aid of the interaction between antigens and antibodies, the peak current of HQ to BQ showed an upward trend with increasing concentration of cTnI, thus the quantitative detection of cTnI could be achieved. Under optimal conditions, the biosensor prepared in this work has a wider linear range (1.0 × 10 -4 -200 ng mL -1 ) and a lower detection limit (0.031 pg mL -1 ) than other sensors reported in literatures, coupled by good stability and high sensitivity. More importantly, it also performed well in complex serum environment, proving that the electrochemical sensor has a practical application potential in this field., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Hydroquinone (HQ) exposure is common as it is a natural component of plant-based foods and is used in some fingernail polishes, hair dyes, and skin lighteners. Industrially it is used as an antioxidant, polymerization inhibitor, and reducing agent. The current study was undertaken to determine whether HQ may cause DNA damage in an in vivo comet assay in F344 rats. DNA strand breaks were assessed in the duodenum as a direct tissue contact site, the testes, and the liver and kidneys, which were tumor sites in bioassays. Rats were exposed to HQ by gavage at 0, 105, 210, or 420 mg/kg/day. At all dose levels, mean % tail intensity and tail moment values for all tissues in animals given HQ were similar to the control. There were no statistically significant increases in tail intensity in any tissue following HQ treatment of male and female rat and data for all animals fell within the available historical control ranges for each tissue. There was no evidence of induction of DNA damage in cells isolated from duodenum, kidney or liver of male and female rats or in the testes of male rats following exposure to HQ at a dose levels up to 420 mg/kg/day, which caused acute renal necrosis.

Carbonaceous nanostructures stand out as an excellent electrode material to enhance the electrocatalytic, electroconductivity, and long-term stability of the electrochemical sensor in recent years. This review article focus on the important advancement in developing carbonaceous nanomaterials-based electrochemical sensors for simultaneous electrochemical sensing (binary and ternary mixtures) of environmental contaminants dihydroxybenzene isomers. The fabrication of electrochemical sensors such as graphene/carbon nanotubes hybrid composite, graphene/ carbon nanotubes supported nanomaterials, mesoporous carbon, carbon nanofiber, carbon nano-fragment and biochar modified electrode was presented coupled with suitable applications. This review discussed the selective reports on the application of dihydroxybenzene sensors during the period from 2015 to 2020.

Pyrocatechol is a coffee ingredient that exhibits anti-inflammatory activity. We herein identified hydroquinone and 4-ethylcatechol as novel coffee ingredients inhibiting LPS-induced inflammatory responses. Similar to pyrocatechol, hydroquinone and 4-ethylcatechol significantly inhibited LPS-induced nitric oxide (NO) production and CCL2 secretion by suppressing the mRNA expression of iNOS and CCL2 in murine macrophage-like RAW264.7 cells. These ingredients also inhibited the LPS-induced activation of NF-κB, a pivotal transcription factor in inflammation, by preventing its nuclear localization, and induced the expression of Nrf2, a transcription factor negatively regulating LPS-induced inflammation. By utilizing Keap1−/−MEFs reconstituted with Keap1 mutants in which major cysteine residues were substituted, we found that Cys151 in Keap1 was a critical sensor for pyrocatechol, hydroquinone, and 4-ethylcatechol to induce Nrf2 expression. However, the amounts of hydroquinone and 4-ethylcatechol in the coffee decoction were markedly lower than that of pyrocatechol, suggesting that pyrocatechol is the main coffee ingredient exhibiting anti-inflammatory activity.

Hydroquinone (HQ), a key metabolite of benzene, affects cell cycle and apoptosis. Poly (ADP-ribose) polymerase-1 (PARP-1) plays an important role in DNA damage repair. To explore whether PARP-1 is involved in HQ-induced cell cycle and apoptosis, we assessed the effect of PARP-1 suppression and overexpression on induction of cell cycle and apoptosis analyzed by flow cytometry analysis. We observed that HQ induced aberrant cell cycle progression and apoptosis. We further confirmed that PARP-1 suppression accelerated the cell cycle progression and inhibited cell apoptosis via inhibiting p16/pRb signal pathway after acute HQ exposure, while overexpression of PARP-1 displayed the opposite results. Therefore, we concluded that HQ-induced cell cycle and apoptosis were regulated by PARP-1 through activation of p16/pRb signaling pathway.

