Ocean acidification may increase the risk of disease outbreaks that would challenge the future persistence of marine organisms if their immune system and capacity to produce vital structures for survival (e.g., byssus threads produced by bivalves) are compromised by acidified seawater. These potential adverse effects may be exacerbated by microplastic pollution, which is forecast to co-occur with ocean acidification in the future. Thus, we evaluated the impact of ocean acidification and microplastics on the health of a mussel species (Mytilus coruscus) by assessing its physiological performance, immunity and byssus properties. We found that ocean acidification and microplastics not only reduced hemocyte concentration and viability due to elevated oxidative stress, but also undermined phagocytic activity of hemocytes due to lowered energy budget of mussels, which was in turn caused by the reduced feeding performance and energy assimilation. Byssus quality (strength and extensibility) and production were also reduced by ocean acidification and microplastics. To increase the chance of survival with these stressors, the mussels prioritized the synthesis of some byssus proteins (Mfp-4 and Mfp-5) to help maintain adhesion to substrata. Nevertheless, our findings suggest that co-occurrence of ocean acidification and microplastic pollution would increase the susceptibility of bivalves to infectious diseases and dislodgement risk, thereby threatening their survival and undermining their ecological contributions to the community.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a well-known immunotoxic environmental pollutant. However, most immunotoxicology studies of TCDD were based on the animal models and the inner mechanisms have just focused on a few genes/proteins. In this study, the immune functions of THP-1-derived macrophages was measured with in-vitro bioassays after 24-h exposure of TCDD including environmentally relevant concentrations. RNA-seq and Weighted Gene Co-expression Network Analysis were used to characterize the immunotoxicity molecular mechanisms. Our study is the first report on the TCDD-induced effects of cell adhesion, morphology, and multiple cytokines/chemokines production on THP-1 macrophages. After TCDD treatment, we observed an inhibited cell adherence, probably attributed to the suppressed mRNA levels of adhesion molecules ICAM-1, VCAM-1 and CD11b, and a decrease in cell pseudopodia and expression of F-actin. The inflammatory cytokines TNF-α, IL-10 and other 8 cytokines/chemokines regulating granulocytes/T cells and angiogenesis were disrupted by TCDD. Alternative splicing event was found to be a sensitive target for TCDD. Using WGCNA, we identified 10 hub genes (TNF, SRC, FGF2, PTGS2, CDH2, GNG11, BDNF, WNT5A, CXCR5 and RUNX2) highly relevant to these observed phenotypes, suggesting AhR less important in the effects TCDD have on THP-1 macrophages than in other cells. Our findings broaden the understanding of TCDD immunotoxicity on macrophages and provide new potential targets for clarifying the molecular mechanisms.

of bioaugmentation strategies are an obstacle for damage mitigation caused by oil spills in marine environments. Cells added to the contaminated sites are quickly lost by low adherence to the contaminants, rendering ineffective. This study used two hydrocarbonoclastic species - Rhodococcus rhodochrous TRN7 and Nocardia farcinica TRH1 cells - growing in mineral medium containing hexadecane to evaluate cell distribution in a crude-oil contaminated marine water. Cell affinity to hydrophobic compounds was quantified using Microbial Adhesion to Hydrocarbons test and analysis of fatty acids profile was performed using the Microbial Identification System. Bioremediation simulations were set up and cell populations of both strains were quantified by Fluorescent in situ Hybridization. R. rhodochrous and N. farcinica reached up to 97% and 60% of adhesion to hexadecane, respectively. The carbon source had more influence on the fatty acid profiles of both strains than the microbial species. The presence of 45.24% of 13:0 anteiso on total fatty acids in R. rhodochrous and 12.35% of saturated fatty acids with less than 13 carbons atoms in N. farcinica, as well as the occurrence of fatty alcohols only in presence of hexadecane in both species, are indicators that fatty acid changes are involved in the adaptation of the cells to remain at the water/oil interface. Cell quantification after bioremediation simulations revealed an increase in the density of both species, suggesting that the bioremediation strategies resulted on the increase of hydrocarbonoclastic species and up to 27.9% of all prokaryotic microbial populations in the microcosms were composed of R. rhodochrous or N. farcinica. These findings show the potential of application of these two bacterial strains in bioaugmentation of hydrocarbon-contaminated marine ecosystems.R. rhodochrous TRN7 and N. farcinica TRH1 hydrocarbonoclastic strains modify the fatty acid profile and increases density, optimizing hydrocarbons biodegradation.

Marine diatoms have been identified among the most abundant taxa of microorganisms associated with plastic waste collected at sea. However, the impact of nano-sized plastic fragments (nanoplastics) at single cell and population level is almost unknown. We exposed the marine diatom Skeletonema marinoi to model polystyrene nanoparticles with carboxylic acid groups (PS–COOH NPs, 90 nm) for 15 days (1, 10, 50 μg/mL). Growth, reactive oxygen species (ROS) production, and nano-bio-interactions were investigated. No effect on diatom growth was observed, however Dynamic light scattering (DLS) demonstrated the formation of large PS aggregates which were localized at the diatoms’ fultoportula process (FPP), as shown by TEM images. Increase production of ROS and reduction in chain length were also observed upon PS NPs exposure (p < 0.005). The observed PS-diatom interaction could have serious consequences on diatoms ecological role on the biogeochemical cycle of carbon, by impairing the formation of fast-sinking aggregates responsible for atmospheric carbon fixation and sequestration in the ocean sea floor. S. marinoi exposure to PS NPs caused an increase of intracellular and extracellular oxidative stress, the reduction of diatom's chain length and the adhesion of PS NPs onto the algal surface.

