Global warming both reduces global temperature variance and increases the frequency of extreme weather events. In response to these ambient perturbations, animals may be subject to trans- or intra-generational phenotype modifications that help to maintain homeostasis and fitness. Here, we show how temperature-associated transgenerational plasticity in tilapia affects metabolic trade-offs during developmental stages under a global warming scenario. Tropical tilapia reared at a stable temperature of 27 °C for a decade were divided into two temperature-experience groups for four generations of breeding. Each generation of one group was exposed to a single 15 °C cold-shock experience during its lifetime (cold-experienced CE group), and the other group was kept stably at 27 °C throughout their lifetimes (cold-naïve CN group). The offspring at early life stages from the CE and CN tilapia were then assessed by metabolomics-based profiling, and the results implied that parental cold-experience might affect energy provision during reproduction. Furthermore, at early life stages, progeny may be endowed with metabolic traits that help the animals cope with ambient temperature perturbations. This study also applied the feature rescaling and Uniform Manifold Approximation and Projection (UMAP) to visualize metabolic dynamics, and the result could effectively decompose the complex omic-based datasets to represent the energy trade-off variability. For example, the carbohydrate to free amino acid conversion and enhanced compensatory features appeared to be hypothermic-responsive traits. These multigenerational metabolic effects suggest that the tropical ectothermic tilapia may exhibit transgenerational phenotype plasticity, which could optimize energy allocation under ambient temperature challenges. Knowledge about such metabolism-related transgenerational plasticity effects in ectothermic aquatic species may allow us to better predict how adaptive mechanisms will affect fish populations in a climate with narrow temperature variation and frequent extreme weather events.

Seed coating (‘seed treatment’) is the leading delivery method of neonicotinoid insecticides in major crops such as soybean, wheat, cotton and maize. However, this prophylactic use of neonicotinoids is widely discussed from the standpoint of environmental costs. Growing soybean plants from neonicotinoid-coated seeds in field, we demonstrate that soybean aphids (Aphis glycines) survived the treatment, and excreted honeydew containing neonicotinoids. Biochemical analyses demonstrated that honeydew excreted by the soybean aphid contained substantial concentrations of neonicotinoids even one month after sowing of the crop. Consuming this honeydew reduced the longevity of two biological control agents of the soybean aphid, the predatory midge Aphidoletes aphidimyza and the parasitic wasp Aphelinus certus. These results have important environmental and economic implications because honeydew is the main carbohydrate source for many beneficial insects in agricultural landscapes.

Pharmaceuticals and personal care products (PPCPs) have been widely distributed and posed ecotoxicological risks in the aquatic environment. This study aims to evaluate the toxic effects after chronic exposure to PPCPs mixture at the environment relevant concentrations (ERCs). Our results indicated that PPCPs induced serious metabolic effects by disturbing the carbohydrate and lipid metabolism pathways. Chronic exposure caused a significant reduction in the hepatosomatic index (HSI), the gut weight ratios, and histological alterations in liver and gut tissues. Further, exposure to the combined PPCPs disrupted the carbohydrate metabolism via significant upregulation of hk1, gk, pck1, and insr genes. The lipid metabolism was affected with higher ppars expression levels that increased the fatty acid β-oxidation and ultimately decreased the lipidogenesis. Moreover, the altered responses of the insulin growth factor (IGF) pathway more in male gut tissue than that of female revealed sex-dependent disturbance in the gut homeostasis induced by PPCPs mixture. In conclusion, chronic exposure to PPCPs mixtures at ERCs can induce developmental effects and metabolic dysfunction in both male and female fish. The consumption and environmental disposal of these PPCPs should be regulated to ensure ecological health and environmental safety.