Nosocomial pathogens cause various health problems in human and many novel drugs are under investigation to combat the pathogens. The present study explains the naturally derived hydroquinone possible mode of action against Pseudomonas aeruginosa MTCC 741 and Staphylococcus aureus MTCC 740. Time kill studies, cell viability assays, membrane potential assays, and potassium release assays were carried out to study the mode of action. Time kill studies revealed the rapid death of bacterial pathogens exposed to 4X MIC (Minimum inhibitory concentration) of the hydroquinone. Cell viability assay results showed that nearly half of the cell destruction of test pathogens occurred within one hour. Transmission electron microscopic (TEM) observations revealed the disruption of the cell membrane, which caused severe ultrastructural changes in both test pathogens. Hydroquinone dissipated the membrane potential of test pathogens, as confirmed by the depolarization of membrane potential, increases in permeability and leakage of intracellular potassium ions. At the concentration of 2X MIC hydroquinone in 5 min, about 91.41% and 84.85% potassium ions were released from P. aeruginosa MTCC 741 and S. aureus MTCC 740, respectively. This is the first report on the mode of action of naturally derived hydroquinone against clinical pathogens.

It is of great significance to establish an effective method for removing Cr(VI) from wastewater. Herein, Fe-doped g-C 3 N 4 (namely Fe-g-C 3 N 4 -2) was synthesized and then employed as photocatalyst to conduct the test of Cr(VI) reduction. Notably, the embedding of Fe ion in g-C 3 N 4 can offer the Fe 2+ /Fe 3+ 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-C 3 N 4 after the introduction of Fe ion, thereby boosting the light absorption capacity of catalyst. Thus, Fe-g-C 3 N 4 -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-C 3 N 4 -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 H 2 O 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 O 2 •‒ must be given carefully consideration., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Benzene, a widely used industrial chemical, has been clarified to cause hematotoxicity. Our previous study suggested that miR-451a may play a role in benzene-induced impairment of erythroid differentiation. However, the mechanism underlying remains unclear. In this study, we explored the role of miR-451a and its underlying mechanisms in hydroquinone (HQ)-induced suppression of erythroid differentiation in K562 cells. 0, 1.0, 2.5, 5.0, 10.0, and 50 μM HQ treatment of K562 cells resulted in a dose-dependent inhibition of erythroid differentiation, as well as the expression of miR-451a. Bioinformatics analysis was conducted to predict potential target genes of miR-451a and dual-luciferase reporter assays confirmed that miR-451a can directly bind to the 3'-UTR regions of BATF, SETD5, and ARHGEF3 mRNAs. We further demonstrated that over-expression or down-regulation of miR-451a altered the expression of BATF, SETD5, and ARHGEF3, and also modified erythroid differentiation. In addition, BATF, SETD5, and ARHGEF3 were verified to play a role in HQ-induced inhibition of erythroid differentiation in this study. Knockdown of SETD5 and ARHGEF3 reversed HQ-induced suppression of erythroid differentiation while knockdown of BATF had the opposite effect. On the other hand, we also identified c-Jun as a potential transcriptional regulator of miR-451a. Forced expression of c-Jun increased miR-451a expression and reversed the inhibition of erythroid differentiation induced by HQ, whereas knockdown of c-Jun had the opposite effect. And the binding site of c-Jun and miR-451a was verified by dual-luciferase reporter assay. Collectively, our findings indicate that miR-451a and its downstream targets BATF, SETD5, and ARHGEF3 are involved in HQ-induced erythroid differentiation disorder, and c-Jun regulates miR-451a as a transcriptional regulator in this process., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper, (Copyright © 2024 Elsevier B.V. All rights reserved.)

