Structural supercapacitors require electrolytes that can efficiently transport ions while bearing mechanical loads, known as structural electrolytes (SEs). Here, we report the addition of the multi-oxirane epoxies, reactive epoxy additives (REAs), as a strategy to tune the microstructure of an established bicontinuous SE, formed by reaction induced phase separation (RIPS). Specifically, trimethylolpropane triglycidyl ether (TGETMP), 4-(diglycidylamino)phenyl glycidyl ether (GEDGP), tris(4-hydroxyphenyl)methane triglycidyl ether (TGETHP), and tetraglycidyl-4,4'-methylenedianiline (TGEMDA) were introduced into an SE based on a blend of bisphenol A diglycidyl ether (DGEBA) and 1-ethyl-3-methylimidazolium bis(trifluoromethylsulfonyl) imide (EMIM-TFSI), (DGEBA_IL40). Additive concentrations were varied between 1 and 50 wt% and the SEs were characterized using scanning electron microscopy, impedance spectroscopy, three-point bending tests and dynamic mechanical thermal analysis. At 2.5 wt% addition, all REAs enhanced ionic conductivity, but reduced Young's modulus, relative to the unmodified SE based on DGEBA_IL40. TGETMP showed the most promising performance by increasing ionic conductivity by 90% and reducing Young's modulus only by 20%. Small-angle neutron scattering of the curing process of DGEBA_IL40 with the addition of 2.5 wt% TGETMP showed a delay in phase separation kinetics and an increase in the cluster correlation length from about 30 Å to 63 Å compared to the unmodified system. Carbon aerogel-modified carbon fibre (CF-CAG) structural electrodes were introduced into the SEs, to explore whether the bicontinuous microstructure would be retained in a multifunctional device. The unmodified SE (DGEBA_IL40) showed epoxy sheathing on CF-CAG with bead-like morphology around fibres and strut-like morphology in the bulk, showing that the presence of CF-CAG influenced local curing of the SE at the electrode/electrolyte interface. Encouragingly, the addition of 2.5 wt% TGETMP to DGEBA_IL40 reduced both epoxy sheathing and bead formation around CF-CAG.

Restrictions on bisphenol A (BPA), continued exposure to phthalates, and the emergence of micro- and nanoplastics (MNPs) have altered the plastic-associated exposure landscape relevant to human reproduction. Existing reviews commonly address these exposures separately or summarize broad reproductive outcomes. This review instead develops a comparative mechanistic framework centered on two connected mechanisms: disruption of gonadotropin-responsive steroidogenesis and oxidative stress, inflammation, and barrier dysfunction. Human biomonitoring, reproductive-tissue, fertility-clinic, and epidemiological evidence are prioritized, while experimental studies are used to resolve mechanisms that cannot be tested directly in humans. Replacement bisphenols can reproduce BPA-like estrogenic, anti-androgenic, and steroidogenic effects, but their actions are analogue-, tissue-, dose-, and time-dependent. Selected phthalates and metabolites have been shown in experimental and ex vivo studies to impair androgen synthesis through altered gonadotropin signaling, cholesterol transport, mitochondrial function, and steroidogenic enzymes. MNPs are heterogeneous particulate exposures whose biological effects depend on polymer composition, size, shape, surface properties, weathering, corona formation, additives, and co-contaminants. Experimental studies using specific MNP models suggest mainly indirect effects on steroidogenesis through particle uptake, altered gonadotropin-responsive signaling, organelle stress, inflammation, and barrier injury. Despite different initiating mechanisms, evidence across the three exposure classes implicates steroidogenesis, redox regulation, inflammatory signaling, and reproductive tissue barriers, although the strength and directness of evidence differ. Human evidence is strongest for phthalates, emerging and analogue-specific for replacement bisphenols, and still methodologically limited for MNP-related clinical outcomes. The framework separates direct catalytic inhibition from altered expression, tissue detection from toxicity, and mechanistic plausibility from demonstrated human effect, supporting targeted research, cautious clinical communication, safer chemical substitution, and MNP exposure mitigation.