Most microplastics are expected to sink and end up in marine sediments. However, very little is known concerning their potential impact on sediment-dwelling organisms. We studied the long-term impact of microplastic exposure on two sediment-dwelling bivalve species. Ennucula tenuis and Abra nitida were exposed to polyethylene microparticles at three concentrations (1; 10 and 25 mg/kg of sediment) for four weeks. Three size classes (4–6; 20–25 and 125–500 μm) were used to study the influence of size on microplastic ecotoxicity. Microplastic exposure did not affect survival, condition index or burrowing behaviour in either bivalve species. However, significant changes in energy reserves were observed. No changes were observed in protein, carbohydrate or lipid contents in E. tenuis, with the exception of a decrease in lipid content for one condition. However, total energy decreased in a dose-dependent manner for bivalves exposed to the largest particles. To the contrary, no significant changes in total energy were observed for A. nitida, although a significant decrease of protein content was observed for individuals exposed to the largest particles, at all concentrations. Concentration and particle size significantly influenced microplastic impacts on bivalves, the largest particles and higher concentrations leading to more severe effects. Several hypotheses are presented to explain the observed modulation of energy reserves, including the influence of microplastic size and concentration. Our results suggest that long-term exposure to microplastics at environmentally relevant concentrations can impact marine benthic biota.

Mercury (Hg) is recognized as a dangerous contaminant due to its bioaccumulation and biomagnification within trophic levels, leading to serious health risks to aquatic biota. Therefore, there is an urgent need to unravel the mechanisms underlying the toxicity of Hg. To this aim, a metabolomics approach based on protonic nuclear magnetic resonance (1H NMR), coupled with chemometrics, was performed on the gills of wild golden grey mullets L. aurata living in an Hg-polluted area in Ria de Aveiro (Portugal). Gills were selected as target organ due to their direct and continuous interaction with the surrounding environment. As a consequence of accumulated inorganic Hg and methylmercury, severe changes in the gill metabolome were observed, indicating a compromised health status of mullets. Numerous metabolites, i.e. amino acids, osmolytes, carbohydrates, and nucleotides, were identified as potential biomarkers of Hg toxicity in fish gills. Specifically, decrease of taurine and glycerophosphocholine, along with increased creatine level, suggested Hg interference with the ion-osmoregulatory processes. The rise of lactate indicated anaerobic metabolism enhancement. Moreover, the increased levels of amino acids suggested the occurrence of protein catabolism, further supported by the augmented alanine, involved in nitrogenous waste excretion. Increased level of isobutyrate, a marker of anoxia, was suggestive of onset of hypoxic stress at the Hg contaminated site. Moreover, the concomitant reduction in glycerophosphocholine and phosphocholine reflected the occurrence of membrane repair processes. Finally, perturbation in antioxidant defence system was revealed by the depletion in glutathione and its constituent amino acids. All these data were also compared to the differential Hg-induced metabolic responses previously observed in liver of the same mullets (Brandão et al., 2015). Overall, the environmental metabolomics approach demonstrated its effectiveness in the evaluation of Hg toxicity mechanisms in wild fish under realistic environmental conditions, uncovering tissue-specificities regarding Hg toxic effects namely in gills and liver.

Concerns about the environmental and human health implications of TiO₂ nanoparticles (nTiO₂) are growing with their increased use in consumer and industrial products. Investigations of the underlying molecular mechanisms of nTiO₂ tolerance in organisms will assist in countering nTiO₂ toxicity. In this study, the countermeasures exhibited by the slime mold Physarum polycephalum macroplasmodium against nTiO₂ toxicity were investigated from a physiological, transcriptional, and metabolic perspective. The results suggested that the countermeasures against nTiO₂ exposure include gene-associated metabolic rearrangements in cellular pathways involved in amino acid, carbohydrate, and nucleic acid metabolism. Gene-associated nonmetabolic rearrangements involve processes such as DNA repair, DNA replication, and the cell cycle, and occur mainly when macroplasmodia are exposed to inhibitory doses of nTiO₂. Interestingly, the growth of macroplasmodia and mammal cells was significantly restored by supplementation with a combination of responsive metabolites identified by metabolome analysis. Taken together, we report a novel model organism for the study of nTiO₂ tolerance and provide insights into countermeasures taken by macroplasmodia in response to nTiO₂ toxicity. Furthermore, we also present an approach to mitigate the effects of nTiO₂ toxicity in cells by metabolic intervention.

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.