The nucleophilic substitution and Friedel-Crafts alkylation were performed for chloromethylated polystyrene, and the hydroquinone-modified hyper-crosslinked polymer, namely, PS-KHQ-HCP, was prepared accordingly. The nucleophilic substitution offered plentiful oxygen for PS-KHQ-HCP and the Friedel-Crafts alkylation provided PS-KHQ-HCP with hyper-crosslinking frameworks. As a result, PS-KHQ-HCP possessed abundant oxygen (13.04 wt.%) and high Brunauer-Emmett-Teller surface area (437 m2/g). The adsorption experiments indicated that PS-KHQ-HCP displayed efficient adsorption to aniline with a maximum adsorption capacity of 166.8 mg/g at the original solution pH of 7.8, and the adsorption enthalpy (ΔH: -18.62 kJ/mol) and adsorption entropy (ΔS: -62.87 J/(mol·K)) were predicted to be negative. The kinetic curve displayed that it was sufficient for the adsorption to reach equilibrium within 120 min. The adsorption mechanism revealed that the introduced oxygen was beneficial for the adsorption because of the possible hydrogen bonding and acid-base interaction.

Single-atom nanozymes (SANs) can significantly enhance the sensitivity and selectivity of electrochemical sensing platforms due to the homogeneity of their active sites, full atom utilization, and high catalytic activity. In this study, we demonstrate the synthesis and characterization of a high-density Co-based single-atom nanozyme anchored on activated MOF-derived porous carbon (Co-AcNC-3) via a cascade anchoring strategy for ultrasensitive, simultaneous electrochemical detection of catechol (CC) and hydroquinone (HQ). The Co-AcNC-3 displays a large specific surface area, high defectivity, and abundant oxygen-containing groups, with Co atoms being atomically dispersed throughout the carbon support via Co-N bonds. The Co-AcNC-3 biosensor exhibits superior electrochemical signals for CC and HQ, with linear ranges of 4.0 μM-300.0 μM. and detection limits of 0.072 μM and 0.034 μM, respectively. Moreover, the Co-AcNC-3 biosensor has shown excellent performance in accurately detecting CC and HQ in actual samples. Our findings highlight the potential of the proposed Co-AcNC-3 biosensor as a reliable and promising sensing platform for determining CC and HQ., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Hydroquinone (HQ), a major metabolite of benzene and known hematotoxic carcinogen. MicroRNA 1246 (miR-1246), an oncogene, regulates target genes in carcinogenesis including leukemia. This study investigates the impact of exosomal derived miR-1246 from HQ-transformed (HQ19) cells on cell-to-cell communication in recipient TK6 cells., Methods: RNA sequencing was used to identify differentially expressed exosomal miRNAs in HQ19 cells and its phosphate buffered solution control cells (PBS19), which were then confirmed using qRT-PCR. The impact of exosomal miR-1246 derived from HQ-transformed cells on cell cycle distribution was investigated in recipient TK6 cells., Results: RNA sequencing analysis revealed that 34 exosomal miRNAs were upregulated and 158 miRNAs were downregulated in HQ19 cells compared with PBS19 cells. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses predicted that their targets are enriched in cancer development-related pathways, such as MAPK signaling, microRNAs in cancer, apoptosis, PI3K-Akt signaling, cell cycle, Ras signaling, and Chronic myeloid leukemia. Eleven miRNAs were confirmed to have differential expression through qRT-PCR, with 6 upregulated (miR-140-3p, miR-551b-3p, miR-7-5p, miR-1290, miR-92a-3p, and miR-1246) and 5 downregulated (miR-183-5p, miR-26a-5p, miR-30c-5p, miR-205-5p, and miR-99b-3p). Among these, miR-1246 exhibited the highest expression level. HQ exposure resulted in a concentration-dependent increase in miR-1246 levels and decrease Cyclin G2 (CCNG2) levels in TK6 cells. Similarly, exosomes from HQ19 exhibited similar effects as HQ exposure. Dual luciferase reporter gene assays indicated that miR-1246 could band to CCNG2. After HQ exposure, exosomal miR-1246 induced cell cycle arrest at the S phase, elevating the expression of genes like pRb, E2F1, and Cyclin D1 associated with S phase checkpoint. However, silencing miR-1246 caused G2/M-phase arrest., Conclusion: HQ-transformed cells' exosomal miR-1246 targets CCNG2, regulating TK6 cell cycle arrest, highlighting its potential as a biomarker for HQ-induced malignant transformation., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Polymer-based hybrid was widely fabricated and applied in heavy metal removal and other inorganic pollutants. The present study deals with the sorption efficiency of metal adsorption through the chemically modified PAA with dihydroxybenzenes into the polymeric matrix present in the tannery effluents and a parallel investigation of chromium (VI) ions in aqueous solution was carried out. From the Langmuir model the removal of chromium (VI) has the maximum adsorption capacity with 181.4 mg g−1. Batch sorption to remove chromium (VI) and lead (II) from the tannery effluents was investigated by using different parameters. The sorption efficiency was found to be 75% and 99% for chromium (VI) and lead (II), respectively, present in the tannery effluents. The chemical and structural characteristics of the adsorbents were determined by UV, FT-IR, TGA, DSC, XRD and SEM-EDS analyses.

