Investigating the levels, spatial distribution, and trophic transfer patterns of short-chain chlorinated paraffins in the Southern Bohai Sea, China.

The marine environment of the southern Bohai Sea is severely polluted by short-chain chlorinated paraffins (SCCPs). To improve understanding of how SCCPs occur and of how they migrate, are transformed, and transferred in this area, we collected seawater, sediment, and organism samples, and determined the SCCP contents using a new approach based on high-resolution mass spectrometry. The ΣSCCP concentrations in the seawater, sediment, and organism samples ranged from 57.5 to 1150.4 ng/L, 167.7-1105.9 ng/g (dry weight), and 11.4-583.0 ng/g (wet weight), respectively. Simulation of the spatial distribution of SCCPs using Kriging interpolation showed that SCCPs were markedly influenced by land-based pollution. Substantial quantities of SCCPs were transported to the marine environment via surface runoff from rivers that passed through areas of major SCCP production. Once discharged from such rivers into the Bohai Sea, these SCCPs were further dispersed under the influence of ocean currents. Furthermore, the logarithmic bioaccumulation factor that varied from 2.12 to 3.20 and the trophic magnification factor that reached 5.60 (r2 = 0.750, p < 0.01) suggest that organisms have the ability to accumulate and biomagnify SCCPs through the food chain, which could potentially present risks to both marine ecosystems and human health.

Amantadine Toxicity in Apostichopus japonicus Revealed by Proteomics.

Amantadine exposure can alter biological processes in sea cucumbers, which are an economically important seafood in China. In this study, amantadine toxicity in Apostichopus japonicus was analyzed by oxidative stress and histopathological methods. Quantitative tandem mass tag labeling was used to examine changes in protein contents and metabolic pathways in A. japonicus intestinal tissues after exposure to 100 µg/L amantadine for 96 h. Catalase activity significantly increased from days 1 to 3 of exposure, but it decreased on day 4. Superoxide dismutase and glutathione activities were inhibited throughout the exposure period. Malondialdehyde contents increased on days 1 and 4 but decreased on days 2 and 3. Proteomics analysis revealed 111 differentially expressed proteins in the intestines of A. japonicus after amantadine exposure compared with the control group. An analysis of the involved metabolic pathways showed that the glycolytic and glycogenic pathways may have increased energy production and conversion in A. japonicus after amantadine exposure. The NF-κB, TNF, and IL-17 pathways were likely induced by amantadine exposure, thereby activating NF-κB and triggering intestinal inflammation and apoptosis. Amino acid metabolism analysis showed that the leucine and isoleucine degradation pathways and the phenylalanine metabolic pathway inhibited protein synthesis and growth in A. japonicus. This study investigated the regulatory response mechanisms in A. japonicus intestinal tissues after exposure to amantadine, providing a theoretical basis for further research on amantadine toxicity.