Decay of algal blooms in eutrophic lakes generates detritus-rich, redox-dynamic microhabitats that modulate the degradation of emerging pollutants as antibiotics. The degradation pathways of antibiotics within algal-detritus accumulation zones and the associated microbial assimilators remain insufficiently understood. In this study, localized algal bloom decay zones were simulated using static lake microcosms, and DNA-stable isotope probing (DNA-SIP) combined with metagenomic analysis were employed to elucidate ciprofloxacin (CIP) degradation pathways and to identify microorganisms potentially involved in CIP assimilation under elevated CIP exposure. Results demonstrate that ecological succession linked to algal decomposition was closely synchronized with CIP degradation, which primarily proceeded via defluorination, decarboxylation, and piperazine ring modification. The bottom detritus layer showed enrichment of aromatic compound-degrading bacteria, including Hydrogenophaga, Reyranella, and Rhodoblastus, in heavy DNA fractions, indicating their potential role in CIP assimilation. This layer also contained functional genes associated with benzoate, halogenated aromatic compounds, and polycyclic aromatic hydrocarbon degradation pathways. In addition, enrichment of the AAC(6')-Ib-cr gene family in the bottom layer coincided with detection of N-acetylated CIP products, suggesting a possible acetylation-mediated inactivation mechanism. Collectively, the study identified candidate microorganisms and genes linked to CIP-derived assimilation and degradation in algal-detritus-rich microhabitats, providing mechanistic insights into antibiotic degradation in polluted algal decay hotspots.
Manganese (Mn) overexposure induces neurocognitive deficits associated with hippocampal neuronal injury and neuroinflammation, but the cellular mechanisms underlying Mn-induced hippocampal damage remain incompletely understood. Microglial pyroptosis may amplify neuroinflammation and contribute to secondary neuronal injury; however, its involvement in Mn neurotoxicity and modulation by melatonin (Mel) remain unclear. This study investigated the protective role of Mel against Mn-induced neurological deficits using C57BL/6 mice in vivo and SIM-A9 microglial cells in vitro. Mn exposure impaired learning and memory and promoted hippocampal neuronal injury, accompanied by increased NOD-like receptor family pyrin domain-containing 3 (NLRP3)-mediated pyroptotic signaling in hippocampal microglia. Mel attenuated microglial pyroptosis and neuronal injury without substantially reducing Mn levels in the hippocampus, blood, or urine. Mn disrupted the thioredoxin (Trx)/thioredoxin-interacting protein (TXNIP) redox axis and enhanced TXNIP-NLRP3 interaction. Txnip overexpression strengthened this interaction and weakened the protective effect of Mel on microglial pyroptosis. Furthermore, Mel enhanced Sirtuin 6 (SIRT6) activity and nuclear SIRT6 expression, reduced H3K9ac and H3K56ac enrichment at the Txnip promoter, and suppressed Mn-induced TXNIP overexpression. These findings suggest that Mel mitigates Mn-associated hippocampal neuroinflammatory injury by partially restoring SIRT6-mediated epigenetic repression of Txnip and reducing TXNIP/NLRP3-driven microglial pyroptosis.
Perfluorooctane sulfonate (PFOS) and cadmium (Cd) are persistent contaminants that frequently coexist in aquatic environments, yet their combined effects on early neurodevelopment remain unclear. Here, zebrafish embryos were exposed to environmentally relevant concentrations of Cd, PFOS, or their mixtures from 2 to 120 h post-fertilization. Developmental endpoints, light-dark locomotor behavior, transcriptomics, and qPCR validation were assessed. Cd caused marked developmental toxicity and abnormal light-dependent behavior, whereas PFOS induced weaker and non-monotonic effects. Co-exposure partially attenuated several Cd-induced developmental and behavioral abnormalities, indicating an endpoint-dependent interaction rather than uniform enhancement of Cd toxicity. Transcriptomics analysis showed that Cd mainly affected glutathione metabolism, ferroptosis-related, tight junction, and phototransduction pathways, while PFOS affected DNA replication/repair, spliceosome function, redox regulation, and metabolic remodeling. Combined exposure retained enrichment of ferroptosis and phototransduction pathways and involved iron/transition-metal ion transport, metal-ion homeostasis, and heme/iron-binding processes. qPCR confirmed altered expression of tnfa, ptgs2b, opn1lw1, pde6ha, and cldn5a, supporting inflammatory, ferroptosis-related pathways, visual, and barrier-associated molecular responses. These findings show that PFOS modifies Cd toxicity in a pathway-specific manner, with attenuation of several phenotypic responses accompanied by persistent molecular perturbations. The coordinated perturbation of phototransduction, metal-ion homeostasis, and ferroptosis-related/inflammatory pathways provides a molecular framework for improving early-life risk assessment of mixed PFAS-metal contamination.
