Urban ecosystems and remnant habitat 'islands' therein, provide important strongholds for many wildlife species including those of conservation significance. However, the persistence of these habitats can be undermined if their structure and function are too severely disrupted. Urban wetlands, specifically, are usually degraded by a monoculture of invasive vegetation, disrupted hydrology, and chronic-contamination from a suite of anthropogenic pollutants. Top predators—as bioindicators—can be used to assess and monitor the health of these ecosystems. We measured eight health parameters (e.g., parasites, wounds and scars, tail loss and body condition) in a wetland top predator, the western tiger snake, Notechis scutatus occidentalis. For three years, snakes were sampled across four wetlands along an urban gradient. For each site, we used GIS software to measure the area of different landscapes and calculate an urbanisation–landscape score. Previously published research on snake contamination informed our calculations of a metal-pollution index for each site. We used generalised linear mixed models to assess the relationship between all health parameters and site variables. We found the metal-pollution index to have the most significant association with poor body condition. Although parasitism, tail loss and wounds differed among sites, none of these parameters influenced body condition. Additionally, the suite of health parameters suggested differing health status among sites; however, our measure of contemporary landscape urbanisation was never a significant predictor variable. Our results suggest that the health of wetland predators surrounding a rapidly growing city may be offset by higher levels of environmental pollution.

This study reports the shapes, dimensional classes, types and counts of microplastics (MPs) found in 23 individuals of N. norvegicus collected from two wild populations of the Adriatic Sea (Mediterranean basin). The focus was on three different anatomical compartments (gut, hepatopancreas and tail), which were analysed separately. MPs were found in all the investigated individuals with an average of about 17 MPs/individual. Fragments were predominant over fibers with a ratio of about 3:1. The majority of MPs were in the dimensional range 50–100 μm. The predominant polymers were polyester, polyamide 6, polyvinyl chloride and polyethylene, which together constitute about 61% of all the MPs found. Fragments were more concentrated in the hepatopancreas, with no significant difference between gut and tail, while fibers were more concentrated in the gut than in the tail with hepatopancreas somehow in between. The dimensional class of the MPs influences their anatomical distribution. There were no statistical differences among individuals from the two sampling sites. Sex of the individual did not influence the level of retained MPs, while length had a very marginal effect. The information reported here contributes to understanding of the possible risks linked to human consumption of different tissues from contaminated Norway lobsters.

Bisphenol A (BPA), an endocrine-disrupting chemical that is largely produced and used in the plastics industry, causes environmental pollution and is absorbed by humans through consumption of food and liquids in polycarbonate containers. BPA exerts developmental and genetic toxicities to embryos and offsprings, but the embryotoxicity mechanism of this chemical is unclear. This study aimed to explore the toxic effect of BPA on embryonic development and elucidate its toxicity mechanism. Embryos of Xenopus laevis as a model were treated with different concentrations (0.1, 1, 10, and 20 μM) of BPA at the two-cell stage to investigate the developmental toxicity of BPA. Embryonic development and behaviors were monitored 24 h–96 h of BPA exposure. BPA concentrations greater than 1 μM exerted significant teratogenic effects on the Xenopus embryos, which showed short tail axis, miscoiled guts, and bent notochord as the main malformations. The 20 μM BPA-treated embryos were seriously damaged in all aspects and exhibited deformity, impaired behavioral ability, and tissue damage. The DNA integrity and apoptosis of the Xenopus embryos were also investigated. Exposure to BPA concentrations higher than 0.1 μM significantly induced DNA damage (p < 0.05). The 10 and 20 μM BPA-treated embryos exhibited higher levels of cleaved caspase-3 protein than the control. The ratios of bax/bcl-2 mRNA were significantly higher in the 10 μM and 20 μM-treated embryos than the ratio in the control group. Overall, data indicated that BPA can delay the early development, induce DNA damage and apoptosis, and eventually cause multiple malformations in Xenopus embryos.

