Evaluation of the toxicity of pesticide residues on non-target organisms in the ecosystem is an important part of pesticide environmental risk assessment. Flupyradifurone is a new type of butenolide insecticide produced by Bayer, who claims it to be “low toxic” to non-target organisms in the environment. However, there is little evidence in the literature to show how flupyradifurone affects aquatic organism development. In the current study, zebrafish embryos were treated with 0.1, 0.15, and 0.2 mg/mL of flupyradifurone within 6.0–72 h past fertilization (hpf). We found that the half-lethal concentration (LC₅₀) of flupyradifurone for zebrafish embryos at 96 hpf was 0.21 mg/mL. Flupyradifurone decreases the heart rate, survival rate, and body length of zebrafish embryos. The flupyradifurone treatment also led to the failure of heart looping, and pericardial edema. Moreover, flupyradifurone increased the level of reactive oxygen species (ROS) and decreased the enzymatic catalysis of catalase (CAT) and superoxide dismutase (SOD). Alterations were induced in the transcription of apoptosis-related genes (bcl-2, bax, bax/bcl-2, p53 and caspase-9) and the heart development-related genes (gata4, myh6, nkx2.5, nppa, tbx2b, tbx5 and vmhc). In the current study, new evidences have been provided regarding the toxic effects of flupyradifurone and the risk of its residues in agricultural products and the environment.

Pyriproxyfen is a juvenile hormone analogue insecticide used worldwide. At present, the potential threat of pyriproxyfen to aquatic organism has not been well explored. In this work, the bioaccumulation, metabolic profile and toxicity of pyriproxyfen and its metabolites to zebrafish were studied, and the enantioselectivity of pyriproxyfen and the major chiral metabolites were also determined. Sixteen metabolites of pyriproxyfen in zebrafish were identified. Hydroxylation, ether linkage cleavage and oxidation in phase I metabolism, followed by sulfate and glucuronic acid conjugation. The bioconcentration factors ranged from 1175 to 1246. Hydroxylation metabolites of pyriproxyfen showed enantioselective behavior in zebrafish with enantiomer fractions (EFs) of 4′–OH– pyriproxyfen and 5″–OH– pyriproxyfen ranged from 0.50 to 0.71. Toxicological indexes including acute toxicity, joint toxicity and oxidative stress were tested. Among all the metabolites, 4′–OH– pyriproxyfen was found 2 folds more toxic to zebrafish than pyriproxyfen. (−)-Pyriproxyfen was found 2 folds more toxic than rac- and (+)-pyriproxyfen. Antagonistic effects were found in binary joint toxicity of pyriproxyfen and its hydroxylated metabolites. Pyriproxyfen and its metabolites also showed oxidative stress damage by inhibiting the activity of CAT and SOD and increasing MDA. This work provided deep insight into the metabolism and the potential risks of pyriproxyfen to aquatic organisms.

Chemicals such as triclosan are a concern because of their presence on daily products (soap, deodorant, hand sanitizers …), consequently this compound has an ubiquitous presence in the environment. Little is known about the effect of this bactericide on aquatic life. The aim of this study is to analyze triclosan exposure (24 h) to an in vitro model, zebrafish hepatocytes cell line (ZF-L), if it can be cytotoxic (mitochondrial activity, membrane stability and apoptosis) and if can activate ATP-binding cassette (ABC) proteins (activity, expression and protein/compound affinity). Triclosan was cytotoxic to hepatocytes when exposed to concentrations (1–4 mg/L). The results showed impaired mitochondria function, as well, plasma membrane rupture and an increase of apoptotic cells. We observed an ABC proteins activity inhibition in cells exposed to 0.5 and 1 mg/L. When ABCBs and ABCC2 proteins expression were analyzed, there was an increase of protein expression in both ABC proteins families on cells exposed to 1 mg/L of triclosan. On molecular docking results, triclosan and the fluorescent used as substrate (rhodamine) presented high affinity with all ABC proteins family tested, showing a greater affinity with ABCC2. In conclusion, this study showed that triclosan can be cytotoxic to ZF-L. Molecular docking indicated high affinity between triclosan and the tested pumps.

