In this study, we treated harmful Microcystis aeruginosa cyanobacteria using chitosan-modified nanobubbles. The chitosan-modified nanobubbles (255 ± 19 nm) presented a positive zeta potential (15.36 ± 1.17 mV) and generated significantly (p < 0.05) more hydroxyl radicals than the negatively charged nanobubbles (−20.68 ± 1.11 mV). Therefore, the interaction between the positively charged chitosan-modified nanobubbles and negatively charged M. aeruginosa (−34.81 ± 1.79 mV) was favored. The chitosan-modified nanobubble treatment (2.20 × 10⁸ particles mL⁻¹) inactivated 73.16% ± 2.23% of M. aeruginosa (2.00 × 10⁶ cells mL⁻¹) for 24 h without causing significant cell lysis (≤0.25%) and completely inhibited the acute toxicity of M. aeruginosa toward Daphnia magna. The inactivation was correlated (r² = 0.97) with the formation of reactive oxygen species (ROS) in M. aeruginosa. These findings indicated that the hydroxyl radicals generated by the chitosan-modified nanobubbles disrupted cell membrane integrity and enhanced oxidative stress (ROS formation), thereby inactivating M. aeruginosa. Moreover, the penetration of the chitosan-modified nanobubbles and cell alterations in M. aeruginosa were visually confirmed. Our results suggested that the chitosan-modified nanobubble treatment is an eco-friendly method for controlling harmful algae. However, further studies are required for expanding its practical applications.

Increasing levels of artificial light at night (ALAN) are a major threat to global biodiversity and can have negative impacts on a wide variety of organisms and their ecosystems. Nocturnal species such as bats are highly vulnerable to the detrimental effects of ALAN. A variety of lighting management strategies have been adopted to minimise the impacts of ALAN on wildlife, however relatively little is known about their effectiveness. Using an experimental approach, we provide the first evidence of negative impacts of part-night lighting (PNL) strategies on bats. Feeding activity of Myotis spp. was reduced along rivers exposed to PNL despite no reduction in overall bat activity. We also provide the first evidence of negative effects of PNL on both feeding and activity for Pipistrellus pipistrellus which has previously been recorded feeding under artificial light. Despite having considerable energy-saving benefits, we outline the potential negative impacts of PNL schemes for bats in riparian habitats. PNL are unlikely to provide desired conservation outcomes for bats, and can potentially fragment important foraging habitats leading to a breakdown of functional connectivity across the landscape. We highlight the potential dichotomy for strategies which attempt to simultaneously address climate change and biodiversity loss and recommend alternative management strategies to limit the impacts of ALAN on biodiversity.

Ecotoxicological effects of photolytic degradation mixtures of the two brominated flame retardants PolymericFR and Tetrabromobisphenol A-bis (2,3-dibrom-2-methyl-propyl) Ether (TBBPA-BDBMPE) have been studied in vitro and in vivo. Both substances were experimentally degraded separately by exposure to artificial UV-light and the resulting degradation mixtures from different time points during the UV-exposure were applied in ecotoxicological tests. The in vitro investigation showed no effects of the degraded flame retardants on the estrogenic and androgenic receptors via the CALUX (chemically activated luciferase gene expression) assay. Short-term exposures (up to 96 h) of Lumbriculus variegatus lead to temporary physiological reactions of the annelid. The exposure to degraded PolymericFR lead to an increased activity of Catalase, while the degradation mixture of TBBPA-BDBMPE caused increases of Glutathione-S-transferase and Acetylcholine esterase activities. Following a chronic exposure (28 d) of L. variegatus, no effects on the growth, reproduction, fragmentation and energy storage of the annelid were detected. The results indicate that the experimental degradation of the two flame retardants causes changes in their ecotoxicological potential. This might lead to acute physiological effects on aquatic annelids, which, however, do not affect the animals chronically according to our results.

