Biodigested coffee processing wastewater (CPW) presents a high organic load and does not meet the limits imposed by legislation (namely in Brazil) for discharge into water bodies. Anaerobic digestion generally cannot provide a satisfactory organic matter reduction in CPW as a significant fraction of recalcitrant compounds still persists in the treated effluent. So, this study aims to find alternative ways to remove refractory organic compounds from this wastewater in order to improve the biodegradability and reduce the toxicity, which will allow its recirculation back into the anaerobic digester. Three treatment approaches (Fenton’s oxidation - Approach 1, Coagulation/flocculation (C/F) - Approach 2, and the combination of C/F with Fenton’s process - Approach 3) were selected to be applied to the biodigested CPW in order to achieve that objective.The application of the Fenton process under the optimal operating conditions (initial pH = 5.0; T = 55 °C, [Fe³⁺] = 1.8 g L⁻¹ and [H₂O₂] = 9.0 g L⁻¹) increased the biodegradability (the BOD₅:COD ratio raised from 0.34 ± 0.02 in biodigested CPW to 0.44 ± 0.01 after treatment) and eliminated the toxicity (0.0% of Vibrio fischeri inhibition) along with moderate removals of organic matter (51.3%, 55.7% and 39.7% for total organic carbon – TOC, chemical oxygen demand – COD and biochemical oxygen demand - BOD₅, respectively). The implementation of a coagulation/flocculation process upstream from Fenton’s oxidation, under the best operating conditions (pH 10–11 and [Fe³⁺] = 250 mg L⁻¹), also allowed to slightly increase the biodegradability (from 0.34 to 0.47) and reduce the toxicity, whereas providing a higher removal of organic matter (TOC = 76.2%, COD = 76.5 and BOD₅ = 66.3% for both processes together). Approach 1 and Approach 3 showed to be the best ones, implying similar operating costs (∼74 R$ m⁻³/∼17 € m⁻³) and constitute an attractive option for managing biodigested CPW.

Ionic liquids (ILs) are extensively used in various fields, posing a potential threat in the ecosystem because of their high stability, excellent solubility, and biological toxicity. In this study, the toxicity mechanism of three ILs, 1-octyl-3-methylimidazolium chloride ([C₈MIM]Cl), 1-decyl-3-methylimidazolium chloride ([C₁₀MIM]Cl), and 1-dodecyl-3-methylimidazolium chloride ([C₁₂MIM]Cl) on Arabidopsis thaliana were revealed. Reactive oxygen species (ROS) level increased with higher concentration and longer carbon chain length of ILs, which led to the increase of malondialdehyde (MDA) content and antioxidase activity, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and peroxidase (POD) activities. SOD, CAT, and GPX activities decreased in high ILs concentration due to the excessive ROS. Differentially expressed protein was analyzed based on Gene ontology (GO) and KEGG pathways analysis. 70, 45, 84 up-regulated proteins, and 72, 104, 79 down-regulated proteins were identified in [C₈MIM]Cl, [C₁₀MIM]Cl, and [C₁₂MIM]Cl treatment, respectively (fold change ≥ 1.5 with ≥95% confidence). Cellular aldehyde metabolic process, mitochondrial and mitochondrial respiratory chains, glutathione transferase and oxidoreductase activity were enriched as up-regulated proteins as the defense mechanism of A. thaliana to resist external stresses. Chloroplast, photosynthetic membrane and thylakoid, structural constituent of ribosome, and transmembrane transport were enriched as the down-regulated protein. Compared with the control, 8 and 14 KEGG pathways were identified forup-regulated and down-regulated proteins, respectively, in three IL treatments. Metabolic pathways, carbon metabolism, biosynthesis of amino acids, porphyrin and chlorophyll metabolism were significantly down-regulated. The GO terms annotation demonstrated the oxidative stress response and effects on photosynthesis of A. thaliana in ILs treatment from biological process, cellular component, and molecular function categories.

