Ocean acidification impedes gustation-mediated feeding behavior by disrupting gustatory signal transduction in the black sea bream, Acanthopagrus schlegelii.

Growing evidence suggests that ocean acidification (OA) may affect animal behaviors such as feeding. Although gustation plays a crucial role in evaluating the quality and palatability of food and ultimately influences whether or not teleosts consume the food, the potential impact of OA on gustation-mediated feeding behavior remains unknown. In this study, gustation mediated-feeding behavior, as indicated by the consumption rate (CR) and swallowing rate (SR) of agar pellets with or without feed upon OA exposure was investigated in black sea bream (Acanthopagrus schlegelii). Results showed that the exposure to acidified seawater led to significant reductions in the CR and SR of feed-containing agar pellets. In addition, the in vivo contents of three neurotransmitters and expression of genes from the gustatory signal transduction pathway were all significantly suppressed by the OA treatment. In general, the data obtained indicated that OA may hinder the gustation-mediated feeding behavior of A. schlegelii by disrupting gustatory signal transduction, which may aggravate the issue of food shortage for wild populations of black sea bream.

Immunotoxicity of microplastics and two persistent organic pollutants alone or in combination to a bivalve species.

Both microplastics and persistent organic pollutants (POPs) are ubiquitously present in natural water environment, posing a potential threat to aquatic organisms. While it has been suggested that the immune responses of aquatic organisms could be hampered by exposure to microplastics and POPs, the synergistic immunotoxic impact of these two types of pollutants remain poorly understood. In addition, little is known about the mechanism behind the immunotoxic effect of microplastics. Therefore, in the present study, the immunotoxicity of microplastics and two POPs, benzo[a]pyrene (B[a]P) and 17ß-estradiol (E2), were investigated alone or in combination in a bivalve species, Tegillarca granosa. Evident immunotoxicity, as indicated by alterations of haemocyte count, blood cell composition, phagocytic activity, intracellular content of ROS, concentration of Ca2+ and lysozyme, and lysozyme activity, was revealed for both microplastics and the two POPs examined. In addition, the expression of six immune-, Ca2+ signalling-, and apoptosis-related genes was significantly altered by exposure of clams to the contaminants studied. Furthermore, the toxicity of POPs was generally aggravated by smaller microplastics (500 nm) and mitigated by larger ones (30 µm). This size dependent effect on POP toxicity may result from size dependent interactions between microplastics and POPs. Data obtained in this study also indicate that similar to exposure to B[a]P and E2, exposure to microplastics may hamper the immune responses of clams through a series of interdependent physiological and molecular processes.

Exposure to Waterborne nTiO2 Reduces Fertilization Success and Increases Polyspermy in a Bivalve Mollusc: A Threat to Population Recruitment.

Fertilization success is crucial for the population recruitment of an organism. However, little is known about the threat of nanoparticles (NPs) to the fertilization of broadcast spawners. Therefore, the effects of nTiO2 on fertilization success, polyspermy rate, sperm velocity, gametic DNA damage, sperm-egg collision probability, gamete fusion, and oocyte ultrastructure were investigated in a broadcast spawning bivalve, Tegillarca granosa. The results obtained show that fertilization success significantly decreased, whereas polyspermy risk markedly increased upon nTiO2 exposure. In addition, nTiO2 exposure led to a significant reduction in sperm swimming velocity, which would subsequently constrain gamete collisions. In addition, nTiO2 exposure resulted in a significant decline in gamete fusion per collision along with aggravated DNA damage in gametes. Furthermore, ultrastructural analysis illustrated the attachment of nTiO2 to the oocyte surface, which subsequently resulted in microvillus disassociation and plasma membrane damage. In conclusion, the results obtained suggest a significant threat from NP pollution to the recruitment of broadcast spawning invertebrates.

Immunotoxicity of four nanoparticles to a marine bivalve species, Tegillarca granosa.

The increasing application of nanomaterials drives the unintentional release of nanoparticles (NPs) into the ocean, which may pose a potential threat to marine organisms. It has been demonstrated that exposure to NPs could chanllenge the immune responses of marine species. However, the affecting mechanism behind remains poorly understood. In this study, the immunotoxic impacts and the mechanisms underpinning the effects of four major NPs, including nZnO, nFe2O3, nCuO, and carbon nanotube (MWCNT), were investigated in blood clam, Tegillarca granosa. The results showed that exposure to tested NPs resulted in reduced total counts, altered cell composition, and constrained phagocytic activities of haemocytes. The intracellular contents of reactive oxygen species (ROS) and the degree of DNA damage of haemocytes were significantly induced, whereas the haemocyte viability was suppressed. Furthermore, NP exposures led to significant increases in the in vivo contents of neurotransmitters. Down-regulations of the immune- and neurotransmitter-related genes were detected as well. Our data suggest that NP exposures hampered the immune responses of blood clams most likely through (1) inducing ROS, causing DNA damage, and reducing cell viability of haemocytes, (2) altering the in vivo contents of neurotransmitters, and (3) affecting the expression of immune- and neurotransmitter-related genes.