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder in which exposure to environmental endocrine-disrupting chemicals may contribute to disease susceptibility. Here, we integrated network toxicology, bulk transcriptomics, machine learning, immune deconvolution, single-nucleus transcriptomics, competing endogenous RNA (ceRNA) analysis, molecular docking, and 100-ns molecular dynamics (MD) simulations to investigate the potential molecular links between bisphenol A (BPA) exposure and AD. Cross-database integration identified 248 shared BPA-AD targets, from which 47 network-central genes and 19 differentially expressed genes were prioritized. Five genes-GSK3B, BCL2, EGFR, APP, and PPARD-were subsequently retained as a candidate gene signature. Although the resulting model showed strong discriminatory performance in the discovery cohort, substantially lower performance in validation cohorts indicated limited generalizability and potential overfitting. Functional analyses implicated neuroinflammatory signaling, mitochondrial apoptosis, amyloid-related processes, and lipid and metabolic dysregulation in the molecular association between BPA and AD. LM22-based CIBERSORT analysis revealed alterations in peripheral leukocyte-like immune signatures, which were interpreted cautiously because this reference matrix does not directly represent resident brain immune populations. Single-nucleus transcriptomic analysis of GSE163577 further localized key genes across biologically plausible cerebrovascular and neuroimmune cell populations. CeRNA analysis suggested potential post-transcriptional regulatory relationships associated with the identified hub genes, while molecular docking identified putative interactions between BPA and candidate target proteins. Subsequent 100-ns MD simulations further characterized the dynamic behavior and conformational stability of the selected BPA-protein complexes, providing complementary evidence for the docking-derived structural hypotheses. Collectively, these findings suggest that BPA-related molecular targets may converge on immune, vascular, metabolic, and neurodegenerative processes relevant to AD. However, the present findings remain primarily computational and hypothesis-generating, and experimental studies are required to establish causal and mechanistic relationships.

4-Hydroxy-4'-isopropoxydiphenylsulfone (BPSIP), an emerging substitute for bisphenol A (BPA), has been increasingly detected in the environment, yet its toxicological profile remains poorly understood. In this study, zebrafish larvae were exposed to BPSIP at various concentrations, including an environmentally relevant level (50 μg/L), for 5 days. Transcriptomic analysis indicated that BPSIP predominantly disrupted biological processes associated with optic nerve development, including oxidative stress and energy metabolism. Corresponding biochemical assays confirmed metabolic disturbance, marked by altered levels of adenosine triphosphate (ATP), pyruvate, and lactate. Oxidative stress was further demonstrated by elevated superoxide dismutase (SOD) activity, coupled with reduced catalase (CAT) activity, total antioxidant capacity (T-AOC), and glutathione (GSH) content. Multi-level toxicological endpoints confirmed optic nerve dysfunction: locomotor behavior assays revealed impaired photoresponse, which was consistent with systemic downregulation of key phototransduction-related genes and histopathological damage in the retina and lens. Additionally, increased thyroid hormone levels and altered expression of hypothalamic-pituitary-thyroid (HPT) axis-related genes indicated thyroid disruption. Together, these results demonstrate that BPSIP exposure disrupts visual function in zebrafish larvae, likely mediated by interference in phototransduction, oxidative homeostasis, energy metabolism, and thyroid signaling. This study provides new insights into the toxicity of BPSIP and underscores its potential ecological and health risks.

