Exploring the Hawaiian Ala Wai Watershed with Zebrafish.

The Ala Wai Canal is an artificial waterway in the tourist district of Waikiki in Honolulu, HI. Originally built to collect runoff from industrial, residential, and green spaces dedicated to recreation, the Ala Wai Canal has since experienced potent levels of toxicity due to this runoff entering the watershed and making it hazardous for both marine life and humans at current concentration, including Danio rerio (zebrafish). A community of learners at educations levels from high school to postbaccalaureate from Oahu, HI was connected through the Consortium for Increasing Research and Collaborative Learning Experiences (CIRCLE) distance research program. This team conducted research with an Investigator and team from Mayo Clinic in Rochester, MN, with the Ala Wai Canal as its primary subject. Through CIRCLE, research trainees sent two 32 oz bottles of Ala Wai- acquired water to a partnered laboratory at the Mayo Clinic in which zebrafish embryos were observed at differing concentrations of the sampled water against a variety of developmental and behavioral assays. Research trainees also created atlases of developmental outcomes in zebrafish following exposure to environmental toxins and tables of potential pesticide contaminants to enable the identification of the substances linked to structural defects and enhanced stress during Ala Wai water exposure experiments.

Microplastics' toxic effects and influencing factors on microorganisms in biological wastewater treatment units.

Prior to entering the water body, microplastics (MPs) are mostly collected at the sewage treatment plant and the biological treatment unit is the sewage treatment facility's central processing unit. This review aims to present a comprehensive analysis of the detrimental impacts of MPs on the biological treatment unit of a sewage treatment plant and it covers how MPs harm the effluent quality of biological treatment processes. The structure of microbial communities is altered by MPs presence and additive release, which reduces functional microbial activity. Extracellular polymers, oxidative stress, and enzyme activity are explored as micro views on the harmful mechanism of MPs on microorganisms, examining the toxicity of additives released by MPs and the harm caused to microorganisms by harmful compounds that have been adsorbed in the aqueous environment. This article offers a theoretical framework for a thorough understanding of the potential problems posed by MPs in sewage treatment plants and suggests countermeasures to mitigate those risks to the aquatic environment.

Effects of 2,4-dichlorophenol on non-specific immunity, histopathological lesions, and redox balance in African Catfish, clarias gariepinus (Burchell, 1822).

The toxic effects of 2, 4-dichlorophenol (2, 4-DCP) on aquatic organisms are well-established; however, the details regarding the mechanisms underlying the toxicity, especially immunotoxicity are poorly understood. Consequently, the aim of this study was to investigate the histopathologic, oxidative stress and immunotoxic effects attributed to exposure to sublethal concentrations of 2,4-DCP in the African catfish, Clarias gariepinus. Juvenile C. gariepinus were exposed to 0.4, 0.8, or 1.6 mg/L 2, 4-DCP for 28 days after which blood and head kidney were extracted for the determination of various nonspecific innate immune parameters while the liver was excised for histopathology examination and measurement of oxidative stress biomarkers. Control fish were maintained in water spiked 10 µL/L ethanol, representing the solvent control. A significant increase was noted in the activities of lactate dehydrogenase and superoxide dismutase as well as in levels of lipid peroxidation and DNA fragmentation in a dose-dependent manner, with higher adverse effects observed at the highest concentration tested (1.6 mg/L). The total white blood cells (WBC) count was significantly elevated in fish exposed to 2,4-DCP compared to control. Myeloperoxidase content was decreased significantly in fish exposed to 2,4-DCP especially at the highest concentration (1.6 mg/L) compared to controls. The respiratory burst activity did not differ markedly amongst groups. Histopathological lesions noted included edema, leucocyte infiltration, and depletion of hemopoietic tissue in the head kidney of exposed fish. There was significant upregulation in the mRNA expression of tumor necrosis factor (TNF-α) and heat shock protein 70 (HSP 70) but downregulation of major histocompatibility complex 2 (MHC 2) in exposed fish. Data demonstrated that exposure to 2,4-DCP resulted in histopathological lesions, oxidative stress, and compromised immune system in C. gariepinus.

Poly- and perfluoroalkyl substances (PFASs) in amphibians and reptiles - exposure and health effects.