Antifouling booster biocides are chemicals used in protective paints to tackle the adhesion of fouling organisms to maritime artificial structures. However, they are also known to exert toxic effects on non-target organisms. Recent research developments have highlighted the potential use of engineered micro/nanomaterials (EMNMs) as carriers of antifouling booster biocides in order to control their release and to reduce the harmful effects on living biota. In the present study, we sought to assess the toxicity of two commercially-available booster biocides: (zinc pyrithione (ZnPT) and copper pyrithione (CuPT)); three unloaded engineered micro/nanomaterials (EMNMs); layered double hydroxides (LDH), silica nanocapsules (SiNC), polyurea microcapsules (PU); , and six novel EMNMs (loaded with each of the two biocides). The exposure tests were conducted on the larval stage (nauplii) of the brine shrimp Artemia salina and on two embryonic developmental stages of the European purple sea urchin Paracentrotus lividus. The findings indicate that the unloaded LDH and PU (i.e. both biocide-free EMNMs) have non/low toxic effects on both species. The unloaded SiNC, in contrast, exerted a mild toxic effect on the A. salina nauplii and P. lividus embryos. The free biocides presented different toxicity values, with ZnPT being more toxic than CuPT in the P. lividus assays. LDH-based pyrithiones demonstrated lower toxicity compared to the free forms of the state-of-the-art compounds, and constitute good candidates in terms of their antifouling efficacy.

Diesel exhaust particles (DEP) and their ultrafine fraction (UFP) are known to induce cardiovascular effects in exposed subjects. The mechanisms leading to these outcomes are still under investigation, but the activation of respiratory endothelium is likely to be involved. Particles translocation through the air-blood barrier and the release of mediators from the exposed epithelium have been suggested to participate in the process. Here we used a conditioned media in vitro model to investigate the role of epithelial-released mediators in the endothelial cells activation.Diesel UFP were sampled from a Euro 4 vehicle run over a chassis dyno and lung epithelial BEAS-2B cells were exposed for 20 h (dose 5 μg/cm2). The exposure media were collected and used for endothelial HPMEC-ST1.6R cells treatment for 24 h. The processes related to oxidative stress and inflammation were investigated in the epithelial cells, accordingly to the present knowledge on DEP toxicity. The release of IL-6 and VEGF was significantly augmented in diesel exposed cells. In endothelial cells, VCAM-1 and ICAM-1 adhesion molecules levels were increased after exposure to the conditioned media. By interfering with IL-6 binding to its endothelial receptor, we demonstrate the role of this interleukin in inducing the endothelial response.

Numerous studies have established that acute or chronic exposure to environmental pollutants like particulate matter (PM) leads to the development of accelerated aging related pathologies including pulmonary and cardiovascular diseases, and thus air pollution is one of the major global threats to human health. Air pollutant particulate matter 2.5 (PM₂.₅)-induced cellular dysfunction impairs tissue homeostasis and causes vascular and cardiopulmonary damage. To test a hypothesis that elevated plasminogen activator inhibitor-1 (PAI-1) levels play a pivotal role in air pollutant-induced cardiopulmonary pathologies, we examined the efficacy of a drug-like novel inhibitor of PAI-1, TM5614, in treating PM₂.₅-induced vascular and cardiopulmonary pathologies. Results from biochemical, histological, and immunohistochemical studies revealed that PM₂.₅ increases the circulating levels of PAI-1 and thrombin and that TM5614 treatment completely abrogates these effects in plasma. PM₂.₅ significantly augments the levels of pro-inflammatory cytokine interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF), and this also can be reversed by TM5614, indicating its efficacy in amelioration of PM₂.₅-induced increases in inflammatory and pro-thrombotic factors. TM5614 reduces PM₂.₅-induced increased levels of inflammatory markers cluster of differentiation 107 b (Mac3) and phospho-signal transducer and activator of transcription-3 (pSTAT3), adhesion molecule vascular cell adhesion molecule 1 (VCAM1), and apoptotic marker cleaved caspase 3. Longer exposure to PM₂.₅ induces pulmonary and cardiac thrombosis, but TM5614 significantly ameliorates PM₂.₅-induced vascular thrombosis. TM5614 also reduces PM₂.₅-induced increased blood pressure and heart weight. In vitro cell culture studies revealed that PM₂.₅ induces the levels of PAI-1, type I collagen, fibronectin (Millipore), and sterol regulatory element binding protein-1 and 2 (SREBP-1 and SREBP-2), transcription factors that mediate profibrogenic signaling, in cardiac fibroblasts. TM5614 abrogated that stimulation, indicating that it may block PM₂.₅-induced PAI-1 and profibrogenic signaling through suppression of SREBP-1 and 2. Furthermore, TM5614 blocked PM₂.₅-mediated suppression of nuclear factor erythroid related factor 2 (Nrf2), a major antioxidant regulator, in cardiac fibroblasts. Pharmacological inhibition of PAI-1 with TM5614 is a promising therapeutic approach to control air pollutant PM₂.₅-induced cardiopulmonary and vascular pathologies.