Bisphenol TMC (BPTMC), a novel bisphenol A substitute, is widely used as a plastic additive and frequently co-occurs with microplastics (MPs) in various environmental media. Their coexistence may alter biological effects, adding complexity to environmental risk assessment. This study investigated the reproductive and transgenerational toxicity of BPTMC and polylactic acid (PLA) MPs on zebrafish, both individually and in combination, focusing on sex-specific endocrine-disrupting mechanisms. Both BPTMC and PLA impaired gonadal function and germ cell development. BPTMC exhibited sex-specific endocrine disruption, significantly increasing 17β-estradiol in males while decreasing it in females, alongside a more pronounced reduction in testosterone in males. Parental exposure also induced transgenerational developmental toxicity in F1 offspring, including increased mortality and malformations, reduced heart rate, and decreased body length. These effects were linked to the dysregulation of key hypothalamic-pituitary-gonadal axis genes (gnrh3, fshβ, cyp19a1a, esr2a, esr2b). Molecular docking further confirmed that BPTMC activates Esr2a and Esr2b, contributing to reproductive dysfunction. Notably, co-exposure to PLA mitigated BPTMC toxicity, likely by adsorbing BPTMC, reducing its aqueous concentration by 35 % and lowering its bioavailability. This study offers new insights into the biological interactions between plastic additives and MPs, enhancing our understanding of the combined ecological risks posed by emerging contaminants.

Surfactants are widely employed to engineer electrode interfaces with improved electrochemical properties, such as enhanced analyte preconcentration through adsorption, faster electron-transfer kinetics, and increased selectivity. Moreover, surfactant layers can suppress electrode fouling during the oxidation of analytes. Nevertheless, the mechanistic relationship between analyte adsorption and the antifouling behavior imparted by surfactants remains largely unexplored. In this work, a carbon paste electrode modified with cetyltrimethylammonium bromide (CTAB/CPE) was selected as a simple model system for the electrochemical detection of BPA, with the aim of minimizing excessive intermolecular interactions at the electrode interface and facilitating the investigation of the adsorption mechanism and antifouling behavior. Our study was investigated using cyclic voltammetry, supported by adsorption modeling and molecular simulations. The results revealed that CTAB significantly improves electrode performance by reducing surface fouling, improving current response, and enhancing sensitivity and reproducibility. The electrochemical oxidation process was found to involve an adsorption-controlled mechanism. Adsorption studies showed that the experimental data were best described by the Freundlich isotherm, indicating a heterogeneous surface with adsorption sites of different affinities toward BPA, while the Frumkin model suggested negligible lateral interactions between adsorbed BPA molecules. In addition, thermodynamic analysis revealed that the adsorption process is favorable and predominantly physical in nature, driven by ion-dipole and π-cation interactions. Density Functional Theory (DFT), Topological Quantum Theory of Atoms in Molecules (QTAIM), and The Noncovalent Interaction (NCI) analyses further confirmed favorable interfacial charge-transfer properties and the predominance of physisorption at the CTAB/CPE interface. Overall, BPA adsorption on CTAB/CPE occurs through weak intermolecular interactions with negligible lateral interactions which may suppress the polymerization of BPA oxidation products, thus improving the anti-fouling performance of the CTAB/CPE electrode.

Exposure to environmental chemicals such as bisphenol A (BPA) may affect neural circuit function in subtle and spatially distributed ways that are difficult to attribute to a single circuit element. Here, we developed a voltage-sensitive dye (VSD) imaging analysis pipeline for acute male mouse hippocampal slices. This approach measures stimulus-evoked fractional changes in VSD fluorescence (ΔF/F 0) to generate pixel-wise normalized maps, averages response magnitude within anatomically defined regions of interest (ROIs), and visualizes control-versus-compound differences using pixel-wise statistical maps before and after false discovery rate (FDR) adjustment. We applied this pipeline to compare the acute effects of BPA with those of two structurally related phenolic analogs. Evoked responses were quantified by their peak amplitude and time integral across hippocampal trisynaptic pathways at two stimulation levels determined from input-output relationships, with or without the GABAA receptor antagonist gabazine (SR-95531; 10 μM). The phenolic analogs reduced circuit responses across multiple ROI-defined conditions, whereas BPA produced comparatively limited effects. These alterations varied with pathway, subfield, age, response metric, and inhibitory state. These findings demonstrate the utility of integrating ROI averages with pixel-wise statistical maps for detecting condition-dependent circuit-level differences between structurally related compounds and indicate that BPA-related phenolic analogs can differ from BPA itself in their acute effects on hippocampal circuitry.Significance Statement Exposure to environmental chemicals may alter brain circuit activity in subtle, spatially distributed ways. We developed a voltage-sensitive dye imaging pipeline for acute mouse hippocampal slices that combines regional summaries with pixel-wise statistical maps, quantifying regional response magnitude while localizing where statistically supported differences are expressed within evoked response fields. Using this framework, we compared the acute hippocampal circuit effects of bisphenol A (BPA) with those of two structurally related phenolic analogs. Under acute slice conditions, statistically supported response reductions were detected more consistently for the phenolic analogs than for BPA, depending on age, inhibitory state, hippocampal subfield, and response metric. These results show how integrated regional and pixel-wise analysis improves circuit-level phenotyping of structurally related compounds.