Many prey organisms adaptively respond to predation risk by inducible defenses with underlying tradeoffs in resource allocation. Cyanobacterial blooms expose zooplankton to poor food conditions, affecting the herbivores’ fitness. Given the interferences on resources allocation and life history traits, poor-quality cyanobacteria are predicted to affect the adaptive predator-induced responses in zooplankton. Here, we exposed two clones (i.e., clones SH and ZJ) of the cladoceran Daphnia mitsukuri to different combinations of fish predation cues and diets containing toxic Microcystis aeruginosa (0%–30%). D. mitsukuri matured at a small size and had elongated relative tail spine as adaptive responses to fish cues. Despite the comparable tail spine defense, fish cue-induced changes in growth and reproduction in the clone SH were more pronounced than those in the clone ZJ under no M. aeruginosa. Animals accumulated microcystin in the whole body with increasing abundance of M. aeruginosa. However, the inducible enhanced tail spine allometry was not affected, resulting in unchanged tail spine defense by Daphnia under all M. aeruginosa treatments. By contrast, M. aeruginosa remarkably decreased the adaptive maturation size and the offspring number in all animals. However, the inducible reproductive effort tended to increase or remain unchanged depending on clones associated with the constant or decreased responses of the somatic growth effort under increasing M. aeruginosa. Our results suggested that toxic M. aeruginosa did not alter the resource allocation to antipredator morphological defense but affected the somatic growth and reproduction in D. mitsukuri under fish cues. The present study highlights the different effects of toxic cyanobacteria on adaptive predator-induced responses in zooplankton, promoting the understanding for the morphological defense-mediated predator–prey interactions in eutrophic environments.

The aim of this study was to investigate the long-term effects of a short exposure to natural sediments within the Athabasca oil sand formation to critical stages of embryo-larval development in fathead minnows (Pimephales promelas). Three different sediments were used: Ref sediment from the upper Steepbank River tested at 3 g/L (containing 12.2 ng/g ∑PAHs), and two bitumen-rich sediments tested at 1 and 3 g/L; one from the Ells River (Ells downstream, 6480 ng/g ∑PAHs) and one from the Steepbank River (Stp downstream, 4660 ng/g ∑PAHs). Eggs and larvae were exposed to sediments for 21 days, then transferred to clean water for a 5-month grow-out and recovery period. Larval fish had significantly decreased survival after exposure to 3 g/L sediment from Stp downstream, and decreased growth (length and weight at 16 days post hatch) in Ells and Stp downstream sediments at both 1 and 3 g/L. Decreased tail length was a sensitive endpoint in larval fish exposed to Ells and Stp downstream sediments for 21 days compared to Ref sediment. After the grow-out in clean water, all growth effects from the bitumen-containing sediments recovered, but adult fish from Stp downstream 3 g/L sediment had significant increases in jaw deformities. The study shows the potential for fish to recover from the decreased growth effects caused by sediments containing oil sands-related compounds, but that some effects of the early-life sediment exposure occur later on in adult fish.

Hydraulic fracturing to extract oil and natural gas reserves is an increasing practice in many international energy sectors. Hydraulic fracturing flowback and produced water (FPW) is a hyper saline wastewater returned to the surface from a fractured well containing chemical species present in the initial fracturing fluid, geogenic contaminants, and potentially newly synthesized chemicals formed in the fracturing well environment. However, information on FPW toxicological mechanisms of action remain largely unknown. Both cardiotoxic and respirometric responses were explored in zebrafish (Danio rerio) embryos after either an acute sediment-free (FPW-SF) or raw/sediment containing (FPW-S) fraction exposure of 24 and 48 h at 2.5% and 5% dilutions. A 48 h exposure to either FPW fraction in 24–72 h post fertilization zebrafish embryos significantly increased occurrences of pericardial edema, yolk-sac edema, and tail/spine curvature. In contrast, larval heart rates significantly decreased after FPW fraction exposures. FPW-S, but not FPW-SF, at 2.5% doses significantly reduced embryonic respiration/metabolic rates (MO2), while for 5% FPW, both fractions reduced MO2. Expression of select cardiac genes were also significantly altered in each FPW exposure group, implicating a cardiovascular system compromise as the potential cause for reduced embryonic MO2. Collectively, these results support our hypothesis that organics are major contributors to cardiac and respiratory responses to FPW exposure in zebrafish embryos. Our study is the first to investigate cardiac and respiratory sub-lethal effects of FPW exposure, demonstrating that FPW effects extend beyond initial osmotic stressors and verifies the use of respirometry as a potential marker for FPW exposure.

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.