As persulfate activator, Metal organic frameworks (MOFs) and derivatives are widely concerned in degradation of emerging environmental pollutants by advanced oxygen technology dominated by sulfate radical (▪) (SR-AOPs). However, the poor stability and low catalytic efficiency limit the performance of MOFs, requiring multiple strategies to further enhance their catalytic activity. The aim of this paper is to improve the catalytic activity of MOFs and their derivatives by physical and chemical enhancement strategies. Physical enhancement strategies mainly refer to the activation strategies including thermal activation, microwave activation and photoactivation. However, the physical enhancement strategies need energy consumption and require high stability of MOFs. As a substitute, chemical enhancement strategies are more widely used and represented by optimization, modification, composites and derivatives. In addition, the identification of reactive oxygen species, active site and electron distribution are important for distinguishing radical and non-radical pathways. Finally, as a new wastewater treatment technology exploration of unknown areas in SR-AOPs could better promote the technology development.

Arsenite (As(III)) is more toxic, mobilizable and bioavailable than arsenate (As(V)). Hence, the transformations between As(III) and As(V) are crucial for the toxicity and mobility of arsenic (As). However, As transformation and microbial communities involved in alkaline soils are largely unknown. Here we investigate two major pathways of As transformation, i.e., As(III) oxidation and As(V) reduction, and identify the bacteria involved in the alkaline soil by combining stable isotope probing with shotgun metagenomic sequencing. As(III) oxidation and significant increase of the aioA genes copies were observed in the treatments amended with As(III) and NO₃⁻, suggesting that As(III) oxidation can couple with nitrate reduction and was mainly catalyzed by the microorganisms containing aioA genes. As(V) reduction was detected in the treatments amended with As(V) and acetate where the abundance of arrA gene significantly increased, indicating that microorganisms with arrA genes were the key As(V) reducers. Acidovorax, Hydrogenophaga, and Ramlibacter were the putative nitrate-dependent As(III) oxidizers, and Deinococcus and Serratia were the putative respiratory As(V) reducers. These findings will improve our understanding of As metabolism and are meaningful for mapping out bioremediation strategies of As contamination in alkaline environment.

Risk assessments of the ecotoxicological effects insecticides impose on ectotherms have increasingly considered temperature. However, the changes toxicants induce in thermoregulatory behavioral traits may lead to a divergence of thermal selection and temperature-dependent changes of contaminant toxicity. This study demonstrated the interaction of behavioral thermoregulation and temperature-dependent toxicity of beta-cyfluthrin (BC) in the lizard Eremias argus. Based on the negative relationship between temperature and BC toxicity, seeking a warming environment was assumed to represent a self-rescue behavior (and vice versa). The results showed that BC-treated lizards (0–20 μg/g body weight (bw)) showed such self-rescue behavior, while lizards exposed to an extremely high BC dose (200 μg/g bw) sought a cooler environment. Biochemical assays showed that BC affected neurotransmitter systems, caused oxidative stress, and interfered with ion-transport in the central nervous system. Biomarkers of the cholinergic and glutamatergic system, ion-transport function, and oxidative stress were identified as potential biochemical variables related to thermoregulatory behavior. Apparently, seeking a warmer environment is a survival strategy with the aim to neutralize BC toxicity, while seeking a cooler environment aims to attenuate the harmful effects of metabolic and oxidative stress, and to decelerate internal BC diffusion. This phenomenon could be also explained by the concept of the “cooling trap”, i.e., a behavior where cooler temperatures are sought. This impairs survival after exposure to BC at it has a negative temperature coefficient, derived from a dysfunction of the central nervous system regarding thermoregulation caused by the high dosage of neurotoxicant and resulting temperature maladaptation. Implications of the interaction between thermoregulatory behavior and temperature-dependent toxicity are presented, which may aid further temperature-dependent risk assessments.