Aquatic macrophytes play a significant role in nutrients removal in constructed wetlands, yet nutrients could be re-released due to plant debris decomposition. In this study, Myriophyllum aquaticum was used as a model plant debris and three debris biomass levels of 3 g, 9 g dry biomass, and 20 g fresh biomass (D3, D9, and F20, respectively) were used to simulate 120-d plant debris decomposition in a sediment-water system. The biomass first-order decomposition rate constants of D3, D9, and F20 treatments were 0.0058, 0.0117, and 0.0201 d⁻¹, respectively with no significant difference of decomposition rate among three mass groups (p > 0.05). Plant debris decomposition decreased nitrate and total nitrogen concentrations but increased ammonium, organic nitrogen, and dissolved organic carbon (DOC) concentrations in overlying water. The parallel factor analysis confirms that three components of DOC in overlying water changed over decomposition time. Emission fluxes of methane and nitrous oxide in the plant debris treatments were several to thousands of times higher than the control group within the initial 0–45 d, which was mainly attributed to DOC released from the plant debris. Plant debris decomposition can affect the gas emission fluxes for relatively shorter time (30–60 d) than water quality (>120 d). The 16S rRNA, nirK, nirS and hazA gene abundance increased in the early stage for plant debris treatments, and then decreased to the end of 120-d incubation time while ammonia monooxygenase α-subunit A gene abundance of ammonia-oxidizing archaea and bacteria had no large variations during the entire decay time compared with no plant debris treatment. The results demonstrate that decomposition of M. aquaticum debris could affect greenhouse gas emission fluxes and microbial gene abundance in the sediment-water system besides overlying water quality.

Stibnite (Sb₂S₃) dissolution and transformation on mineral surfaces are the fundamental steps controlling the fate of antimony (Sb) in the environment. The molecular-level understanding of Sb₂S₃-mineral-water interfacial reactions is of great importance. Herein, Sb₂S₃ oxidative dissolution and sequestration on pyrite (FeS₂) were explored. The results show that FeS₂ accelerated the rate of Sb₂S₃ oxidative dissolution by a factor of 11.4-fold under sunlight due to heterogeneous electron transfer. The electron transfer from Sb₂S₃ to FeS₂ separated photogenerated hole (h⁺) and electron (e⁻) pairs, facilitating the generation of hydroxyl radicals (OH) on Sb₂S₃ and FeS₂, and superoxide radicals (O₂⁻) on FeS₂. Surface O₂⁻ was the dominant oxidant for Sb(III) oxidation with 91% contribution, as evidenced by radical trapping experiments. OH was preferentially adsorbed on Sb₂S₃, but was released with Sb₂S₃ dissolution, and subsequently contributable to Sb(III) oxidation in solution. The Sb(III) oxidation and sequestration on FeS₂ surface coupled Fe²⁺/Fe³⁺ cycling and inhibited FeS₂ dissolution, as evidenced by X-ray absorption near edge structure and X-ray photoelectron spectroscopy. The insights gained from this study further our understanding of Sb₂S₃ transformation and transport at the environmental mineral-water interfaces.

Microplastic pollution is pervasive in aquatic environments, but the potential effects of microplastics on aquatic organisms are still under debate. Given that tissue damage is unavoidable in fish and the available data mostly concentrate on healthy fish, there is a large chance that the ecotoxicological risk of microplastic pollution is underrated. Therefore, in this study, the effects of microplastics on the regenerative capacity of injured fish were investigated using a zebrafish caudal fin regeneration model. After fin amputation at 72 h post fertilization, the larvae were exposed to polystyrene microplastics (0.1–10 mg/L) with diameters of 50 or 500 nm. Microplastic exposure significantly inhibited fin regeneration, both morphologically and functionally. Furthermore, the signaling networks that regulate fin regeneration, as well as reactive oxygen species signaling and the immune response, both of which are essential for tissue repair and regeneration, were altered. Transcriptomic analyses of the regenerating fin confirmed that genes related to fin regeneration were transcriptionally modulated in response to microplastic exposure and that metabolic pathways were also extensively involved. In conclusion, this study demonstrated for the first time that microplastic exposure could disrupt the regenerative capacity of fish and might eventually impair their fitness in the wild.