With conventional plastics posing a great threat to marine organisms, and potentially also to humans, bio-based, biodegradable plastics are being offered as an ecological solution by which to reduce the environmental impact. Inside compost facilities, bioplastics that comply with the EN 13432:2000 international standard biodegrade almost completely within 180 days. However, outside compost facilities, and specifically in marine environments, these bioplastics may have a similar effect to that of fossil-fuel based plastics. Here we investigated the effects of polyethylene terephthalate (PET) and polylactic acid (PLA) single-use cups and plates on a solitary ascidian’s biological and ecological features. Both PET and PLA microparticles reduced the fertilization rate of Microcosmus exasperatus, with no significant difference between materials. Accumulation rates in adult M. exasperatus exposed to micronized PET and PLA particles at two concentrations were similar for both the bioplastic material and the conventional plastic particles, with no significant difference between the two materials. A microbial-based digestive protocol was developed in order to recover the bioplastic material from ascidian tissue and reduce any material-loss caused by the known digestion protocols. Finally, PET plates submerged for three months in the Red Sea exhibited a significantly higher community richness and cover area in comparison to PLA plates, which did not provide a firm substrate for settlers. Indeed, coverage by the solitary ascidian Herdmania momus was significantly higher on PET plates. The current study demonstrates that discarded bioplastic products may have similar effects to those of conventional plastics on marine organism fertilization and biological accumulation, emphasizing the need to revise both the production and marketing of “biodegradable” and “compostable” plastics in order to prevent a further negative impact on ecosystems due to the mismanagement of bioplastic products.

Organic ultraviolet filters (OUVFs) are used in a wide range of manufactured products including personal care (e.g. sunscreens) and plastic items. This review summarizes the available data regarding the toxic effects of OUVFs on marine and freshwater organisms and generates the predicted no-effect concentration (PNEC) values necessary for assessing ecological risk. Through a systematic search of the literature, 89 studies were identified and ecotoxicological data extracted. Collectively, these studies described toxicity testing with 39 OUVF from 10 structural classes, with derivatives of benzophenones (49%) and camphors (16%) most studied. There was a bias towards selecting freshwater species (61%), and evaluating single OUVF effects (87%) rather than OUVF mixtures. Short-term (acute) experimentation (58%) was marginally more common than long-term (chronic) testing (42%). Reproductive, developmental, genetic, and neurological toxicity were the most commonly identified effects in aquatic organism, and were associated with molecular interactions with steroid receptors, DNA, or the production of reactive oxygen species. Species sensitivity distribution and/or assessment factors were used to calculate PNECs for 22 OUVFs and the risk quotients for 12 OUVFs. When using maximum concentrations, high risk was observed for six OUVFs in marine environments (4-methylbenzylidene-camphor, octocrylene, padimate-O, benzophenone-1, and oxybenzone, ethylhexyl-4-methoxycinnamate), and for four OUVFs in freshwater environments (ethylhexyl-4-methoxycinnamate, octocrylene, avobenzone and oxybenzone). When using median concentrations, a risk to marine environments was observed for oxybenzone. The results of this review underline that there is limited knowledge of the pathological effects of OUVFs and their metabolites in aquatic environments, and this inhibits the development of informed water-quality guidelines.

Several studies highlighted the ubiquitous presence of ibuprofen and aluminum in the aquatic environment around the world and demonstrated their potential to induce embryotoxic and teratogenic defects on aquatic species individually. Although studies that evaluate developmental alterations induced by mixtures of these pollutants are scarce; and, since environmental contamination presented in the form of a mixture of toxicants with different chemical properties and toxicity mechanisms capable of generating interactions; the objective of this study was to evaluate the developmental defects, teratogenic alterations, and oxidative stress induced by individual forms and the mixture of ibuprofen (IBU) and aluminum (Al) on zebrafish embryos. Oocytes exposed to environmentally relevant concentrations of IBU (0.1–20 μg L-1) and Al (0.01–8 mg L-1) and one binary mixture. The LC50 and EC50 were obtained to calculate the teratogenic index (TI). The IBU LC50, EC50, and TI were 8.06 μg L-1, 2.85 μg L-1 and 2.82. In contrast, Al LC50 was 5.0 mg L-1with an EC50 of 3.58 mg L-1 and TI of 1.39. The main alterations observed for individual compounds were hatching alterations, head malformation, skeletal deformities, hypopigmentation, pericardial edema, and heart rate impairment. The mixture also showed significant delays to embryonic development. Moreover, oxidative stress biomarkers of cellular oxidation and antioxidant defenses at 72 and 96 hpf significantly increased. Results show that environmentally relevant concentrations of ibuprofen (IBU), aluminum (Al), and their mixture promote a series of developmental defects, teratogenic effects, and oxidative disruption on D. rerio embryos, and the interaction of both substances altered the response. In conclusion, morphological and biochemical tests are suitable tools for assessing the health risk of aquatic wildlife by exposure to individual and mixed pollutants in freshwater bodies.

