Energy strategy alteration, rather than toxicity itself, interferes with the population fluctuation of Brachionus plicatilis exposed to water-accommodated fractions (WAFs) of crude oil.

Oil spills are reported to have conflicting impacts of either injury or resilience on zooplankton communities, and physiological plasticity is speculated to be the possible causative factor. But how? An explanation was sought by exposing the marine rotifer Brachionus plicatilis to a series of water-accommodated fractions (WAFs) of crude oil under controlled laboratory conditions, and population dynamics, which is the core issue for zooplankton facing external stress, were analyzed. The total hydrocarbon concentration of WAFs was quickly degraded from a concentration of 5.0 mg L-1 to half within 24 h and then remained stable. No acute lethality was observed; only motion inhibition was observed in the group treated with 10 %, 50 % and 100 % WAFs, which occurred simultaneously with inhibition of feeding and filtration. However, sublethal exposure to the WAFs concentration series presented stimulation impacts on reproduction and even the population of B. plicatilis. The negative correlation between motion and reproduction seemed to indicate that a shift in the distribution of individual energy toward reproduction rather than motion resulted in increased reproduction after exposure to WAFs. More evidence from transmission electron microscopy (TEM) revealed ultrastructural impairment in both the ovaries and cilia in each treated group, and imbalance in mitochondrial numbers was one of the distinct features of alteration. WAFs stress may alter the energy utilization and storage paradigm, as indicated by the significant elevation in glycogen and the significant decrease in lipid content after WAFs exposure. Further evidence from metabolomics analysis showed that WAFs stress increased the level of lipid metabolism and inhibited some of the pathways in glucose metabolism. Sublethal acute toxicity was observed only in the first 24 h with WAFs exposure, and an energy strategy consisting of changes in the utilization and storage paradigm and reallocation is responsible for the population resilience of B. plicatilis during oil spills.

Antioxidant Systematic Alteration Was Responsible for Injuries Inflicted on the Marine Blue Mussel Mytilus edulis Following Strontium Exposure.

The ionic properties of strontium (Sr), a significant artificial radionuclide in the marine environment, were estimated using a stable nuclide-substituting experimental system under controlled laboratory conditions. The bio-accumulation of Sr and its impacts, as well as any possible hidden mechanisms, were evaluated based on the physiological alterations of the sentinel blue mussel Mytilus edulis. The mussels were exposed to a series of stress-inducing concentrations, with the highest solubility being 0.2 g/L. No acute lethality was observed during the experiment, but sublethal damage was evident. Sr accumulated in a tissue-specific way, and hemolymph was the target, with the highest accumulating concentration being 64.46 µg/g wet weight (ww). At the molecular level, increases in the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) and changes in ROS components (H2O2, O2-, and -OH) and antioxidant system activity indicated that the redox equilibrium state in hemocytes was disturbed. Furthermore, the rise in the hemocyte micronucleus (MN) rate (4‱ in the high-concentration group) implied DNA damage. At the cellular level, the structures of hemocytes were damaged, especially with respect to lysosomes, which play a crucial role in phagocytosis. Lysosomal membrane stability (LMS) was also affected, and both acid phosphatase (ACP) and alkaline phosphatase (AKP) activities were reduced, resulting in a significant decline in phagocytosis. The hemolymph population structure at the organ level was disturbed, with large changes in hemocyte number and mortality rate, along with changes in component ratios. These toxic effects were evaluated by employing the adverse outcome pathway (AOP) framework. The results suggested that the disruption of intracellular redox homeostasis is a possible explanation for Sr-induced toxicity in M. edulis.

Polystyrene microplastics mitigate lead-induced neurotoxicity by reducing heavy metal uptake in zebrafish larvae.

The combined pollution of lead (Pb) and polystyrene microplastics (PS-MPs) is common in aquatic environments. However, the combined neurotoxicity of these two pollutants is still poorly understood. In this study, zebrafish (Danio rerio) larvae were used to assess the combined neurotoxicity and mechanism of Pb and PS-MPs at environmentally relevant concentrations. The results showed that Pb (10 µg/L) induced abnormal behavior including significantly reduced movement distance, maximum acceleration, and average velocity (P < 0.05) along with altered expression of neurodevelopment-related genes (gap43 and α1-tubulin) (P < 0.05). PS-MPs (25 µg/L, 250 µg/L; diameter at 25 µm) co-exposure not only significantly reduced the concentration of Pb in the exposed solution (P < 0.01), but also decreased the uptake of Pb by downregulating the divalent metal transporter 1 gene (dmt1) (P < 0.01), thereby alleviating Pb-induced neurotoxicity. However, to demonstrate that PS-MPs alleviate the neurotoxicity of Pb by reducing Pb uptake, upregulation of dmt1 by addition of deferoxamine (DFO, an efficient iron chelator, 100 µM) significantly increased the Pb uptake and exacerbated neurotoxicity in zebrafish. In summary, our results demonstrated that PS-MPs alleviate Pb neurotoxicity by downregulating the mRNA level of dmt1 and decreasing the Pb uptake. This study provides a new insight into the combined neurotoxicity and underlying mechanisms of PS-MPs and Pb on zebrafish.

Hemocytes in blue mussel Mytilus edulis adopt different energy supply modes to cope with different BDE-47 exposures.

The energetic response of blue mussel Mytilus edulis when coping with tetrabromodiphenyl ether (BDE-47) exposure was evaluated from the perspective of alterations in energy supply mode, and the possible regulating mechanism was discussed based on a 21-day bioassay. The results showed that the energy supply mode changed with concentration: 0.1 µg/L BDE-47 decreased the activity of isocitrate dehydrogenase (IDH), succinate dehydrogenase (SDH), malate dehydrogenase and oxidative phosphorylation, suggesting inhibition of the tricarboxylic (TCA) acid cycle and aerobic respiration. The coincident increase in phosphofructokinase and the decrease in lactate dehydrogenase (LDH) indicated that glycolysis and anaerobic respiration were increased. When exposed to 1.0 µg/L BDE-47, M. edulis mainly utilized aerobic respiration, but lowered glucose metabolism as indicated by the decrease in glutamine and l-leucine was suggested to be involved in this process, which was differed from that in the control. The reoccurrence of IDH and SDH inhibition as well as LDH elevation indicated attenuation of aerobic and anaerobic respiration when the concentration increased to 10 µg/L, but severe protein damage was evidenced based on the elevation of amino acids and glutamine. Under the 0.1 µg/L BDE-47, activation of the AMPK-Hif-1a signaling pathway promoted the expression of glut1, which was the potential mechanism for the improvement of anaerobic respiration, and further activated glycolysis and anaerobic respiration. This study shows that the energy supply mode experienced a conversion from aerobic respiration under normal conditions to anaerobic mode in the low BDE-47 treatment and back to aerobic respiration with increasing BDE-47 concentrations, which may represent a potential mechanism for mussel physiological responses when faced with different levels of BDE-47 stress.