Cerium oxide (CeO2) nanoparticles are used as in-fuel catalysts and in manufacturing processes, creating a potential for release to aquatic environments. Exposures at 1 and 10 μg/L CeO2-nanoparticles were made to assess effects during the development of river biofilm communities. Scanning transmission x-ray microscopy (STXM) indicated extensive sorption of nanoparticles to the community and co-localization with lipid moieties. Following 8 weeks of development, polycarbonate coupons were removed from the reactors and used for molecular analyses, denaturing gradient gel electrophoresis analysis (DGGE-16S rRNA) and 16S rRNA amplicon sequencing. Microscopic imaging of the biofilm communities (bacterial, photosynthetic biomass, exopolymer composition, thickness, protozoan numbers), as well as carbon substrate utilization fingerprinting was performed. There was a trend toward reduced photosynthetic biomass, but no significant effects of CeO2 exposure were found on photosynthetic and bacterial biomass or biofilm thickness. Sole carbon source utilization analyses indicated increased utilization of 10 carbon sources in the carbohydrate, carboxylic acid and amino acids categories related to CeO2 exposures; however, predominantly, no significant effects (p < 0.05) were detected. Measures of microbial diversity, lectin binding affinities of exopolymeric substances and results of DGGE analyses, indicated significant changes to community composition (p < 0.05) with CeO2 exposure. Increased binding of the lectin Canavalia ensiformis was observed, consistent with changes in bacterial-associated polymers. Whereas, no significant changes were observed in binding to residues associated with algal and cyanobacterial exopolymers. 16S rRNA amplicon sequencing of community DNA indicated changes in diversity and shifts in community composition; however, these did not trend with increasing CeO2 exposure. Counting of protozoans in the biofilm communities indicated no significant effects on this trophic level. Thus, based on biomass and functional measures, CeO2 nanoparticles did not appear to have significant effects; however, there was evidence of selection pressure resulting in significant changes in microbial community composition.

Spirotetramat, a member of tetronic and tetramic acid derivatives, is a unique insecticide and acaricide. Although the effect on zebrafish embryos lipid biosynthesis of spirotetramat has been characterized, the energy metabolism and toxic effect mechanism warrant further investigation. To investigate the toxic mechanism of spirotetramat on energy metabolism, zebrafish embryos were exposed to 100, 500 and 1000 µg/L of spirotetramat for 4 days. Untargeted metabolomics showed the synthesis and degradation of ketone pathway metabolites (R)-3-Hydroxybutyric acid and Acetoacetate significantly decreased, as well as increasing the abundance of Anti-Acetyl Coenzyme A Carboxylase protein (ACC1). Down-regulation of the genes related to ß-oxidation and the tricarboxylic acid cycle in the embryos show decreased energy metabolism. Carnitine palmitoyltransferase 1 (CPT- I) significantly decreased while citrate synthase (CS) significantly increased. Additionally, mitochondrial lesions in embryos were found using electron microscopy. Our study provides novel and robust perspectives, which show that spirotetramat treatment in embryos leads to metabolic disturbances that adversely affect cellular energy homeostasis.