BONR, a newly developed fluorescent probe, was prepared through the fusion of bisphenol A, dicyanoisophorone, and Rhodamine ethylenediamine. This probe enables the specific detection of Fe[3+] ions, resulting in a synergistic enhancement of both its spectral properties and practical application. In an EtOH/HEPES (1:1, v/v, pH =7.0) system, BONR exhibits high selectivity for Fe[3+], producing an "off-on" fluorescence switching response. The probe undergoes a color transition from pale yellow to orange-red under natural light, with a significant increase in fluorescence intensity when exposed to 365 nm ultraviolet (UV) light. This behavior remains stable in the coexistence of over 20 interfering ions. The binding of probe to Fe[3+] occurs in a 1:1 stoichiometry, characterized by a binding constant of 2.38 × 10[5] M[-1]. It achieves a minimum detection limit of 2.92 × 10[-7] M, maintains outstanding stability over the pH range of 4 to 10, and demonstrates reversible response characteristics. BONR has been effectively employed for accurate determination of Fe[3+] in real water samples, rapid on-site colorimetric analysis, plant and cell imaging, and visualization of fingerprint tertiary structures. This probe represents tool for efficient Fe[3+] detection in diverse contexts, underscoring its promising utility across environmental monitoring and biomedical fields.

Bisphenol S (BPS), an endocrine-disrupting chemical used in thermal paper and hard plastics, is a common replacement for bisphenol A. Human exposure to BPS is widespread, raising concern about potential effects on pregnancy and fetal development. We conducted a meta-analysis of studies published before July 2025 that evaluated associations between BPS exposure and two outcomes: preterm birth and gestational age. Eligible studies used cohort, case-control, or cross-sectional designs; measured BPS in humans; reported adjusted associations; and detected BPS concentrations in over 50% of participant samples. We standardized published effect estimates to reflect changes in the odds of preterm birth or difference in gestational age per one ng/mL increase in natural log-transformed BPS. We used mixed-effects meta-analysis to estimate trimester-specific pooled odds ratios (for preterm birth) and beta coefficients (for gestational age). Nine studies met inclusion criteria. Most showed low-to-medium threats of bias, primarily due to potential misclassification of BPS exposure. Pooled associations for BPS measured between preconception and second trimester produced a statistically significant finding of -0.04 weeks (95% CI: -0.05, -0.02) for gestational age as well as a non-significant increase in the odds of preterm birth. No pooled estimates for BPS measured between third trimester were statistically significant, however the associations changed direction. Variation in median BPS concentrations and detection rates contributed to heterogeneity across studies. These results suggest that timing of gestational BPS exposure may influence pregnancy outcomes. Future research should incorporate repeated exposure measurements to better capture sensitive windows of vulnerability.