Poly- and perfluoroalkyl substances (PFASs) are commonly used in various industries and everyday products, including clothing, electronics, furniture, paints, and many others. PFASs are primarily found in aquatic environments, but also present in soil, air and plants, making them one of the most important and dangerous pollutants of the natural environment. PFASs bioaccumulate in living organisms and are especially dangerous to aquatic and semi-aquatic animals. As endocrine disruptors, PFASs affect many internal organs and systems, including reproductive, endocrine, nervous, cardiovascular, and immune systems. This manuscript represents the first comprehensive review exclusively focusing on PFASs in amphibians and reptiles. Both groups of animals are highly vulnerable to PFASs in the natural habitats. Amphibians and reptiles, renowned for their sensitivity to environmental changes, are often used as crucial bioindicators to monitor ecosystem health and environmental pollution levels. Furthermore, the decline in amphibian and reptile populations worldwide may be related to increasing environmental pollution. Therefore, studies investigating the exposure of amphibians and reptiles to PFASs, as well as their impacts on these organisms are essential in modern toxicology. Summarizing the current knowledge on PFASs in amphibians and reptiles in a single manuscript will facilitate the exploration of new research topics in this field. Such a comprehensive review will aid researchers in understanding the implications of PFASs exposure on amphibians and reptiles, guiding future investigations to mitigate their adverse effects of these vital components of ecosystems.

Biofilm enhances the interactive effects of microplastics and oxytetracycline on zebrafish intestine.

The enhanced adsorption of pollutants on biofilm-developed microplastics has been proved in many studies, but the ecotoxicological effects of biofilm-developed microplastics on organisms are still unclear. In this study, adult zebrafish were exposed to original microplastics, biofilm-developed microplastics, original microplastics absorbed with oxytetracycline (OTC), and biofilm-developed microplastics absorbed with OTC for 30 days. The intestinal histological damage, intestinal biomarker response, gut microbiome and antibiotic resistance genes (ARGs) profile of zebrafish were measured to explore the roles of biofilm in the effects of microplastics. The results showed that biofilm-developed microplastics significantly increased the number of goblet cells in intestinal epithelium compared with the control group. The biofilm-developed microplastics also induced the oxidative response in the zebrafish intestines, and biofilm changed the response mode in the combined treatment with OTC. Additionally, the biofilm-developed microplastics caused intestinal microbiome dysbiosis, and induced the abundance of some pathogenic genera increasing by several times compared with the control group and the original microplastics treatments, regardless of OTC adsorption. Furthermore, the abundance of ARGs in biofilm-developed microplastics increased significantly compared with the control and the original microplastic treatments. This study emphasized the significant influence and unique role of biofilm in microplastic studies.

Interactive effects between water temperature, microparticle compositions, and fiber types on the marine keystone species Americamysis bahia.

Recently, there has been an increasing emphasis on examining the ecotoxicological effects of anthropogenic microparticles (MPs), especially microplastic particles, and related issues. Nevertheless, a notable deficiency exists in our understanding of the consequences on marine organisms, specifically in relation to microfibers and the combined influence of MPs and temperature. In this investigation, mysid shrimp (Americamysis bahia), an important species and prey item in estuarine and marine food webs, were subjected to four separate experimental trials involving fibers (cotton, nylon, polyester, hemp; 3 particles/ml; approximately 200 µm in length) or fragments (low-density Polyethylene: LDPE, polylactic acid: PLA, and their leachates; 5, 50, 200, 500 particles/ml; 1-20 µm). To consider the effects in the context of climate change, three different temperatures (22, 25, and 28 °C) were examined. Organismal growth and swimming behavior were measured following exposure to fragments and microfibers, and reactive oxygen species and particle uptake were investigated after microfiber exposure. To simulate the physical characteristics of MP exposure, such as microfibers obstructing the gills, we also assessed the post-fiber-exposure swimming behavior in an oxygen-depleted environment. Data revealed negligible fragment, but fiber exposure effects on growth. PLA leachate triggered higher activity at 25 °C and 28 °C; LDPE exposures led to decreased activity at 28 °C. Cotton exposures led to fewer behavioral differences compared to controls than other fiber types. The exposure to hemp fibers resulted in significant ROS increases at 28 °C. Microfibers were predominantly located within the gastric and upper gastrointestinal tract, suggesting extended periods of residence and the potential for obstructive phenomena over the longer term. The combination of increasing water temperatures, microplastic influx, and oxidative stress has the potential to pose risks to all components of marine and aquatic food webs.