Fluoxetine suppresses the immune responses of blood clams by reducing haemocyte viability, disturbing signal transduction and imposing physiological stress.

The antidepressant fluoxetine (FLX), a selective serotonin reuptake inhibitor, is widely prescribed for the treatment of depression and anxiety disorders. Nowadays, measurable quantities of FLX have been frequently detected in the aquatic ecosystems worldwide, which may pose a potential threat to aquatic organisms. Although the impacts of FLX exposure on immune responses are increasingly well documented in mammals, they remain poorly understood in aquatic invertebrates. Therefore, to gain a better understanding of the ecotoxicological effects of FLX, the impacts of waterborne FLX exposure on the immune responses of blood clam, Tegillarca granosa, were investigated in this study. Results obtained showed that both cellular and humoural immune responses in T. granosa were suppressed by exposure to waterborne FLX, as indicated by total counts of haemocytes (THC), phagocytic rate, and activities of superoxide dismutases (SOD) and catalase (CAT), suggesting that waterborne FLX renders blood clams more vulnerable to pathogen challenges. To ascertain the mechanisms explaining how waterborne FLX affects immune responses, haemocyte viabilities, intracellular Ca2+ levels, in vivo concentrations of neurotransmitters, physiological stress conditions (as indicated by in vivo concentrations of cortisol), and expressions of key regulatory genes from Ca2+ and neurotransmitter signal transduction, as well as immune-related signalling pathways, were examined after 10 days of FLX exposure by blood clams via 1, 10 and 100 µg/L waterborne FLX. The results obtained indicated that immune response suppression caused by waterborne FLX could be due to (i) inhibited haemocyte viabilities, which subsequently reduce the THC; (ii) altered intracellular Ca2+ and neurotransmitter concentrations, which lead to constrained phagocytosis; and (iii) aggravated physiological stress, which thereafter hampers immune-related NFκB signalling pathways.

Anthropogenic Noise Aggravates the Toxicity of Cadmium on Some Physiological Characteristics of the Blood Clam Tegillarca granosa.

Widespread applications of cadmium (Cd) in various products have caused Cd contamination in marine ecosystems. Meanwhile, human activities in the ocean have also generated an increasing amount of noise in recent decades. Although anthropogenic noise and Cd contaminants could be present simultaneously in marine environments, the physiological responses of marine bivalve mollusks upon coexposure to anthropogenic noise and toxic metal contaminants, including Cd remain unclear. Therefore, the combined effects of anthropogenic noise and Cd on the physiological characteristics of the blood clam Tegillarca granosa were investigated in this study. The results showed that 10 days of coexposure to anthropogenic noise and Cd can enhance adverse impacts on metabolic processes, as indicated by the clearance rate, respiration rate, ammonium excretion rate, and O:N ratio of T. granosa. In addition, both the ATP content, ATP synthase activity and genes encoding important enzymes in ATP synthesis significantly declined after coexposures to anthropogenic noise and Cd, which have resulted from reduced feeding activity and respiration. Furthermore, the expressions of neurotransmitter-related genes (MAO, AChE, and mAChR3) were all significantly down-regulated after coexposure to anthropogenic noise and Cd, which suggests an enhanced neurotoxicity under coexposure. In conclusion, our study demonstrated that anthropogenic noise and Cd would have synergetic effects on the feeding activity, metabolism, and ATP synthesis of T. granosa, which may be due to the add-on of stress responses and neurotransmitter disturbances.

Ocean Acidification Affects the Cytoskeleton, Lysozymes, and Nitric Oxide of Hemocytes: A Possible Explanation for the Hampered Phagocytosis in Blood Clams, Tegillarca granosa.