Understanding the vertical transport and fate of microplastics (MPs) in freshwater systems is critical for clarifying their redistribution and downstream transfer. However, in river-connected lakes, the mechanisms controlling the downward transport of buoyant MPs remain poorly quantified. Here, we developed a three-dimensional hydrodynamic-particle tracking model for Lake Poyang to investigate the vertical transport of buoyant MPs under contrasting river-lake exchange regimes, incorporating sediment flocculation as a dynamic process modifying the size and effective density. The simulations revealed size-dependent and spatially heterogeneous settling behavior: 69, 210, and 750μm MPs initiated settling after 4.5, 35.4, and 756.8 h on average, with maximum spatial differences exceeding 60% for the same size. Sediment flocculation shortened the settling timescale of small MPs from weeks to hours, whereas hydrodynamic mixing advanced the downward transport of larger particles. Riverine conditions favored export and deposition, lacustrine conditions enhanced surface retention; during backflow, Yangtze River input increased in-lake MP abundance, allowing suspended-sediment-induced densification to promote rapid deposition of small buoyant MPs. These findings highlight the importance of coupling particle-size-dependent responses with sediment flocculation and river-lake hydrodynamics to understand buoyant MP transport and fate in river-connected lakes, providing process-based insights for prediction and risk assessment.
Manganese (Mn) oxide-mediated adsorption-oxidation critically controls antimony (Sb) mobility and transformation in contaminated aquatic and terrestrial environments, yet its Sb(Ⅲ) isotope fractionation mechanism remains unclear. Here, α-MnO2 exposing the (100) and (310) facets was used as a model system to resolve Sb isotope fractionation during coupled Sb(III) transformation at Mn oxide-water interfaces. For the (100) facet, surface-bound Sb(III) was initially oxidized to Sb(V) and partly released into solution, whereas rapid transformation on the (310) facet obscured this early signal. The similar corner-sharing Sb-Mn coordination environments indicate that the contrasting isotope responses were not mainly controlled by Sb complexation. Light Sb isotopes were preferentially enriched in the solid phase during initial adsorption, followed by lighter Sb(V) release that modified the aqueous isotope composition. Facets primarily control the extent of Sb isotope fractionation by regulating the oxidation rate and Sb(V) release, rather than altering the Sb-Mn structure. Different oxidation and Sb release kinetics led to contrasting isotope responses, with slower transformation preserving larger apparent fractionation (Δ¹²³Sbaq-solid ≈ -3.8 ε) and faster transformation approaching negligible fractionation. These findings show that Mn oxide-mediated transformation can rework aqueous Sb isotope signatures beyond adsorption-driven fractionation, providing a basis for interpreting Sb isotopes in Mn oxide-bearing environments.
An ultrasensitive method for rapid detection of norfloxacin (NOR) is crucial for ensuring the food safety and environmental protection. Ratiometric fluorescent sensors have attracted increasing attention as an effective detection strategy. However, there is still an urgent demand to design novel multi-color fluorescent beads with independent optical signals and hydrophilic functionalization. Herein, a novel strategy was proposed by combining poly (styrene-co-maleic anhydride) (PSMA) mediated with a layer-by-layer assembly approach to construct functionalized quantum dots (QDs) encoded molecularly imprinted microspheres with two strong fluorescence signals. Using PSMA molecules as mediator, the encapsulation of QDs and carboxylation of the microspheres were integrated in one-pot route, improving the preparation efficiency. Based on these dual-encoded microspheres, a ratiometric fluorescent sensor was fabricated for the fast quantitative detection of NOR by monitoring changes in fluorescence response with varying NOR concentrations. The hydrophilic modification endows the sensor with applicability in aqueous system. Under the optimum detection conditions, satisfactory spiked recoveries (92.08-103.55%) and precision (RSD < 4.84%) in chicken, pork, fish, and milk were obtained. The method limit of detection (LOD) value was measured to be 0.1 μg L-1. Moreover, the unique hollow structure facilitated mass transfer, thereby reducing the detection time to 8 min. This work provides a pioneering and effective strategy for dual-encoded imprinted fluorescent microspheres and high-performance chemical sensing of food contaminants.
In this study, carbon isotope analysis was employed to investigate hydrolysis and natural pyrite-activated persulfate (NP/PDS) degradation of TCPP. EPR and radical quenching experiments revealed that •OH and SO4•⁻ were the dominant reactive oxygen species. The XPS, XRD, and FTIR results indicated Fe(Ⅱ) served as the primary active site, generating •OH and SO4•⁻. For acidic and neutral hydrolysis, the apparent kinetic isotope effects (13C-AKIE = 1.031 ± 0.004 and 1.030 ± 0.004, respectively) were consistent with the intrinsic KIE associated with C-O bond cleavage (1.00-1.03), suggesting that C-O bond cleavage was the initial rate-limiting step. In contrast, negligible carbon isotope fractionation during alkaline hydrolysis indicated that P-O bond cleavage was the initial rate-limiting step. For degradation in the NP/PDS, the observed 13C-AKIEs were 1.009 ± 0.001, 1.004 ± 0.000, and 1.005 ± 0.001, respectively. These values were inconsistent with intrinsic KIEs expected for C-H (1.01-1.03) and C-Cl (1.02-1.03) bond cleavage but corresponded to the lower end of the intrinsic KIEs range for C-O bond cleavage, indicating that P-O bond cleavage was the initial rate-limiting step. Overall, this study demonstrates isotope analysis is a powerful tool for identifying the geochemical mechanisms of OPFRs in contaminated fields.
