416 research outputs found

    Interactive effects of nanoparticles with other contaminants in aquatic organisms: Friend or foe?

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    The increasing production and use of nanoparticles (NPs) will lead to their release into the aquatic environment, posing a potential threat to the health of aquatic organisms. Both in the water phase and in the sediments NPs could mix and interact with other pollutants, such as organic xenobiotics and heavy metals, leading to possible changes in their bioavailability/bioconcentration/toxicity. However, whether these interactive effects may lead to increased harmful effects in marine organisms is largely unknown. In this work, available data mainly obtained on carbon based NPs and n-TiO2, as examples of widespread NPs, in aquatic organisms are reviewed. Moreover, data are summarized on the interactive effects of n-TiO2 with 2,3,7,8-TCDD and Cd(2+), chosen as examples of common and persistent organic and inorganic contaminants, respectively, in the model marine bivalve Mytilus. The results reveal complex and often unexpected interactive responses of NPs with other pollutants, depending on type of contaminant and the endpoint measured, as well as differences in bioaccumulation. The results are discussed in relation with data obtained in freshwater organisms. Overall, information available so far indicate that interactive effects of NPs with other contaminants do not necessarily lead to increased toxicity or harmful effects in aquatic organisms

    Insight Into the Microbial Communities Associated With First Larval Stages of Mytilus Galloprovincialis: Possible Interference by Estrogenic Compounds

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    The microbiota, the host-associated community of microbes, play important roles in health status and whole body homeostasis of all organisms, including marine species. In bivalves, the microbiota composition has been mainly investigated in adults, whereas little information is available during development. In this work, the microbiota composition of the first larval stages of Mytilus galloprovincialis was evaluated by 16S rRNA gene-based profiling, at 24 and 48 hours post fertilization in comparison with those of eggs and sperm. The main genera detected in both larvae (Vibrio, Pseudoalteromonas, Psychrobium, Colwellia) derived from eggs. However, a clear shift in microbiota was observed in developing larvae compared to eggs, both in terms of core microbiome and relative abundance of different genera. The results provide a first insight into the composition of the microbial communities associated with gametes and early larvae of mussels. Moreover, the impact on larval microbiome of estrogenic chemicals that potentially affect Mytilus early development, 17βestradiol-E2, Bisphenol A-BPA and Bisphenol F-BPF (10 μg/L), was investigated. Exposure to estrogenic chemicals leads to changes in abundance of different genera, with distinct and common effects depending on the compound and larval stage. Both potential pathogens (Vibrio, Arcobacter, Tenacibaculum) and genera involved in xenobiotic biotransformation (Oleispira, Shewanella) were affected. The effects of estrogenic compounds on larval microbiome were not related to their developmental effects: however, the results address the importance of evaluating the impact of emerging contaminants on the microbiota of marine invertebrates, including larval stages, that are most sensitive to environmental perturbations

    Hg(2+) and Cu(2+) interfere with agonist-mediated Ca(2+) signaling in isolated Mytilus digestive gland cells

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    The effects of mercury and copper on agonist-mediated Ca-signaling were investigated in isolated cells from the marine mussel: Mytilus galloprovincialis Lam., by single cell fluorescence microscopy. In isolated digestive gland cells, short-term exposure (10 min) to both Hg2+, a highly toxic metal and Cu2+, essential metal, in the nano-low mu M range caused a sustained increase in cytosolic [Ca2+]. The effect of mercury on resting [Ca2+] was stronger than that of copper. The Hg-induced elevation in [Ca2+] seemed to be mainly due to an increased influx through Verapamil-sensitive Ca-channels, whereas the effect of Cu2+ was related to a release from thapsigargin-sensitive intracellular stores. Agonists, such as epidermal growth factor (EGF), bradykinin (BK) and ATP, evoked Ca2+ transients in isolated digestive gland cells through different mechanisms similar to those observed in mammalian cells, demonstrating the presence of common pathways of Ca-mediated cell signaling in both invertebrates and vertebrates. The agonist-mediated Ca2+ response was affected by exposure to Hg2+ and Cu2+ in a concentration dependent manner: both metals significantly reduced the amplitude of the Ca2+ spikes elicited by BK and ATP and decreased the percentage of EGF-responsive cells. The effects of Hg2+ and Cu2+ were apparently independent of their different type of interaction with the mechanisms involved in Ca2+ homeostasis. The results clearly demonstrate that, in marine invertebrate cells, short-term exposure to heavy metal concentrations comparable to environmental exposure levels results in alterations of intracellular Ca2+ homeostasis which compromise the cell response to extracellular stimuli involving Ca-mediated signaling. The mechanisms of heavy metal interference with Ca-homeostasis and signaling are discussed. (C) 2000 Elsevier Science B.V. All rights reserved