Transcriptome analyses in juvenile yellow perch (Perca flavescens) exposed in vivo to clothianidin and chlorantraniliprole: Possible sampling bias.

The St. Lawrence River is an important North American waterway that is subject to anthropogenic pressures including intensive urbanization, and agricultural development. Pesticides are widely used for agricultural activities in fields surrounding the yellow perch (Perca flavescens) habitat in Lake St. Pierre (Quebec, Canada), a fluvial lake of the river where the perch population has collapsed. Clothianidin and chlorantraniliprole were two of the most detected insecticides in surface waters near perch spawning areas. The objectives of the present study were to evaluate the transcriptional and biochemical effects of these two pesticides on juvenile yellow perch exposed for 28d to environmental doses of each compound alone and in a mixture under laboratory/aquaria conditions. Hepatic mRNA-sequencing revealed an effect of chlorantraniliprole alone (37 genes) and combined with clothianidin (251 genes), but no effects of clothianidin alone were observed in perch. Dysregulated genes were mostly related to circadian rhythms and to Ca2+ signaling, the latter effect has been previously associated with chlorantraniliprole mode of action in insects. Moreover, chronic exposure to clothianidin increased the activity of acetylcholinesterase in the brain of exposed fish, suggesting a potential non-target effect of this insecticide. Further analyses of three clock genes by qRT-PCR suggested that part of the observed effects of chlorantraniliprole on the circadian gene regulation of juvenile perch could be the result of time-of-day of sacrifice. These results provide insight into biological effects of insecticides in juvenile perch and highlight the importance of considering the circadian rhythm in experimental design and results analyses.

Comparative evaluation of SPE methods for biotoxicity assessment of water and wastewater: Linkage between chemical extracting efficiency and biotoxicity outcome.

Biotoxicity assessment results of environmental waters largely depend on the sample extraction protocols that enrich pollutants to meet the effect-trigger thresholds of bioassays. However, more chemical mixture does not necessarily translate to higher combined biotoxicity. Thus, there is a need to establish the link between chemical extracting efficiency and biotoxicity outcome to standardize extraction methods for biotoxicity assessment of environmental waters. This study compares the performance of five different extraction phases in solid phase extraction (SPE), namely HLB, HLB+Coconut, C18 cartridge, C18 disk and Strata-X, and evaluated their chemical extracting efficiencies and biotoxicity outcomes. We quantitatively assessed cytotoxicity, acute toxicity, genotoxicity, estrogenic activity, and neurotoxicity of the extracts using in vitro bioassays and characterized the chemical extracting efficiencies of the SPE methods through chemical recoveries of 23 model compounds with different polarities and total organic carbon. Using Pareto ranking, we identified HLB+Coconut as the optimal SPE method, which exhibited the highest level of water sample biotoxicity and recovered the most chemicals in water samples. We found that the biotoxicity outcomes of the extracted water samples significantly and positively correlated with the chemical extracting efficiencies of the SPE methods. Moreover, we observed synchronous changing patterns in biotoxicity outcome and chemical extracting efficiencies in response to increasing sample volumes per cartridge (SVPC) during SPE. Our findings underscore that higher chemical extracting efficiency of SPE corresponds to higher biotoxicity outcome of environmental water samples, providing a scientific basis for standardization of SPE methods for adequate assessment of biotoxicities of environmental waters.

The combined neurotoxicity of DBP and nano-TiO2 in embryonic zebrafish (Danio rerio) revealed by oxidative activity, neuro-development genes expression and metabolomics changes.

Dibutyl phthalate (DBP) is a commonly used plasticizer that is frequently detected in water samples due to its widespread use. Titanium dioxide nanoparticles (n-TiO2) have been found to enhance the harmful effects of organic contaminants by increasing their bioavailability in aquatic environments. However, the combined toxic effects of DBP and n-TiO2 on aquatic organisms remain unclear. This study aimed to investigate the neurotoxicity of DBP and n-TiO2 synergistic exposure during the early life stage of zebrafish. The results of the study revealed that co-exposure of DBP and n-TiO2 led to an increase in deformities and a significant reduction in the active duration of zebrafish larvae. Furthermore, the co-exposure of DBP and n-TiO2 resulted in elevated levels of oxidative stress and altered gene expression related to neurodevelopment and apoptosis. Notably, n-TiO2 exacerbated the oxidative damage and apoptosis induced by DBP alone exposure. Additionally, co-exposure of the 1.0 mg/L DBP and n-TiO2 significantly affected the expression of genes associated with neurodevelopment. Moreover, disturbances in amino acid metabolism and interference with lipid metabolism were observed as a result of DBP and n-TiO2 co-exposure. In general, n-TiO2 aggravated the neurotoxicity of DBP in the early life stage of zebrafish by increasing oxidative stress, apoptosis, and disrupting amino acid synthesis and lipid metabolism. Therefore, it is essential to consider the potential risks caused by DBP and nanomaterials co-existence in the aquatic environment.

