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.

The present study was undertaken to examine the impact of varying concentrations of divalent zinc cation (Zn²⁺) on the growth, antioxidant levels, fatty acid composition, and related gene expression in a pennate diatom, Phaeodactylum tricornutum. As a prevalent environment contaminant, zinc is introduced into aquatic ecosystems via agricultural and industrial processes, exerting toxic effects on aquatic biota. P. tricornutum was exposed to gradient Zn²⁺ concentrations (0.99–1000.23 μM), with growth tracked spectrophotometrically. Antioxidant biomarkers, fatty acid profiles, and Zn-responsive gene expression were analyzed via biochemical assays, gas chromatography, and qRT-PCR, respectively. The results showed that appropriate concentrations of Zn²⁺ were essential for the growth of P. tricornutum, but high concentrations of Zn²⁺ (1000.23 μM) significantly inhibited its growth. Zinc stress also led to the production of reactive oxygen species (ROS), which in turn triggered oxidative stress, as evidenced by changes in antioxidant enzyme activities and lipid peroxidation levels. Furthermore, zinc stress affected the fatty acid composition of P. tricornutum, particularly in the group exposed to high concentrations of Zn²⁺. There was a notable reduction in the levels of polyunsaturated fatty acids (PUFAs) and highly unsaturated fatty acids (HUFAs), while the levels of saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs) increased. Gene expression analyses indicated alterations in the expression of zinc transporter proteins and antioxidant-related genes, suggesting that P. tricornutum adapts to zinc stress through the regulation of gene expression. These findings provide new insights into the understanding of the physiological and molecular responses of microalgae to zinc pollution and a scientific basis for evaluating the potential impacts of zinc pollution on aquatic ecosystems and developing bioremediation strategies.