Bisphenol A bis(diphenyl phosphate) (BDP), an emerging oligomeric organophosphate ester, has been increasingly detected in the environment. However, its effects on host defense at environmentally relevant concentrations remain unclear. Using Caenorhabditis elegans, we examined whether developmental exposure to 2, 20, or 200 ng/L BDP impaired resistance to the pathogenic bacterium Pseudomonas aeruginosa PA14 and affected related immune processes. Among the three exposure windows, continuous L1-to-adult exposure produced the broadest response profile. BDP did not markedly affect lifespan or growth but significantly shortened survival during PA14 infection at 2 and 200 ng/L. RNA-seq and qRT-PCR revealed alterations in antimicrobial gene expression involving epidermal nlp/cnc effectors, intestinal lys/spp-type genes, and the p38 MAPK and DAF-2/FOXO pathways. These changes coincided with increased intestinal permeability, disrupted antioxidant status, and mild apoptosis-associated responses. Mutant assays and genotype × exposure interaction analysis showed that the PA14-sensitive phenotype at 2 ng/L differed between wild-type and tir-1 mutant worms, whereas pmk-1, skn-1, and dbl-1 mutants retained similar susceptibility patterns. TJ356 assays further showed increased cytosolic retention of DAF-16, suggesting insufficient nuclear activation during BDP-induced PA14 susceptibility. Overall, these findings indicate that environmentally relevant BDP exposure can disrupt host immune homeostasis and weaken resistance to pathogen challenge, suggesting that such susceptibility may represent an underrecognized toxicological consequence of emerging organophosphate esters with broader ecological and health implications.

Bisphenol BP (BPBP), a structural analog of bisphenol A (BPA), is increasingly utilized in industrial applications; however, its potential hazards to the cardiovascular system remain unexplored. This study employed an integrated strategy combining network toxicology, molecular docking, and in vivo zebrafish models to systematically elucidate the cardiovascular toxicity of BPBP. Network toxicology identified several candidate hub genes and pathways potentially associated with BPBP-induced cardiotoxicity. Molecular docking further suggested favorable predicted interactions between BPBP and selected candidate hub proteins. In vivo zebrafish experiments revealed dose-dependent cardiovascular developmental abnormalities, including cardiac looping defects, pericardial edema, and impaired cardiac function. Additionally, BPBP exposure significantly suppressed angiogenesis, resulting in compromised vascular sprouting and aberrant vessel morphogenesis. Behavioral profiling further demonstrated that BPBP-exposed larvae exhibit substantial locomotor deficits and blunted sensorimotor responsiveness. BPBP exposure was associated with altered expression of key cardiogenesis-related genes. Furthermore, BPBP exposure was associated with excessive reactive oxygen species (ROS) accumulation, redox imbalance, and enhanced apoptosis-related responses. Collectively, our findings demonstrate that BPBP induces marked cardiovascular developmental toxicity under the tested exposure conditions, raising significant concerns regarding its safety as a BPA alternative and highlighting the need for further mechanistic investigation and toxicological assessment of BPBP, particularly under environmentally relevant exposure conditions.

Metal-free photocatalysts activated under visible solar irradiation offer a promising and sustainable approach for the efficient remediation of organic contaminants in the environment. However, developing a highly efficient metal-free visible light photocatalyst remains a significant challenge, primarily due to the rapid recombination of photogenerated carriers and the inherently low specific surface area. Here, we designed a dual-modified MCNUGQD photocatalyst using a green synthesis approach to address these two critical challenges. The π-π stacked interface of graphene quantum dots (GQDs) and exfoliated carbon nitride (CN) promotes photogenerated carriers separation, enhancing electron utilization efficiency. The synergistic effects of GQDs grafting and efficient nanosheet exfoliation achieved the complete removal of 1 mg/L bisphenol A (BPA) within 5 min, achieving a high reaction rate constant of 0.983 min[-1] and a total organic carbon (TOC) removal efficiency of 44.5%, under the optimized conditions. Moreover, MCNUGQD demonstrated excellent adaptability under various environmental conditions and maintained high reusability over four consecutive recycling tests. This study highlights that metal-free visible-light photocatalysts can outperform metal-based/modified systems and further demonstrates their practical applicability and potential for future development.