The occurrence of iodinated contrast agents (ICAs) in the aquatic environment is relatively well documented, showing that these compounds can be found at several µg/L in natural waters, and up to hundreds of µg/L in waste water treatment plants inlets. Nevertheless, only few studies address their potential impacts and fate in aquatic organisms mainly because these compounds are considered non-toxic due to their intrinsic properties. However, as aquatic organisms are continuously exposed to these compounds, they could nonetheless induce some adverse effects on aquatic populations like filter feeder organisms. To verify this, we exposed model organisms, Dreissena polymorpha mollusks, to 100 µg/L of an ICA, diatrizoic acid (DTZ), to determine the potential biological effects caused by this compound using a non-targeted metabolomic approach based on liquid chromatography coupled to high resolution mass spectrometry. Metabolic profiles showed a slight effect of DTZ, with some metabolome variations linked to exposure. Indeed, to avoid any misinterpretation of DTZ effects, we also studied the natural evolution of the metabolome over time in unexposed mussels, showing that control mussels exhibited metabolomic changes over the exposure period. During DTZ exposure, we showed that the carnitine shuttle pathway of fatty acids and pyrimidine metabolisms were impacted, leading to dysregulation of mussels’ energy metabolism. Thus, this study demonstrates for the first time that compounds considered non-toxic like ICAs can have an impact on aquatic organisms such as bivalves by slightly modulating their metabolome.
Nano-zinc oxide (ZnO NPs), as widely used nanomaterials, are inevitably released into aquatic environments, posing potential threats to aquatic organisms. Mytilus galloprovincialis is a bivalve species sensitive to changes in marine ecological environments, but there has been limited research on its toxicity response to ZnO NPs. Therefore, we selected M. galloprovincialis as the research subject and exposed them to 50 µg/L ZnO NPs for 96 h and 30 days to determine the dissolution of ZnO NPs in seawater and their distribution in M. galloprovincialis. The toxicity of ZnO NPs in M. galloprovincialis was then evaluated through gene expression, tissue pathology, and cellular immune response. The results showed that ZnO NPs could enrich Zn in various tissues of the mussel, in the order of gills > hepatopancreas > adductor muscle > mantle. Seven immune-related genes including four heat shock protein genes (HSPA12A, sHSP24.1, sHSP22, TCTP) and three apoptotic genes (Ras, p63 and Bcl-2) were altered to varying degrees. There was a downward trend in lysosomal membrane stability of M. galloprovincialis after exposure to ZnO NPs for 96 h and 30 days, while ROS and apoptosis rates increased significantly. Furthermore, the seven genes, apoptosis, LMS, and ROS were dependent on exposure time, treatment, and their interaction. Histopathological damage included disorganisation of hepatopancreas epithelial cells, gill filament swelling, and contraction of blood sinuses. These results indicated that ZnO NPs exerted toxicity in M. galloprovincialis, affecting the immune system, resulting in changes in the expression of immune-related genes and ultimately leading to histopathological changes. Our research findings could contribute to systematically understand the impact of ZnO NPs on bivalves in aquatic environments and provide a theoretical basis for marine pollution assessment.
Yangtze finless porpoises (YFP) accumulate high levels of per- and polyfluoroalkyl substances (PFASs). However, the health impacts of PFASs to YFP are still unknown because it is technically and ethically unfeasible to use the critically endangered YFP in toxicological exposures. To uncover the potential toxicities of PFASs to YFP, this study exposed a YFP umbilical cord fibroblast cell line to perfluorobutane sulfonate (PFBS), an emerging PFASs pollutant in the aquatic environments. After exposure, the cytotoxicity and mechanisms of PFBS were explored. Our preliminary experiments found that PFBS compromised the cell viability in a concentration and duration dependent manner. In an exposure of 48-h duration, the maximum no observed effect concentration (NOEC) of PFBS was determined to be 400 µM. High-throughput proteomics were then conducted to identify the differentially expressed proteins in YFP cells exposed to 400 µM PFBS for 48 h. The results found that PFBS exposure significantly perturbed the proteome fingerprints of YFP umbilical cord fibroblast cells. Functional annotation of differential proteins showed that PFBS had the potential to impair a variety of biological processes associated with the immunity, oxidative stress, metabolism, and proteolysis. Consistently, the intracellular levels of reactive oxygen species (ROS) and proinflammatory cytokine IL-1β were significantly increased by PFBS in YFP umbilical cord fibroblast cells. Overall, this study highlights the toxic effects of emerging PFASs on YFP and provides reference data to evaluate the health risks of aquatic pollution under the context of national YFP protection. To our knowledge, this is the first omics study using YFP umbilical cord fibroblast cells in ecotoxicology of PFASs, which is applicable to various cetacean species and pollutants.
New evidence regarding the risks that microplastics (MP) ingestion pose to human and wildlife health are being revealed with progress made in ecotoxicological research. However, comprehensive and realistic approaches that evaluate multiple physiological responses simultaneously are still scarce despite their relevance to understand whole-organism effects. To address this information gap, we performed an experiment to assess the effects of MP on freshwater fish physiology from the molecular to the organismal level. Using a model species of global commercial importance (Cyprinus carpio) and MP type (recycling industry fragments), size (range between 125-1000 µm), and two concentrations of environmental relevance (0.75 and 8.25 µg/L). Experimental design included 5 blocks containing 3 treatment levels each one: control, low, and high MP concentration, with 6 fish each aquarium (5 blocks x 3 treatments x 6 fish per aquarium = 90 fish). Our results suggest that, under the experimental conditions applied, MP exposure did not cause adverse effects at the morphological (variation in size of gut), metabolic (variation of standard metabolic rate), or ecological (growth performance) levels. Nonetheless, we observed an increased frequency of micronucleated cells with increasing MP concentration (df = 42, t-value = 3.68, p-value < 0.001), showing the potential genotoxicity of MP, which can clearly harm fish health in long-term. Thus, despite being a highly resistant species, exposure to MP may generate negative effects in juvenile C. carpio at cellular or subcellular levels. Our findings highlight that the manifestation of MP effects may vary over time, emphasizing the need for future studies to consider longer exposure durations in experimental designs.