With the growing production and use of carbon nanomaterials (CNMs), the risk of their releases to the environment has drawn much attention. However, their potential effect on soil invertebrates has not yet been systematically assessed. Herein, the toxic effects of graphene oxide (GO) on earthworms (Eisenia fetida) were thoroughly investigated. Exposure to different doses of GO (0, 5, 10, 20, and 30 g kg⁻¹) was conducted for 7, 14, 21, and 28 days. The results showed that enzymatic activity was stimulated at the early stages of exposure (7 days and 14 days) and inhibited after 14 days for catalase (CAT) and after 21 days for peroxidase (POD) and superoxide dismutase (SOD), especially at high GO doses. The content of MDA showed an increasing trend over the whole exposure period and was significantly elevated by GO from 21 days except at the dose of 5 g kg⁻¹on day 21. Lysosomal membrane stability and DNA damage presented dose- and time-dependent relationships. Graphene oxide remarkably decreased lysosomal membrane stability except at the dose of 5 g kg⁻¹ on day 7. The tail DNA%, tail length and olive tail moment increased with increasing GO dose throughout the exposure duration, reaching maximum values at the end of exposure (28 days). These findings suggest that GO induces oxidative stress and genotoxicity in Eisenia fetida, resulting in lipid peroxidation, decreased lysosomal membrane stability and DNA damage. Therefore, attention should be paid to the potential pollution and risk associated with graphene oxide application. The results can provide valuable information for environmental safety assessment of graphene nanomaterials in soil.

Systemic toxicity, particularly, developmental defects of humidifier disinfectant chemicals that have caused lung injuries in Korean children, remains to be elucidated. This study evaluated the mechanisms of the adverse effects of 5-chloro-2-methyl-4-isothiazoline-3-one/2methyl-4-isothiazolin-3-one (CMIT/MIT), one of the main biocides of the Korean tragedy, and identify the most susceptible developmental stage when exposed in early life. To this end, the study was designed to analyze several endpoints (morphology, heart rate, behavior, global DNA methylation, gene expressions of DNA methyl-transferases (dnmts) and protein profiling) in exposed zebrafish (Danio rerio) embryos at various developmental stages. The results showed that CMIT/MIT exposure causes bent tail, pericardial edema, altered heart rates, global DNA hypermethylation and significant alterations in the locomotion behavior. Consistent with the morphological and physiological endpoints, proteomics profiling with bioinformatics analysis suggested that the suppression of cardiac muscle contractions and energy metabolism (oxidative phosphorylation) were possible pivotal underlying mechanisms of the CMIT/MIT mediated adverse effects. Briefly, multi-level endpoint analysis indicated the most susceptible window of exposure to be ≤ 6 hpf followed by ≤ 48 hpf for CMIT/MIT. These results could potentially be translated to a risk assessment of the developmental exposure effects to the humidifier disinfectants.

The potential leakage from marine CO2 storage sites is of increasing concern, but few studies have evaluated the probable adverse effects on marine organisms. Fish, one of the top predators in marine environments, should be an essential representative species used for water column toxicity testing in response to waterborne CO2 exposure. In the present study, we conducted fish life cycle toxicity tests to fully elucidate CO2 toxicity mechanism effects. We tested sub-lethal and lethal toxicities of elevated CO2 concentrations on marine medaka (Oryzias melastigma) at different developmental stages. At each developmental stage, the test species was exposed to varying concentrations of gaseous CO2 (control air, 5%, 10%, 20%, and 30%), with 96 h of exposure at 0–4 d (early stage), 4–8 d (middle stage), and 8–12 d (late stage). Sub-lethal and lethal effects, including early developmental delays, cardiac edema, tail abnormalities, abnormal pigmentation, and mortality were monitored daily during the 14 d exposure period. At the embryonic stage, significant sub-lethal and lethal effects were observed at pH < 6.30. Hypercapnia can cause long-term and/or delayed developmental embryonic problems, even after transfer back to clean seawater. At fish juvenile and adult stages, significant mortality was observed at pH < 5.70, indicating elevated CO2 exposure might cause various adverse effects, even during short-term exposure periods. It should be noted the early embryonic stage was found more sensitive to CO2 exposure than other developmental stages of the fish life cycle. Overall, the present study provided baseline information for potential adverse effects of high CO2 concentration exposure on fish developmental processes at different life cycle stages in marine ecosystems.