In recent years, reports of plastic debris in the gastrointestinal (GI) tract of fish have been well documented in the scientific literature. This, in turn, increased concerns regarding human health exposure to microplastics through the consumption of contaminated fish. Most of the available research regarding microplastic toxicity has focused on marine organisms through direct feeding or waterborne exposures at the individual level. However, little is known about the trophic transfer of microplastics through the aquatic food chain. Freshwater zooplankton Daphnia magna (hereafter Daphnia), and the fathead minnow Pimephales promelas (FHM), are well-known model species used in standard toxicological studies and ecological risk assessments that provide a simple model for trophic transfer. The aim of this study was to assess the tissue translocation, trophic transfer, and depuration of two concentrations (20 and 2000-part ml⁻¹) of 6 μm polystyrene (PS) microplastics particles between Daphnia and FHM. Bioconcentration factors (BCF) and bioaccumulation factors (BAF) were determined. Fluorescent microscopy was used to determine the number of particles in the water media and within the organs of both species. Throughout the five days of exposure, PS particles were only found within the GI tract of both species. The BCF for Daphnia was 0.034 ± 0.005 for the low concentration and 0.026 ± 0.006 for the high concentration. The BAF for FHM was 0.094 ± 0.037 for the low concentration and 0.205 ± 0.051 for the high concentration. Between 72 and 96 h after exposure all microplastic particles were depurated from both species. The presence of food had a significant effect on the depuration of microplastic particles from Daphnia but not for FHM. Based on the low BCF and BAF values for both species, rapid depuration rates, and null translocation of microplastic particles to organs and tissues from the GI tract, there is a low probability that microplastics will bioconcentrate and bioaccumulate under environmental conditions.

Amaranth (Amaranthus mangostanus L.) has superior capability for accumulating cadmium (Cd) and has the potential to be used for phytoremediation of Cd contaminated soils. Iron (Fe) is chemically similar to Cd and may mediate Cd-induced physiological or metabolic impacts in plants. The purpose was to investigate the model of time-dependent and concentration-dependent kinetics of Cd absorption under Fe deficiency, understanding the physiological mechanism of Cd absorption in amaranth roots. The kinetic characteristics of Cd uptake by amaranth grown in Cd enriched nutritional solution with or without Fe addition and with methanol-chloroform, carbonyl cyanide 3-chlorophenylhydrazone (CCCP), and lanthanum chloride (LaCl3) were compared using 109Cd2+ isotope labeling technique. The results showed that Cd uptake was time-dependent and about 90–93% of uptake occurred during the first 150 min. The kinetics of Cd uptake showed that two stages were involved. The saturation stage fitted the Michaelis-Menten model when concentrations of Cd were lower than 12.71 μmol/L and then the absorption of Cd by roots was increased linearly during the second stage. Only linear absorption was observed with methanol-chloroform treatment while the metabolic inhibitor CCCP inhibited only the saturation absorption process, and the Ca channel inhibitor LaCl3 partially inhibited the two stages of absorption. These results indicated that the root absorption of 109Cd2+ was enhanced under Fe deficiency which induced more Fe transporters in the root cell membrane, and the Ca channel, apoplastic and symplastic pathways enhanced the Cd absorption in roots.

While extreme high temperatures are an important aspect of global warming, their effects on organisms are relatively understudied, especially in ecotoxicology. Sequential exposure to heat spikes and pesticides is a realistic scenario as both are typically transient stressors and are expected to further increase in frequency under global warming. We tested the effects of exposure to a lethal heat spike and subsequently to an ecologically relevant lethal pulse exposure of the pesticide chlorpyrifos in the larvae of mosquito Culex pipiens. The heat spike caused direct and delayed mortality, and resulted in a higher heat tolerance and activity of acetylcholinesterase, and a lower fat content in the survivors. The chlorpyrifos exposure caused mortality, accelerated growth rate, and decreased the heat tolerance and the activity of acetylcholinesterase. The preceding heat spike did not change how chlorpyrifos reduced the heat tolerance. Notably, the preceding heat spike did lower the lethal effect of the pesticide, which makes an important novel finding at the interface of ecotoxicology and global change biology, and adds a new dimension to the “climate-induced toxicant sensitivity” (CITS) concept. This may be due to both survival selection and cross-tolerance, and therefore likely a widespread phenomenon. Our results emphasize the importance of including extreme high temperatures as an important transient global change stressor in ecotoxicology.