    Tetrabromobisphenol A acts a neurodevelopmental disruptor in early larval stages of Mytilus galloprovincialis

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    Tetrabromobisphenol A-TBBPA, a widely used brominated flame retardant detected in aquatic environments, is considered a potential endocrine disruptor-ED for its reproductive/developmental effects in vertebrates. In aquatic invertebrates, the modes of action of most EDs are largely unknown, due to partial knowledge of the mechanisms controlling neuroendocrine functions. In the marine bivalve Mytilus galloprovincialis, TBBPA has been previously shown to affect larval development in the 48 h larval toxicity assay at environmental concentrations. In this work, the effects of TBBPA were further investigated at different times post-fertilization. TBBPA, from 1 μg/L, affected shell biogenesis at 48 hours post fertilization-hpf, as shown by phenotypic and SEM analysis. The mechanisms of action of TBBPA were investigated at concentrations of the same order of magnitude as those found in highly polluted coastal areas (10 μg/L). At 28–32 hpf, TBBPA significantly affected deposition of both the organic matrix and CaCO3 in the shell. TBBPA also altered expression of shell-related genes from 24 to 48 hpf, in particular of tyrosinase, a key enzyme in shell matrix remodeling. At earlier stages (24 hpf), TBBPA affected the development of dopaminergic, serotoninergic and GABAergic systems, as shown by in situ hybridization-ISH and immunocytochemistry. These data contribute draw adverse outcome pathways-AOPs, where TBBPA affects the synthesis of neutrotransmitters involved in key events (neurodevelopment and shell biogenesis), resulting in phenotypic changes on individuals (delayed or arrested development) that might lead to detrimental consequences on populations

    Models of non-alcoholic fatty liver disease and potential translational value: The effects of 3,5-L-diiodothyronine

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    Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder in industrialized countries and is associated with increased risk of cardiovascular, hepatic and metabolic diseases. Molecular mechanisms on the root of the disrupted lipid homeostasis in NAFLD and potential therapeutic strategies can benefit of in vivo and in vitro experimental models of fatty liver. Here, we describe the high fat diet (HFD)-fed rat in vivo model, and two in vitro models, the primary cultured rat fatty hepatocytes or the FaO rat hepatoma fatty cells, mimicking human NAFLD. Liver steatosis was invariably associated with increased number/size of lipid droplets (LDs) and modulation of expression of genes coding for key genes of lipid metabolism such as peroxisome proliferator-activated receptors (Ppars) and perilipins (Plins). In these models, we tested the anti-steatotic effects of 3,5-L-diiodothyronine (T2), a metabolite of thyroid hormones. T2 markedly reduced triglyceride content and LD size acting on mRNA expression of both Ppars and Plins. T2 also stimulated mitochondrial oxidative metabolism of fatty acids. We conclude that in vivo and especially in vitro models of NAFLD are valuable tools to screen a large number of compounds counteracting the deleterious effect of liver steatosis. Because of the high and negative impact of liver steatosis on human health, ongoing experimental studies from our group are unravelling the ultimate translational value of such cellular models of NAFLD
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