The impact of chronic and acute problems on sea turtles: The consequences of the oil spill and ingestion of anthropogenic debris on the tropical semi-arid coast of Ceará, Brazil.

Sea turtle mortality is often related to materials that reach the coast from different anthropic activities worldwide. This study aimed to investigate whether sea turtle mortality was related to older marine problems, such as solid waste, or one of the largest oil spill accidents on the Brazilian coast, that occurred in 2019. We posed three questions: 1) Are there solid residues in the digestive tract samples, and which typology is the most abundant? 2) Can meso­ and macro-waste marine pollutants cause mortality? 3) Is the dark material found really oil? A total of 25 gastrointestinal content (GC) samples were obtained, of which 22 ingested waste of anthropogenic origin and 18 were necropsied. These 22 samples were obtained during or after the 2019 oil spill, of which 17 specimens were affected, making it possible to suggest oil ingestion with the cause of death in the animals that could be necropsied. Macroscopic data showed that the most abundant solid waste was plastic (76.05 %), followed by fabrics (12.18 %) and oil-like materials. However, chemical data confirmed only three specimens with oil levels ranging from remnants to high. It was possible to infer possible causes of death in 16 of the total 18 necropsied cases: Most deaths were due to respiratory arrest (62.5 %), followed by pulmonary edema (12.5 %), cachexia syndrome (12.5 %), circulatory shock (6.25 %), and head trauma (6.25 %), which may have been caused by contact with solid waste, oil, or both. The study showed that not all dark material found in the GCs of turtles killed in oiled areas is truly oil, and in this sense, a chemical analysis step to prove the evidence of oil must be added to international protocols.

A study on the subchronic toxicity of triclocarban to the early-life development of oryzias melastigma and focused on the analysis of osmoregulatory regulation mechanisms.

Triclocarban (TCC), a novel antimicrobial agent found in personal care products, has been extensively detected in marine environments. However, research on the toxic effects of TCC on marine organisms remains inadequate. This study delved into the subchronic toxic effects of TCC on the early life stages of marine medaka (Oryzias melastigma, O. melastigma), revealing that TCC could reduce embryo heart rate and hatching rate while diminishing the survival rate of larvae. Biomarker assays indicated that TCC could inflict damage on the embryos' antioxidant and nervous systems. Transcriptomic analysis suggested that TCC could impact cell growth, reproduction, and various life processes, activating cancer signaling pathways, increasing the likelihood of cancer, and exerting toxic effects on the immune and osmoregulatory systems. To validate and enhance our understanding of TCC's unique toxic impact on the osmoregulatory system of O. melastigma, we conducted homology modeling and molecular docking analyses on the protein involved in osmoregulation. The study intuitively revealed the potential binding affinity of TCC to sodium/potassium-transporting ATPase subunit alph (ATP1A1), indicating its ability to disrupt osmotic balance in marine fish by affecting this target protein. In summary, the results of this study will further enhance our comprehension of the potential toxic effects and mechanisms of TCC on the early stages of marine fish, with a specific focus on its unique toxic effects in osmoregulation.

Ocean acidification impact on the uptake of trace elements by mussels and their biochemical effects.

This study delves into the intricate interplay between ocean acidification (OA), metal bioaccumulation, and cellular responses using mussels (Mytilus galloprovincialis) as bioindicators. For this purpose, environmentally realistic concentrations of isotopically labelled metals (Cd, Cu, Ag, Ce) were added to investigate whether the OA increase would modify metal bioaccumulation and induce adverse effects at the cellular level. The study reveals that while certain elements like Cd and Ag might remain unaffected by OA, the bioavailability of Cu and Ce could potentially escalate, leading to amplified accumulation in marine organisms. The present findings highlight a significant rise in Ce concentrations within different mussel organs under elevated pCO2 conditions, accompanied by an increased isotopic fractionation of Ce (140/142Ce), suggesting a heightened potential for metal accumulation under OA. The results suggested that OA influenced metal accumulation in the gills of mussels. Conversely, metal accumulation in the digestive gland was unaffected by OA. The exposure to both trace metals and OA affects the biochemical responses of M. galloprovincialis, leading to increased metabolic capacity, changes in energy reserves, and alterations in oxidative stress markers, but the specific effects on other biomarkers (e.g., lipid peroxidation, some enzymatic responses or acetylcholinesterase activity) were not uniform, suggesting complex interactions between the stressors and the biochemical pathways in the mussels.