The presence of chemicals and the destruction of freshwater habitats have been addressed as one of the reasons for the decline in the amphibians’ populations worldwide. Considering the threat that these animals have been suffering in tropical regions, the present study tested if the Brazilian legislation, concerning the permissive levels of lithium and selenium in water bodies and effluents, warrants the protection of aquatic life. To do so, we assessed the metabolic, immunologic, and histopathologic alterations in liver samples of American bullfrog (Lithobates catesbeianus), at the premetamorphic stage, through biomarkers indicative of general energetic status, i.e., glucose, lipid, and protein metabolism using biochemical and histochemical approaches. The immunologic responses were assessed by the quantification of melanomacrophage centres (MMCs); the histopathologic evaluation of the liver sections was also performed. The assay was carried out over 21 days with two periods of sampling (after 7 and 21 days) to assess the effects of exposure over time. The animals were exposed to the considered safe levels of lithium (2.5 mg L⁻¹) and selenium (10 μg L⁻¹), both, isolated and mixed. The exposed animals showed alterations in glucose and lipid metabolism throughout the experiment. The intense presence of MMCs and histopathological responses are compatible with hepatotoxicity. The toxicity expressed by the employed animal model indicates that the Brazilian environmental legislation for the protection of aquatic life needs to be updated. With this study, we intend to provide data for better environmental policies and bring attention to sublethal effects triggered by the presence of contaminants in the aquatic environment.

Imidacloprid (IMI) is widely used in agriculture, and is toxic to non-target aquatic species. Quercetin (Que) is a flavonoid abundant in fruits and vegetables that exhibits anti-oxidant activity. In the present study, we treated grass carp hepatocytes (L8824) with 0.1 μM Que and/or 1 mM IMI for 24 h to explore the effect of Que on IMI-induced mitochondrial apoptosis. We found that IMI exposure enhanced reactive oxygen species (ROS) generation, inhibiting the activities of SOD, CAT and T-AOC, exacerbating the accumulation of MDA, aggravating the expression of mitochondrial apoptosis pathway (Cyt-C, BAX, Caspase9 and Caspase3) related genes and decreased the expression of anti-apoptosis gene B-cell lymphoma-2 (Bcl-2). In addition, Que and IMI co-treatment significantly restored the activity of anti-oxidant enzymes, downregulated ROS level and apoptosis rate, thereby alleviating the depletion of mitochondrial membrane potential (ΔΨm) and the expression of cytochrome c (Cyt-C), Bcl-2-associated X (BAX), and cysteinyl aspartate specific proteinases (Caspase9 and 3), increasing the Bcl-2 level. Furthermore, we elucidated that Que could inhibit the expression of phosphatase and tensin homolog deleted on chromosome 10 (PTEN), thus activating phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway to attenuate IMI-induced apoptosis. Molecular docking provides assertive evidence for the interaction between Que ligand and PTEN receptor. Consequently, these results indicate that Que effectively antagonizes IMI-induced mitochondrial apoptosis in grass carp hepatocytes via regulating the PTEN/PI3K/AKT pathway.

Microplastics are ubiquitous in the environment, with high concentrations being detected now also in river corridors and sediments globally. Whilst there has been increasing field evidence of microplastics accumulation in the guts and tissues of freshwater and marine aquatic species, the uptake mechanisms of microplastics into freshwater food webs, and the physical and geological controls on pathway-specific exposures to microplastics, are not well understood. This knowledge gap is hampering the assessment of exposure risks, and potential ecotoxicological and public health impacts from microplastics.This review provides a comprehensive synthesis of key research challenges in analysing the environmental fate and transport of microplastics in freshwater ecosystems, including the identification of hydrological, sedimentological and particle property controls on microplastic accumulation in aquatic ecosystems. This mechanistic analysis outlines the dominant pathways for exposure to microplastics in freshwater ecosystems and identifies potentially critical uptake mechanisms and entry pathways for microplastics and associated contaminants into aquatic food webs as well as their risk to accumulate and biomagnify.We identify seven key research challenges that, if overcome, will permit the advancement beyond current conceptual limitations and provide the mechanistic process understanding required to assess microplastic exposure, uptake, hazard, and overall risk to aquatic systems and humans, and provide key insights into the priority impact pathways in freshwater ecosystems to support environmental management decision making.

Sediments are capable of adsorbing and desorbing heavy metals (HMs) under various environmental conditions. This study investigated the impact of pre-set redox potential (Eh) on the release dynamics of HMs (Co, Cr, Cu, Ni, Pb, V, and Zn) from sediment in an automated biogeochemical microcosm. The release of Co, Pb, and V under reducing conditions increased that may increase the potential risks in the aquatic environment. This phenomenon could be attributed to the decrease in pH, the reductive dissolution of FeMn oxides, and the complex of HMs with dissolved organic carbon (DOC). However, the soluble Cr, Cu, Ni, and Zn decreased at redox potentials as low as −150 mV. Co, Ni, Pb, and Zn were observed in mobile fractions while Cu primarily existed in the residual fraction (indicating lithogenic source). HPI and HEI indexes showed that water quality concerning HMs would become more unsuitable for aquatic life by reducing Eh.