Salinity stress severely limits crop productivity worldwide. While plant growth-promoting rhizobacteria (PGPR) are known to alleviate abiotic stress, the specific mechanisms mediated by their volatile organic compounds (VOCs) remain largely elusive. In this study, an in vitro split-plate system was used to investigate the effects of VOCs emitted by Bacillus velezensis SQR9 on Arabidopsis thaliana seedlings under salt stress. Exposure to SQR9 VOCs significantly enhanced Arabidopsis salt tolerance, evidenced by increased biomass and root growth. Mechanistically, SQR9 VOCs mitigated salt-induced damage by increasing chlorophyll content, modulating osmolytes, and reducing malondialdehyde (MDA) levels. SQR9 VOCs alleviated oxidative stress by decreasing ROS (H₂O₂, O₂⁻) accumulation and enhancing antioxidant enzyme (SOD, CAT, POD) activities. Furthermore, SQR9 VOCs maintained ion homeostasis by significantly reducing leaf Na⁺ accumulation, maintaining a high K⁺/Na⁺ ratio, and upregulating key ion transporter genes. Analysis of the headspace from SQR9 cultured on MSgg medium identified 2,3-butanediol (2,3-BD) as a major active VOC. Exogenous application of 2,3-BD successfully mimicked the growth-promoting and salt-tolerance-enhancing effects of SQR9. Our findings demonstrate that SQR9 VOCs, particularly 2,3-BD, systemically prime Arabidopsis for salt tolerance by co-activating the antioxidant defense system and the SOS ion homeostasis pathway.

Microcystin–LR (MC-LR) and phenanthrene (Phen), which commonly co-occur in eutrophic waters, have been extensively studied as individual contaminants, but their combined ecotoxicological effects on submerged macrophytes remain unclear. In this study, we examined the individual and combined toxicity of MC-LR (2, 10, 50, 250, and 1000 μg/L) and Phen (0.2, 1, 5, 25, and 100 μg/L) on the submerged macrophyte Vallisneria natans over a 7-day exposure. Key toxicity biomarkers, including growth, photosynthetic efficiency, and antioxidant responses (catalase, superoxide dismutase, glutathione S-transferase, and malondialdehyde), were evaluated. The results showed that high concentrations of each contaminant alone (MC-LR ≥ 1000 μg/L; Phen ≥ 100 μg/L) significantly inhibited growth and reduced photosynthetic efficiency. In contrast, synergistic toxicity was observed at much lower combined concentrations (≥50 + 5 μg/L), with effects substantially exceeding those of individual exposures. Co-exposure intensified antioxidant activity, but it was insufficient to mitigate oxidative damage. Notably, Phen at concentrations above 25 μg/L significantly enhanced the bioaccumulation of MC-LR in V. natans. These findings demonstrate that environmentally relevant mixtures of MC-LR and Phen induce remarkable toxicity even at concentrations where individual compounds show negligible effects. The results highlight that co-existing cyanotoxins and polycyclic aromatic hydrocarbons may present greater ecological risks than predicted from single-contaminant assessments, underscoring the need to update current ecological risk frameworks for the accurate evaluation of complex pollution scenarios in freshwater systems.

While harmful cyanobacterial blooms (HCBs) are extensively characterized in eutrophic lakes, the ecological dynamics of connected river networks remain oversimplified, obscuring the mechanisms of community assembly and toxin distribution across the lake–river interface. This study investigated the spatial heterogeneity of HCBs and microcystins (MCs) in the Lake Taihu watershed, revealing a complex functional divergence between lotic and lentic ecosystems. The rivers functioned as primary nutrient sources, with Total Nitrogen (3.35 ± 1.52 mg·L⁻¹) and Total Phosphorus (0.21 ± 0.22 mg·L⁻¹) concentrations being 1.7-fold and 1.8-fold higher, respectively, than those in the lake during peak periods. Conversely, the lake acted as a biological sink, supporting a peak cyanobacterial density (3.32 × 10⁷ cells·L⁻¹) nearly 1.5 times that of the river network. Phytoplankton community analysis revealed distinct ecological niches: while the lentic lake environment was almost exclusively dominated by colonial Microcystis (>90% relative abundance), the lotic river networks harbored a diverse assemblage with significant contributions from filamentous Oscillatoria and Dolichospermum. Correspondingly, intracellular MC (IMC) in the lake (up to 14.5 μg·L⁻¹) significantly exceeded riverine levels (generally 0.75, p < 0.01), suggesting a spillover effect where the lake determines the watershed’s toxin burden during rivers outflow period. Redundancy Analysis (RDA) further elucidated that limnetic blooms were primarily regulated by water temperature and pH, whereas riverine communities were strictly constrained by hydrodynamic flow. Consequently, the health risk assessment revealed a highly heterogeneous landscape where, beyond the northern lake bays, specific semi-lentic river segments emerged as cryptic hotspots. These findings demonstrate that while nutrients fuel the system, hydrodynamic conditions act as the ultimate ecological filter determining the spatiotemporal distribution of cyanobacterial risks, necessitating an integrated approach to monitoring the entire lake–river continuum.

Microcystin (MC) risk is often assessed within bloom-affected lakes and reservoirs, although hydrological connectivity can extend exposure into downstream river and estuarine networks. We synthesize evidence using a lake–river continuum framework that treats connected reaches as active processing environments. The framework separates the source pool, export flux, and downstream exposure, and distinguishes advective redistribution, reversible retention, irreversible transformation, and source or remobilization processes. Hydrology sets reaction opportunity, while phase partitioning, photochemical and microbial transformation, sediment exchange, and biological uptake determine how MC mass and bioavailability change during transport. Field evidence shows that downstream occurrence cannot be inferred reliably from visible source blooms: reaches may attenuate, retain, redistribute, or locally renew MC exposure depending on hydraulic state and process coupling. These dynamics shift exposure among water, particles, sediments, cells, and biota. Consequently, source-lake indicators or water concentrations alone can mischaracterize ecological exposure, and drinking-water guideline values are not ecological protection thresholds. Key priorities are flux-resolved monitoring, direct field estimates of process rates and transformation products, chronic ecotoxicology matched to realistic exposure routes, and hierarchical transport–biogeochemical models. This continuum perspective links source, process, pathway, receptor, and effect within a single source-to-risk framework.