Transcriptomics-based analysis reveals the nephrotoxic effects of triphenyltin (TPT) on SD rats by affecting RAS, AQPs and lipid metabolism.

Triphenyltin (TPT) is a class of organotin compounds that are extensively used in industry and agriculture. They have endocrine-disrupting effects and cause severe environmental contamination. Pollutants may accumulate in the kidneys and cause pathological complications. However, the mechanism of TPT's toxicological effects on the kidney remains unclear. This study aimed to investigate the toxic effects and mechanism of action of TPT exposure on renal impairment in rats. Male SD rats were divided into four groups: the Ctrl group (control group), TPT-L group (0.5 mg/kg/d), TPT-M group (1 mg/kg/d), and TPT-H group (2 mg/kg/d). After 28 days of exposure to TPT, we observed the morphology and structure of kidney tissue using HE, PASM, and Masson staining. We also detected serum biochemical indexes, performed transcriptome sequencing of rat kidney tissue using RNA-seq. Furthermore, protein expression levels were measured through immunohistochemistry and gene expression levels were determined using RT-qPCR. The study results indicated a decrease in kidney weight and relative kidney weight after 28 days of exposure to TPT. Additionally, TPT caused damage to kidney structure and function, as evidenced by HE staining, PASM staining, and serum biochemical tests. Transcriptomics identified 352 DEGs, and enrichment analyses revealed that TPT exposure primarily impacted the renin-angiotensin system (RAS). The expression levels of water channel proteins were reduced, and the expression levels of RAS and lipid metabolism-related genes (Mme, Ace, Fasn, Cyp4a8, Cpt1b and Ppard) were significantly decreased in the TPT-treated group. In summary, exposure to TPT may impair renal structure and function in rats by affecting RAS, AQPs, and lipid metabolism.

Toxic interactions at the physiological and biochemical levels of green algae under stress of mixtures of three azole fungicides.

Assessing the interactions between environmental pollutants and these mixtures is of paramount significance in understanding their negative effects on aquatic ecosystems. However, existing research often lacks comprehensive investigations into the physiological and biochemical mechanisms underlying these interactions. This study aimed to reveal the toxic mechanisms of cyproconazole (CYP), imazalil (IMA), and prochloraz (PRO) and corresponding these mixtures on Auxenochlorella pyrenoidosa by analyzing the interactions at physiological and biochemical levels. Higher concentrations of CYP, IMA, and PRO and these mixtures resulted in a reduction in chlorophyll (Chl) content and increased total protein (TP) suppression, and malondialdehyde (MDA) content exhibited a negative correlation with algal growth. The activity of catalase (CAT) and superoxide dismutase (SOD) decreased with increasing azole fungicides and their mixture concentrations, correlating positively with growth inhibition. Azole fungicides induced dose-dependent apoptosis in A. pyrenoidosa, with higher apoptosis rates indicative of greater pollutant toxicity. The results revealed concentration-dependent toxicity effects, with antagonistic interactions at low concentrations and synergistic effects at high concentrations within the CYP-IMA mixtures. These interactions were closely linked to the interactions observed in Chl-a, carotenoid (Car), CAT, and cellular apoptosis. The antagonistic effects of CYP-PRO mixtures on A. pyrenoidosa growth inhibition can be attributed to the antagonism observed in Chl-a, Chl-b, Car, TP, CAT, SOD, and cellular apoptosis. This study emphasized the importance of gaining a comprehensive understanding of the physiological and biochemical interactions within algal cells, which may help understand the potential mechanism of toxic interaction.

Transcriptomic profile in carbendazim-induced developmental defects in zebrafish (Danio rerio) embryos/larvae.