Background: Nanozymes are one of the ideal substitutes for natural enzymes because of their excellent chemical stability and simple preparation methods. However, due to the limited catalytic ability of most reported nanozymes, constructing nanomaterials with low cost and high activity is gradually becoming an exploration focus in the field of nanozymes. Heteroatom doping of metal-organic frameworks is one of potential approaches to design nanozymes with high catalytic performance. Due to their multiple valence states properties, V-doped metal-organic framework (MOF)-derived LDH is expected to be a good enzyme-like catalyst. To our knowledge, the V-doped MOF-derived LDH as nanozyme is not explored before., Results: We report the in-situ synthesis of NiV-layered double hydroxides (LDHs) on nickel-based MOF, i.e. Ni-MOF@NiV-LDHs. The MOF surface is covered by 2D nanosheets. This unique structural design increases the specific surface area of the material, enables more exposure of catalytic active sites to participate in reactions and accelerates the electron transfer rate. The Ni-MOF@NiV-LDHs have high peroxidase-like activity able to catalyze TMB oxidation by H 2 O 2 via the generation of •OH and O 2 •- . Relative to Ni-MOF, the Ni-MOF@NiV-LDHs shows 47-fold peroxidase-like activity rise. It had good affinity to TMB and H 2 , with the Michaelis-Menten constants of 0.12 mM and 0.007 mM, respectively. The hydroquinone (HQ) consumed the reactive oxygen species generated in the TMB + H 2 , with the Michaelis-Menten constants of 0.12 mM and 0.007 mM, respectively. The hydroquinone (HQ) consumed the reactive oxygen species generated in the TMB + H 2 O 2 +Ni-MOF@NiV-LDHs system to inhibit the TMB oxidation. On this basis, a sensitive and rapid assay for determining HQ was developed, with a linear range of 0.50-70 μM and a LOD of 0.37 μM., Significance: This work provided some clues for the further development of novel nanozymes with high catalytic performance via a strategy of heteroatom doping. And the constructed colorimetric analysis method was successfully utilized for the determination of HQ in actual waters, which has the potential for practical application in the analysis of environmental pollutants., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Hydroquinone is a benzene metabolite with a wide range of industrial applications, which has potential for widespread human exposure; however, the toxicity of hydroquinone on human cells remains unclear. The aims of this study are to investigate the cytotoxicity and genotoxicity of hydroquinone in human primary fibroblasts and human colon cancer cells (HCT116). Low doses of hydroquinone (227-454 μM) reduce the viability of fibroblasts and HCT116 cells, determined by resazurin conversion, and induce genotoxic damage (DNA strand breaks), as assessed by alkaline comet assays. Bioremediation may provide an excellent alternative to promote the degradation of hydroquinone, however few microorganisms are known that efficiently degrade it. Here we also investigate the capacity of a halotolerant fungus, Penicillium chrysogenum var. halophenolicum, to remove hydroquinone toxicity under hypersaline condition. The fungus is able to tolerate high concentrations of hydroquinone and can reverse these noxious effects via degradation of hydroquinone to completion, even when the initial concentration of this compound is as high as 7265 μM. Our findings reveal that P. chrysogenum var. halophenolicum efficiently degrade hydroquinone under hypersaline conditions, placing this fungus among the best candidates for the detoxification of habitats contaminated with this aromatic compound.