The use of some systemic insecticides has been banned in Europe because they are toxic to beneficial insects when these feed on nectar. A recent study shows that systemic insecticides can also kill beneficial insects when they feed on honeydew. Honeydew is the sugar-rich excretion of hemipterans and is the most abundant carbohydrate source for beneficial insects such as pollinators and biological control agents in agroecosystems. Here, we investigated whether the toxicity of contaminated honeydew depends on i) the hemipteran species that excretes the honeydew; ii) the active ingredient, and iii) the beneficial insect that feeds on it. HPLC-MS/MS analyses demonstrated that the systemic insecticides pymetrozine and flonicamid, which are commonly used in Integrated Pest Management programs, were present in honeydew excreted by the mealybug Planococcus citri. However, only pymetrozine was detected in honeydew excreted by the whitefly Aleurothixus floccosus. Toxicological studies demonstrated that honeydew excreted by mealybugs feeding on trees treated either with flonicamid or pymetrozine increased the mortality of the hoverfly Sphaerophoria rueppellii, but did not affect the parasitic wasp Anagyrusvladimiri. Honeydew contaminated with flonicamid was more toxic for the hoverfly than that contaminated with pymetrozine. Collectively, our data demonstrate that systemic insecticides commonly used in IPM programs can contaminate honeydew and kill beneficial insects that feed on it, with their toxicity being dependent on the active ingredient and hemipteran species that excretes the honeydew.

For most birds, energy efficiency and conservation are paramount to balancing the competing demands of self-maintenance, reproduction, and other demanding life history stages. Yet the ability to maximize energy output for behaviors like predator escape and migration is often also critical. Environmental perturbations that affect energy metabolism may therefore have important consequences for fitness and survival. Methylmercury (MeHg) is a global pollutant that has wide-ranging impacts on physiological systems, but its effects on the metabolism of birds and other vertebrates are poorly understood. We investigated dose-dependent effects of dietary MeHg on the body composition, basal and peak metabolic rates (BMR, PMR), and respiratory quotients (RQ) of zebra finches (Taeniopygia guttata). Dietary exposure levels (0.0, 0.1, or 0.6 ppm wet weight) were intended to reflect a range of mercury concentrations found in invertebrate prey of songbirds in areas contaminated by atmospheric deposition or point-source pollution. We found adiposity increased with MeHg exposure. BMR also increased with exposure while PMR decreased, together resulting in reduced metabolic scope in both MeHg-exposed treatments. There were differences in RQ among treatments that suggested a compromised ability of exposed birds to rapidly metabolize carbohydrates during exercise in a hop-hover wheel. The elevated BMR of exposed birds may have been due to energetic costs of depurating MeHg, whereas the reduced PMR could have been due to reduced oxygen carrying capacity and/or reduced glycolytic capacity. Our results suggest that environmentally relevant mercury exposure is capable of compromising the ability of songbirds to both budget and rapidly exert energy.

The ecological toxicity of hexabromocyclododecane (HBCD) on animals, including fish and mice, has been reported, but its effects in plants, particularly its toxic mechanism, have rarely been investigated. An untargeted metabolomics approach for comprehensive assessment was selected to study the alterations in the metabolic profiles in pak choi leaves induced by exposure to trace-level amounts of HBCD diastereomers over 30 days. A supervised orthogonal partial least-squares-discriminant analysis (OPLS-DA) was performed to investigate differences between the HBCD and control groups. The discriminating metabolites were identified using public databases. The results indicated that the toxicity of the HBCD diastereomers was ordered as γ-HBCD > α-HBCD > β-HBCD. 13 metabolites were identified as potential biomarkers to discriminate the presence of HBCD toxicity. The lipid, carbohydrate, nucleotide and amino acid metabolic pathways affected were found in accordance with animals and humans, and also HBCD could induce the interference of the secondary metabolite pathways. The system of the stress defences was activated, including signalling pathway, antioxidant defence system, shikimate and phenylpropanoid metabolism. The carbohydrate and amino acid metabolism were disturbed by HBCD intervention, and the lipid, amino acid and secondary metabolite metabolism were regulated for HBCD stress prevention. These results provide insights into the mechanism and degree of HBCD phytotoxicity.