Carbendazim is a widely used fungicide to protect agricultural and horticultural crops against a wide array of fungal species. Published reports have shown that the wide usage of carbendazim resulted in reprotoxicity, carcinogenicity, immunotoxicity, and developmental toxicity in mammalian models. However, studies related to the developmental toxicity of carbendazim in aquatic organisms are not clear. To address this gap, an attempt was made by exposing zebrafish embryos to carbendazim (800 µg/L) and assessing the phenotypic and transcriptomic profile at different developmental stages [24 hour post fertilization (hpf), 48 hpf, 72 hpf and 96 hpf). At 48 hpf, phenotypic abnormalities such as delay in hatching rate, deformed spinal axial curvature, and pericardial edema were observed in zebrafish larvae over its respective controls. At 72 hpf, exposure of zebrafish embryos exposed to carbendazim resulted in scoliosis; however, unexposed larvae did not exhibit signs of scoliosis. Interestingly, the transcriptomic analysis revealed a total of 1253 DEGs were observed at selected time points, while unique genes at 24 hpf, 48 hpf, 72 hpf and 96 hpf was found to be 76.54 %, 61.14 %, 92.98 %, and 68.28 %, respectively. Functional profiling of downregulated genes revealed altered transcriptomic markers associated with phototransduction (24 hpf and 72 hpf), immune system (48 hpf), and SNARE interactions in the vesicular pathway (96 hpf). Whereas functional profiling of upregulated genes revealed altered transcriptomic markers associated with riboflavin metabolism (24 hpf), basal transcription factors (48 hpf), insulin signaling pathway (72 hpf), and primary bile acid biosynthesis (96 hpf). Taken together, carbendazim-induced developmental toxicity could be ascribed to pleiotropic responses at the molecular level, which in turn might reflect phenotypic abnormalities.

Toxicological assessment of bromoxynil and 2-methyl-4-chlorophenoxyacetic acid herbicide in combination on Cirrhinus mrigala using multiple biomarker approach.

The widespread application of herbicides raises concerns about their impact on non-target aquatic organisms. This study aimed to evaluate the toxicity of a commercially available herbicide formulation containing Bromoxynil+MCPA (2-Methyl-4-chlorophenoxyacetic acid) on Cirrhinus mrigala (economically significant fish). A total of 210 juvenile fish were subjected to a triplicate experimental setup, with 70 fish allocated to each replicate, exposed to seven different concentrations of herbicide: 0 mg/L, 0.133 mg/L, 0.266 mg/L, 0.4 mg/L, 0.5 mg/L, 0.66 mg/L, and 0.8 mg/L, respectively, for a duration of 96 h. The median lethal concentration (LC50) was determined to be 0.4 mg/L. Significant hematological alterations were observed, including decreases in RBC counts, hemoglobin, hematocrit, and lymphocyte counts, along with an increase in erythrocyte indices. Biochemical analysis revealed elevated levels of neutrophils, WBCs, bilirubin, urea, creatinine, ALT, AST, ALP, and glucose in treated groups. Morphological abnormalities in erythrocytes and histopathological changes in gills, liver, and kidneys were noted. Pathological alterations in gills, liver and kidneys including epithelial cell uplifting, lamellar fusion, hepatolysis, and renal tubule degeneration were observed. Oxidative stress biomarkers such as TBARS (Thiobarbituric Acid Reactive Substance), ROS (Reactive Oxygen Species), and POD (Peroxides) activity increased, while antioxidant enzymatic activities decreased as toxicant doses increased from low to high concentrations. The study reveals that Bromoxynil+MCPA significantly disrupts physiological and hematobiochemical parameters in Cirrhinus mrigala, which highlights the substantial aquatic risks. In conclusion, the herbicide formulation induced significant alterations in various fish biomarkers, emphasizing their pivotal role in assessing the environmental impact of toxicity. This multi-biomarker approach offers valuable insights regarding the toxicological effects, thereby contributing substantially to the comprehensive evaluation of environmental hazards.

Toxic mechanisms of imazalil, azoxystrobin and their mixture to hook snout carp (Opsariichthys bidens).