The construction of highly sensitive detection methods for hydroquinone (HQ) in environment and cosmetics is of great significance for environmental protection and human health. In this work, a novel detection method for HQ was successfully developed by constructing a metal-organic framework mimic enzyme colorimetric sensor (Mn/Fe-MOF@Pd 1.0 ) with excellent peroxidase-like activity, which was synthesized by doping manganese ions into Fe-MOF by introducing bimetallic active centers, thereby improving the peroxidase-like activity of Fe-MOF, and the acid resistance and stability of Mn/Fe-MOF were improved by supporting palladium (Pd NPs). It is proven that Mn/Fe-MOF@Pd 1.0 promoted the decomposition of hydrogen peroxide (H 2 O 2 ) to generate active species, therefore, oxidized chromogenic substrate discoloration. On this basis, the detection of HQ based on the Mn/Fe-MOF@Pd 1.0 colorimetric sensor was constructed, in which the limit of detection (LOD) was 0.09 μM in the linear range of 0.3-30 μM. Furthermore, Mn/Fe-MOF@Pd 1.0 was successfully used for detecting HQ in hydroquinone whitening cream and actual water samples. The successful synthesis of Mn/Fe-MOF@Pd 1.0 may provide new insights for further study of the enzyme-like activity of metal-organic framework composites, and the constructed facile and sensitive sensor system could broaden the application prospects of HQ detection., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Poly 1-amino-9, 10-anthraquinone (PAAQ) films were prepared by the electropolymerization of 1-amino-9,10-anthraquinone (AAQ) on platinum substrate from aqueous media, where 5.0 × 10−3 mol L−1 AAQ and 6.0 mol L−1 H2SO4 were used. The kinetics of the electropolymerization process was investigated by determining the change of the charge consumed during the polymerization process with time at different concentrations of both monomer and electrolyte. The results have shown that the process follows first order kinetics with respect to the monomer concentration. The order of the reaction with respect to the aqueous solvent i.e. H2SO4 was found to be negative. The polymer films were successfully used as sensors for the electroanalytical determination of many hazardous compounds, e.g. phenols, and biologically important materials like dopamine. The electroanalytical determination was based on the measurements of the oxidation current peak of the material in the cyclic voltammetric measurements. The cyclic voltammograms were recorded at a scan rate of 100 mV s−1 and different analyte concentrations. A calibration curve was constructed for each analyte, from which the determination of low concentrations of catechol and hydroquinone (HQ) as examples of hazardous compounds present in waste water and also for ascorbic acid and dopamine as examples of valuable biological materials can be achieved.