Quantum dots (QDs) have attracted broad attention due to their special optical properties and promising prospect in medical and biological applications. However, the process of QDs on cell membrane is worth further investigations because such process may lead to harmful effects on organisms and also important for QD application. In this study, adhesion of amino- and carboxyl-coated CdTe QDs (A-QDs and C-QDs) on cell membrane and the subsequent internalization are studied using a series of endocytosis-free model membranes, including giant and small unilamellar vesicles, supported lipid bilayers and giant plasma membrane vesicles (GPMVs). The adhered QD amounts on model membranes are quantified by a quartz crystal microbalance. The CdTe QD adhesion on model membranes is governed by electrostatic forces. Positively charged A-QDs adhere on GPMV surface and passively penetrate the plasma membrane via endocytosis-free mechanism, but negatively charged C-QDs cannot. Rat basophilic leukemia (RBL-2H3) cells are exposed to CdTe QDs to monitor the QD internalization process. Both A- and C-QDs are internalized by RBL-2H3 cells mainly via endocytosis. CdTe QDs do not accumulate on the plasma membrane of living cells due to the fast endocytosis and the weakened electrostatic attraction in biological medium, resulting in low chance of passive penetration. The suspended cells after trypsin digestion take more QDs than the adherent cells. A-QDs cause lower cell viability than C-QDs, probably because the approach of positively charged QDs to cells is favored and the smaller aggregates of A-QDs.

Individuals are exposed to brominated flame retardants (BFRs), including tetrabromobisphenol A (TBBPA), on a daily basis because of their widespread usage. These compounds may have adverse effects on human health. In the present study, dermal absorption experiments were conducted in vivo to predict the adhesion, penetration, and bioavailability of TBBPA. TBBPA was administered to Wistar rats for 6 h by repeated dermal exposure at doses of 20, 60, 200, and 600 mg of TBBPA per kg of body weight (bw). The skin adhesion coefficient (AC) was calculated using a difference-value method and ranged from 0.12 to 3.25 mg/cm2 and 0.1 to 2.56 mg/cm2 for the male and female rats, respectively. The adhesion rate was 70.92%. According to Fick's first law of diffusion, the diffusion constant (D) was 1.4 × 10−4 cm2/h and the permeation coefficient (Kp) was 1.26 × 10−5 cm/h for TBBPA. TBBPA levels in the blood, urine, and feces of the male rats were significantly higher than those in the female rats. The dermal bioavailability of TBBPA was 24.71% for male rats and 20.05% for female rats 24 h after exposure.

Polycyclic aromatic hydrocarbons (PAHs) are often detected in the environment and are regarded as endocrine disruptors. We here designated mixtures of PAHs in the environment as environmental PAHs (ePAHs) to discuss their effects collectively, which could be different from the sum of the constituent PAHs. We first summarized the biological impact of environmental PAHs (ePAHs) found in the atmosphere, sediments, soils, and water as a result of human activities, accidents, or natural phenomena. ePAHs are characterized by their sources and forms, followed by their biological effects and social impact, and bioassays that are used to investigate their biological effects. The findings of the bioassays have demonstrated that ePAHs have the ability to affect the endocrine systems of humans and animals. The pathways that mediate cell signaling for the endocrine disruptions induced by ePAHs and PAHs have also been summarized in order to obtain a clearer understanding of the mechanisms responsible for these effects without animal tests; they include specific signaling pathways (MAPK and other signaling pathways), regulatory mechanisms (chromatin/epigenetic regulation, cell cycle/DNA damage control, and cytoskeletal/adhesion regulation), and cell functions (apoptosis, autophagy, immune responses/inflammation, neurological responses, and development/differentiation) induced by specific PAHs, such as benz[a]anthracene, benzo[a]pyrene, benz[l]aceanthrylene, cyclopenta[c,d]pyrene, 7,12-dimethylbenz[a]anthracene, fluoranthene, fluorene, 3-methylcholanthrene, perylene, phenanthrene, and pyrene as well as their derivatives. Estrogen signaling is one of the most studied pathways associated with the endocrine-disrupting activities of PAHs, and involves estrogen receptors and aryl hydrocarbon receptors. However, some of the actions of PAHs are contradictory, complex, and unexplainable. Although several possibilities have been suggested, such as direct interactions between PAHs and receptors and the suppression of their activities through other pathways, the mechanisms underlying the activities of PAHs remain unclear. Thus, standardized assay protocols for pathway-based assessments are considered to be important to overcome these issues.