While combinations of pesticides better represent actual conditions within aquatic ecosystems, the specific toxic effects of these combinations have not been determined yet. The objective of this research was to assess the combined impact of imazalil and azoxystrobin on the hook snout carp (Opsariichthys bidens) and delve into the underlying causes. Our findings indicated that the 4-day LC50 value for imazalil (1.85 mg L-1) was greater than that for azoxystrobin (0.90 mg L-1). When imazalil and azoxystrobin were combined, they presented a heightened effect on the species. Enzyme activities like SOD, CAT, GST, and CarE, along with androgen and estrogen levels, displayed marked differences in most single and combined treatments in comparison to the baseline group. Moreover, four genes (mn-sod, cu-sod, il-1, and esr) related to oxidative stress, immunity, and the endocrine system exhibited more pronounced expression changes when exposed to combined pesticides rather than individual ones. Our tests revealed that the combined use of imazalil and azoxystrobin had more detrimental effect on aquatic vertebrates than when evaluated individually. This finding suggested that future ecological hazard analyses based only on individual tests might not sufficiently safeguard our aquatic ecosystems.

The number of test organisms might influence the toxicity evaluation of hydrophobic micropollutants.

Evaluating the toxicity of micropollutants forms the basis for understanding their potential risks to the ecosystem and/or human health. To accurately evaluate the toxicity of micropollutants in toxicity tests, many factors have been carefully considered, while the impact of the number of test organisms on toxicity results has rarely been taken into account. In this study, the role of the organism number on the developmental toxicity of five micropollutants was investigated using embryos of the marine polychaete Platynereis dumerilii. The toxicity of hydrophobic micropollutants was found to decrease significantly with increasing the number of embryos used in the test. A quantitative model was developed to better describe how the number of embryos affected developmental toxicity. The model showed a satisfactory fit to the raw data in all scenarios tested. The intrinsic half-maximal effective concentration EC50,int was then determined using the model. For a given compound, the EC50,int was a stable parameter that did not depend on the number of test embryos and thus provided an indication of the intrinsic toxicity of the compounds tested. Compared with the EC50 values determined with the commonly used embryo number (around 120), the EC50,int values of all tested hydrophobic micropollutants were lower. The more hydrophobic the compounds tested, the more pronounced the reduction in toxicity. This suggested that hydrophobic micropollutants could be more toxic than reported in the literature. Some suggestions were also made to eliminate the effect of the number of organisms used in the toxicity evaluation.

Enhanced neurotoxic effect of PCB-153 when co-exposed with polystyrene nanoplastics in zebrafish larvae.

Nanoplastics (NPs) and persistent organic pollutants such as polychlorinated biphenyls (PCBs) are ubiquitous aquatic pollutants. The coexistence of these pollutants in the environment emphasises the need to study their combined toxicity. NPs can cross biological membranes and act as vectors for other pollutants, whereas PCBs are known for their ability to bioaccumulate and biomagnify. The present work aimed to study the combined toxicity of polystyrene NPs and PCB-153 using physiological (development, heart rate, respiration), behavioural (swimming behaviour) and molecular (transcriptome) endpoints in zebrafish larvae. The results show that exposure to NPs, PCB and their mixture significantly affected the development and respiration in zebrafish larvae. Larvae co-exposed to NPs and PCB exhibited significant hyperlocomotion, whereas no such effect was observed after exposure to NPs or PCB alone. The transcriptomic results revealed that NPs exposure significantly affected several pathways associated with DNA compaction and nucleosome assembly, whereas PCB exposure significantly affected critical neurogenic pathways. In contrast, co-exposure to NPs and PCB generated multi-faceted toxicity and suppressed neurobehavioural, immune-related and detoxification pathways. The study highlights the complex interplay between NPs and PCBs, and documents how the two toxicants in combination give a stronger effect than the single toxicants alone. Understanding the mixture toxicity of these two pollutants is important to assess the environmental risks and developing effective management strategies, ultimately safeguarding ecosystems and human health.

Plants buffer some of the effects of a pair of cadmium-exposed zebrafish on the un-exposed majority.

Certain individuals have a disproportionate effect on group responses. Characteristics may include susceptibility to pollutants, such as cadmium (Cd), a potent trace metal. Here, we show how a pair of Cd-exposed individuals can impact the behavior of unexposed groups. We used behavioral assessments to characterize the extent of the effects of the Cd-exposed individuals on group boldness, cohesion, foraging, activity, and responses to plants. We found that groups with a pair of Cd-exposed fish remained closer to novel stimuli and plants than did groups with untreated (control) fish. The presence of plants reduced Cd-induced differences in shoal cohesion and delays feeding in male shoals. Shoals with Cd- and water-treated fish were equally active. The results suggest that fish acutely exposed to environmentally relevant Cd concentrations can have profound effects on the un-exposed majority. However, the presence of plants may mitigate the effects of contaminants on some aspects of social behavior.