Reducing the agglomeration and improving the dispersibility in water of two-dimensional (2D) nanozymes is one of the effective ways to improve their enzyme-like activity. In this work, we propose a method by constructing zeolitic imidazolate framework-8 (ZIF-8)-dispersed 2D manganese-based nanozymes to achieve the specific regulated improvement of oxidase-mimicking activity. By in-situ growth of manganese oxides nanosheets of MnO 2 (1), MnO 2 (2) and Mn 3 O 4 on the surface of ZIF-8, the corresponding nanocomposites of ZIF-8 @MnO 2 (1), ZIF-8 @MnO 2 (2), and ZIF-8 @Mn 3 O 4 were prepared at room temperature. The Michaelis-Menton constant measurements indicated that ZIF-8 @MnO 2 (1) exhibits best substrate affinity and fastest reaction rate for 3,3',5,5'-tetramethylbenzidine (TMB). The ZIF-8 @MnO 2 (1)-TMB system was exploited to detection of trace hydroquinone (HQ) based on the reducibility of phenolic hydroxyl groups. In addition, by employing the fact that the cysteine (Cys) with the excellent antioxidant capacity can bind the Hg 2+ based on the formation of "S-Hg 2+ " bonds, the ZIF-8 @MnO 2 (1)-TMB-Cys system was applied to detection of Hg 2+ with high sensitivity and selectivity. Our findings not only provide a better understanding of the relationship between dispersion of nanozyme and enzyme-like activity, but also provide a general method for the detection of environmental pollutants using nanozymes., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)

Benzene is a known hematotoxic and leukemogenic chemical. Exposure to benzene cause inhibition of hematopoietic cells. However, the mechanism of how the hematopoietic cells inhibited by benzene undergo malignant proliferation is unknown. The cells carrying leukemia-associated fusion genes are present in healthy individuals and predispose the carriers to the development of leukemia. To identify the effects of benzene on hematopoietic cells, preleukemic bone marrow (PBM) cells derived from transgenic mice carrying the Mll-Af9 fusion gene were treated with benzene metabolite hydroquinone in serial replating of colony-forming unit (CFU) assay. RNA sequencing was further employed to identify the potential key genes that contributed to benzene-initiated self-renewal and proliferation. We found that hydroquinone induced a significant increase in colony formation in PBM cells. Peroxisome proliferator-activated receptor gamma (Ppar-γ) pathway, which plays a critical role in carcinogenesis in multiple tumors, was significantly activated after hydroquinone treatment. Notably, the increased numbers of the CFUs and total PBM cells induced by hydroquinone were significantly reduced by a specific Ppar-γ inhibitor (GW9662). These findings indicated that hydroquinone can enhance self-renewal and proliferation of preleukemic cells by activating the Ppar-γ pathway. Our results provide insight into the missing link between premalignant status and development of benzene-induced leukemia, which can be intervened and prevented., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)

Glassy carbon electrode (GCE) was modified with electropolymerized films of polyglycine. This polyglycine modified electrode was used to simultaneous electrochemical detection of hydroquinone (HQ) and catechol (CC) and showed an excellent electrocatalytical effect on the oxidation of HQ and CC by cyclic voltammetry (CV) in 0.1 M acetate buffer solution (pH 5.0). In differential pulse voltammetric (DPV) measurements, the polyglycine modified electrode could separate the oxidation peak potentials of HQ and CC present in binary mixtures by about 103 mV though the bare electrode gave a single broad response. A successful elimination of the fouling effect by the oxidized product of HQ on the response of CC has been achieved at the polyglycine modified electrode. The detection limit of HQ in the presence of 0.1 mM CC was 1.0 × 10-6 M and the detection limit of CC in the presence of 0.1 mM HQ was 5.0 × 10-7 M. The proposed method has been applied to simultaneous detection of HQ and CC in a water sample with simplicity and high selectivity.