An enormous amount of anthropogenic carbon dioxide (CO2) has been dissolved into the ocean, leading to a lower pH and changes in the chemical properties of seawater, which has been termed ocean acidification (OA). The impacts of pCO2-driven acidification on immunity have been revealed recently in various marine organisms. However, the mechanism causing the reduction in phagocytosis still remains unclear. Therefore, the impacts of pCO2-driven OA at present and near-future levels (pH values of 8.1, 7.8, and 7.4) on the rate of phagocytosis, the abundance of cytoskeleton components, the levels of nitric oxide (NO), and the concentration and activity of lysozymes (LZM) of hemocytes were investigated in a commercial bivalve species, the blood clam (Tegillarca granosa). In addition, the effects of OA on the expression of genes regulating actin skeleton and nitric oxide synthesis 2 (NOS2) were also analyzed. The results obtained showed that the phagocytic rate, cytoskeleton component abundance, concentration and activity of LZM of hemocytes were all significantly reduced after a 2-week exposure to the future OA scenario of a pH of 7.4. On the contrary, a remarkable increase in the concentration of NO compared to that of the control was detected in clams exposed to OA. Furthermore, the expression of genes regulating the actin cytoskeleton and NOS were significantly up-regulated after OA exposure. Though the mechanism causing phagocytosis seemed to be complicated based on the results obtained in the present study and those reported previously, our results suggested that OA may reduce the phagocytosis of hemocytes by (1) decreasing the abundance of cytoskeleton components and therefore hampering the cytoskeleton-mediated process of engulfment, (2) reducing the concentration and activity of LZM and therefore constraining the degradation of the engulfed pathogen through an oxygen-independent pathway, and (3) inducing the production of NO, which may negatively regulate immune responses.

Neurotoxic impact of acute TiO2 nanoparticle exposure on a benthic marine bivalve mollusk, Tegillarca granosa.

The release of nanoparticles (NPs) into the ocean inevitably poses a threat to marine organisms. However, to date, the neurotoxic effects of NPs remains poorly understood in marine bivalve species. Therefore, in order to gain a better understanding of the physiological effects of NPs, the impact of acute (96 h) TiO2 NP exposure on the in vivo concentrations of three major neurotransmitters, the activity of AChE, and the expression of neurotransmitter-related genes was investigated in the blood clam, Tegillarca granosa. The obtained results showed that the in vivo concentrations of the three tested neurotransmitters (DA, GABA, and ACh) were significantly increased when exposed to relatively high doses of TiO2 NPs (1 mg/L for DA and 10 mg/L for ACh and GABA). Additionally, clams exposed to seawater contaminated with TiO2 NP had significantly lower AChE activity. In addition, the expression of genes encoding modulatory enzymes (AChE, GABAT, and MAO) and receptors (mAChR3, GABAD, and DRD3) for the neurotransmitters tested were all significantly down-regulated after TiO2 NP exposure. Therefore, this study has demonstrated the evident neurotoxic impact of TiO2 NPs in T. granosa, which may have significant consequences for a number of the organism's physiological processes.

Waterborne Cd2+ weakens the immune responses of blood clam through impacting Ca2+ signaling and Ca2+ related apoptosis pathways.

Exposure to heavy metals such as Cadmium (Cd) may exert detrimental impacts on the immune responses of marine bivalve species. However, the immunotoxicity of Cd on blood clams remains unknown to date. Furthermore, though Cd2+ is known to compete with calcium (Ca2+) ions for their binding sites in cells and inhibit Ca2+ influx, whether Cd2+ weakens the immune responses of marine bivalves through inducing intracellular Ca2+ disorders still remains unclear. Therefore, the immunotoxicity of Cd2+ at different waterborne Ca2+ concentrations on blood clam, Tegillarca granosa, were investigated in the present study. Results obtained demonstrated that the total number, phagocytic activity, and red granulocytes ratio of the haemocytes were all significantly reduced after 10 days exposure of individuals to 25 µg/L Cd2+. However, when the waterborne Ca2+ concentrations were elevated by 10% and 20% (approximately 370 and 410 mg/L, respectively), mitigation effects on the immune responses of individuals were detected. In addition, though the expressions of genes from the Ca2+ signaling and Ca2+-related apoptosis pathways were significantly altered by Cd2+ exposure, the expression patterns of these genes were similar to that of the control when the waterborne Ca2+ concentrations were elevated, suggesting a relieving effect of waterborne Ca2+ on Cd2+ induced toxicity to haemocytes. The results obtained in the present study revealed that waterborne Cd2+ may hamper the immune responses of T. granosa through influencing Ca2+ signaling and Ca2+-related apoptosis pathways, which can be partially mitigated by elevating the waterborne Ca2+ concentrations.