Occupational lung cancer caused by coke oven emissions (COE) has attracted increasing attention, but the mechanism is not clear. Many evidences show ceRNA (competing endogenous RNA) networks play important regulatory roles in cancers. In this study, we aimed to construct and verify the ceRNA regulatory network in the occurrence of COE-induced lung squamous cell carcinoma (LUSC). We performed RNA sequencing with lung bronchial epithelial cell (16HBE) and COE induced malignant transformed cell (Rf). Furthermore, we analyzed RNA sequencing data of LUSC and adjacent tissues in the cancer genome atlas (TCGA) database. Combined our data and TCGA data to determine the differentially expressed lncRNAs, miRNAs, mRNAs. lncBASE, miRDB and miRTarBase were used to predict the binding relationship between lncRNA and miRNA, miRNA and mRNA. Based on these, we construct the ceRNA network. FREMSA, dual-luciferase reporter assay, quantitative real-time PCR (qRT-PCR), western-blot were used to verify the regulatory axis. CCK8 assay, phalloidin staining, p53 detection were used to explore the roles of this axis in the COE induced malignant transformation. Results showed 7 lncRNAs, 7 miRNAs and 146 mRNAs were identified. Among these, we constructed a ceRNA network including 1 lncRNA, 2 miRNAs and 9 mRNAs. Further verification confirmed the trend of lncRNA H19, miR-29a-3p and COL1A1 were consistent with sequencing results. H19 and COL1A1 were significantly higher in Rf than in 16HBE and miR-29a-3p was reverse. Regulatory investigation revealed H19 increased COL1A1 expression by sponging miR-29a-3p. Knockdown of H19, COL1A1 or overexpression of miR-29a-3p in Rf cells could inhibit cell proliferation, increased cell adhesion and p53 level. However, knockdown of H19 while suppressing the miR-29a-3p partially rescue the malignant phenotype of Rf caused by H19. In conclusion, all these indicated H19 functioned as a ceRNA to increase COL1A1 by sponging miR-29a-3p and promoted COE-induced cell malignant transformation.

Insufficient evidence exists regarding the effects of microplastics (MPs) on the neuronal toxicity of heavy metals in the early stages of organisms. Herein, the effects of micro-polystyrene (μ-PS; 157 μm) and nano-polystyrene (n-PS; 100 nm) particles on the neurodevelopmental toxicity of mercury (Hg) in zebrafish embryos were compared. Zebrafish embryos exposed to Hg at the concentration of 0.1 mg L⁻¹ revealed blood disorders, delayed hatching, and malformations such as pericardial oedema and tail deformity. The length of the larval head was significantly reduced (P < 0.01) and in vivo expression of atoh1a in the cerebellum of neuron-specific transgenic zebrafish Tg(atoh1a:dTomato) larvae was inhibited by 29.46% under the Hg treatment. Most of the toxic effects were inhibited by the combined exposure to μ-PS or n-PS with Hg, and n-PS decreased the neurodevelopmental toxicity of Hg more significantly than μ-PS. Metabolomic analysis revealed that in addition to inhibiting the amino acid metabolism pathway as in the μ-PS+Hg treatment, the n-PS+Hg treatment inhibited unsaturated fatty acid metabolism in zebrafish larvae, likely because of a greater reduction in Hg bioavailability, thus reducing the oxidative damage caused by Hg in the larvae. The combined effects of MPs and heavy metals differ greatly among different species and their targeted effects. We conclude that the combined toxicity mechanisms of MPs and heavy metals require further clarification.

Estuaries are critical habitats subject to a range of stressors requiring effective management. Microbes are gaining recognition as effective environmental indicators, however, the response of host associated communities to stressors remains poorly understood. We examined microbial communities from seawater, sediments and the estuarine fish Pelates sexlineatus, in Australia's largest urbanised estuary, and hypothesised that anthropogenic contamination would be reflected in the microbiology of these sample types. The human faecal markers Lachno3 and HF183 were not detected, indicating negligible influence of sewage, but a gradient in copy numbers of the class 1 integron (intI-1), which is often used as a marker for anthropogenic contamination, was observed in sediments and positively correlated with metal concentrations. While seawater communities were not strongly driven by metal contamination, shifts in the diversity and composition of the fish gut microbiome were observed, with statistical links to levels of metal contamination (F₂, ₂₁ = 1.536, p < 0.01). Within the fish gut microbiome, we further report increased relative abundance of amplicon sequence variants (ASVs; single inferred DNA sequences obtained in sequencing) identified as metal resistant and potentially pathogenic genera, as well as those that may have roles in inflammation. These results demonstrate that microbial communities from distinct habitats within estuarine systems have unique response to stressors, and alterations of the fish gut microbiome may have implications for the adaptation of estuarine fish to legacy metal contamination.