A high purity, amorphous Bi2S3 thin film composed of loosely packed nanometer-sized spherical grains has been successfully deposited onto ITO substrate at room temperature from non-aqueous bismuth nitrate and sodium thiosulphate solution using a simple, inexpensive, reproducible, and environmentally friendly chemical route method. Film was characterized for structural, surface morphological, optical properties by means of X-ray diffraction (XRD), scanning electron microscopy (SEM) and UV-vis spectrometer, respectively. In last section, Bi2S3 film on ITO substrate was utilized in photo-electrochemical (PEC) solar cell as a working and platinum as a reference electrode in presence of 80 mW/cm2 light intensity in lithium iodide as an electrolyte. Film of non-aqueous Bi2S3 exhibits two separate direct band transitions. Existence of two separate direct transitions was firstly noted in Bi2S3 thin films and explained its possible causes. PEC analysis confirms n-type conductivity.

A simply and high selectively electrochemical method for simultaneous determination of hydroquinone (HQ) and catechol (CC) has been developed at a glassy carbon electrode modified with electropolymerized films of glutamic acid (p-Glu). This p-Glu modified electrode is used to simultaneous electrochemical determination of HQ and CC and shows an excellent electrocatalytical effect on the oxidation of HQ and CC by cyclic voltammetry (CV) in 0.1 M acetate buffer solution (pH 4.5). In differential pulse voltammetric (DPV) measurements, the p-Glu modified electrode could separate the oxidation peak potentials of HQ and CC present in binary mixtures by about 102 mV though the bare electrode gave a single broad response. A successful elimination of the fouling effect by the oxidized product of HQ on the response of CC has been achieved at the p-Pen modified electrode. The determination limit of HQ in the presence of 0.1 M CC was 1.0 × 10-6 M and the determination limit of CC in the presence of 0.1 M HQ was 8.0 × 10-7 M. The proposed method has been applied to simultaneous determination of HQ and CC in a water sample with simplicity and high selectivity.

Glassy carbon electrode (GCE) is modified with electropolymerized films of phenylalanine. Thispoly(phenylalanine) modified electrode is used to simultaneous electrochemical determination of hydroquinone (HQ) and catechol (CC) and shows an excellent electrocatalytical effect on the oxidation of HQ and CC by cyclic voltammetry (CV) in 0.1 M acetate buffer solution (pH 5.0). In differential pulse voltammetric (DPV) measurements, the poly(phenylalanine) modified electrode could separate the oxidation peak potentials of HQ and CC present in binary mixtures by about 104 mV though the bare electrode gave a single broad response. A successful elimination of the fouling effect by the oxidized product of HQ on the response of CC has been achieved at the poly(phenylalanine) modified electrode. The determination limits for HQ and CC in binary mixtures at the poly(phenylalanine) modified electrode were found to be 1.0 × 10-6 M and 7.0 × 10-7 M, respectively. The proposed method has been applied to direct simultaneous determination of HQ and CC in a water sample with simplicity and high selectivity.

Benzene is a frequent component of environmental pollution and is abundant in petrochemicals, decorative materials, motor vehicle exhaust and cigarette smoke. Benzene is a well-known carcinogen in humans and animals, but the molecular mechanism has not yet been elucidated. Our earlier research indicated that hydroquinone (HQ), one of the main reactive metabolites of benzene, could activate aryl hydrocarbon receptor (AhR), which is essential for HQ-induced toxicity, including apoptosis and DNA damage. Since AhR is an important regulator of the immune system that integrates the environmental stimulus and immune response, we examined whether and how HQ-induced AhR activity could lead to NLRP3 inflammasome-dependent pyroptosis in JHP cells. Our results showed that HQ could cause inflammation process and resultant pyroptosis. In JHP cells, HQ also induced endoplasmic reticulum stress (ERS) by releasing excessive reactive oxygen species (ROS). The activation of pyroptosis induced by HQ treatment was reversed by an antioxidant (NAC) and an ERS inhibitor (4-PBA). Interestingly, the treatment of CH223191, an AhR inhibitor, reversed HQ-induced oxidative stress, ERS and pyroptosis. These data suggested that AhR-mediated HQ-induced ERS, ROS and inflammasome activation may play vital roles in the toxic effects of benzene. This work provides insights and prospective strategies into potential mechanisms for reducing benzene-induced hematotoxicity., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)