Toxicology of Anthropogenic Pollutants on Fish

A special issue of Fishes (ISSN 2410-3888). This special issue belongs to the section "Environment and Climate Change".

Deadline for manuscript submissions: 20 October 2025 | Viewed by 1716

Special Issue Editor


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Guest Editor
1. Key Laboratory of Aquaculture in South China Sea for Aquatic Economic Animal of Guangdong Higher Education Institutes, College of Fishery, Guangdong Ocean University, Zhanjiang 524088, China
2. Guangdong Provincial Key Laboratory of Aquatic Animal Disease Control and Healthy Culture, College of Fishery, Guangdong Ocean University, Zhanjiang 524088, China
Interests: environmental endocrine disruptors (EDCs); aquatic toxicology; marine ecological environment; physiology of fish reproduction

Special Issue Information

Dear Colleagues,

As the impacts of human-induced pollution on aquatic ecosystems grow increasingly severe, there is an urgent need to understand the toxicological effects on fish species. We invite researchers from diverse fields, including ecology, environmental science, and toxicology, to contribute to our Special Issue dedicated to exploring the intricate relationships between anthropogenic pollutants and their effects on fish. Topics of interest include, but are not limited to, the physiological impacts of chemicals, microplastics, and trace elements on fish; the use of fish as bioindicators for pollution monitoring; and strategies for mitigating pollution and protecting aquatic ecosystems. Your insights, experimental reports, case studies, and research findings will be crucial in advancing our understanding of this critical issue and fostering effective conservation measures. We look forward to your contributions to this timely and important Special Issue.

Dr. Zhongdian Dong
Guest Editor

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Keywords

  • anthropogenic pollutants
  • fish toxicology
  • aquatic ecosystems
  • organic pollutants
  • microplastics
  • trace elements
  • environmental protection

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Published Papers (2 papers)

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Research

17 pages, 5231 KiB  
Article
Environmentally Relevant Sulfamethoxazole Induces Developmental Toxicity in Embryo-Larva of Marine Medaka (Oryzias melastigma)
by Jianxuan Huang, Lei Ye, Siyi Huang, Zuchun Chen, Jiahao Gao, Yangmei Li, Yusong Guo, Zhongduo Wang, Jian Liao, Zhongdian Dong and Ning Zhang
Fishes 2025, 10(3), 120; https://doi.org/10.3390/fishes10030120 - 8 Mar 2025
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Abstract
Sulfamethoxazole (SMX), a commonly used sulfonamide antibiotic, poses a threat to aquatic life due to its widespread presence in the environment. This study aims to investigate the specific effects of SMX on the development of marine medaka (Oryzias melastigma) embryos and [...] Read more.
Sulfamethoxazole (SMX), a commonly used sulfonamide antibiotic, poses a threat to aquatic life due to its widespread presence in the environment. This study aims to investigate the specific effects of SMX on the development of marine medaka (Oryzias melastigma) embryos and larvae. Marine medaka embryos were exposed to SMX at concentrations of 0 (solvent control group, SC group), 1 μg/L (low concentration group, L group), 60 μg/L (middle concentration group, M group), and 1000 μg/L (high concentration group, H group). The results indicated that SMX exposure significantly accelerated the heart rate of embryos (p < 0.0001) and shortened the hatching time while also causing anomalies such as reduced pigmentation, smaller eye size, spinal curvature, and yolk sac edema. SMX also led to a decrease in the total length of the larvae. The M group and the H group exhibited a significant increase (p < 0.05) in lipid accumulation in the visceral mass of the larvae. In the L group and the M group, there was a significant increase (p < 0.0001) in the swimming distance of the larvae. At the molecular level, SMX exposure affected the transcript levels of the genes involved in the cardiovascular system (ahrra, arnt2, atp2a1, and cacan1da), antioxidant and inflammatory systems (cat, cox-1, gpx, pparα, pparβ, and pparγ), nervous system (gap43, gfap, α-tubulin), intestinal barrier function (claudin-1), detoxification enzymes (ugt2c1-like), and lipid metabolism (rxraa) in the embryos to larval stage. The microbiome analysis showed that at the phylum level, exposure to SMX resulted in an increase in the abundance of Proteobacteria. Additionally, the abundance of Actinobacteriota significantly increased in the L group (p < 0.05). At the genus level, the abundance of Bifidobacterium significantly increased in the L group (p < 0.05), while the abundance of Vibrio significantly increased in the H group (p < 0.05). The alpha diversity analysis revealed a significant decrease in the Chao1 index in the L and H groups, indicating a reduction in microbial richness. The beta diversity analysis showed differences in the microbial communities of marine medaka larvae among different SMX exposure groups. This study elucidates the negative impacts of SMX on the development of marine medaka embryos and larvae and their microbial composition, providing a scientific basis for assessing the risks of SMX in marine ecosystems. Full article
(This article belongs to the Special Issue Toxicology of Anthropogenic Pollutants on Fish)
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13 pages, 4580 KiB  
Article
Transcriptome Analysis of the Effect of Acute Ammonia Stress on Pseudobagrus ussuriensis Liver Tissue
by Shun Shi, Xiaohui Sun, Chunnuan Zhang, Chenran Lv, Yajuan Liu, Juan Du and Qian Qi
Fishes 2025, 10(1), 17; https://doi.org/10.3390/fishes10010017 - 2 Jan 2025
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Abstract
Excess ammonia can damage the growth and development of fish. Pseudobagrus ussuriensis is a scaleless fish with important economic value that is more sensitive to ammonia stress. In this study, P. ussuriensis was explored using different ammonia concentrations [control (0 mg/L), CL; low [...] Read more.
Excess ammonia can damage the growth and development of fish. Pseudobagrus ussuriensis is a scaleless fish with important economic value that is more sensitive to ammonia stress. In this study, P. ussuriensis was explored using different ammonia concentrations [control (0 mg/L), CL; low stress (10 mg/L), T1L; and high stress (50 mg/L), T2L] for 48 h. Compared to the control group, the liver cells in the T1L group showed slight damage, while the T2L group was severely damaged, with the cells being loosely arranged, with nuclei lysis and cell vacuolization. The activities of superoxide dismutase, catalase, and glutathione in the T1L and T2L groups were significantly lower than those in the CL group (p < 0.05), and the malondialdehyde reached the maximum at 48 h. Furthermore, 9301 differentially expressed genes (DEGs) (4583 upregulated and 4718 downregulated) were detected by transcriptome sequencing. Most DEGs were highly enriched in cellular processes (GO:0009987) and cell parts (GO:0044464). Especially, the phosphatidylinositol 3-kinase/protein kinase B (PI3K-Akt) signaling pathway had the maximum quantity of DEGs in all the three groups. In-depth analysis revealed the stress caused multiple substitutions of SNP sites in pik3ca and kras, blocking the PI3K/Akt signaling pathway to prevent cancer cell proliferation and spread, accelerating the apoptosis of damaged cells. These results suggest that ammonia stress induces liver damage in P. ussuriensis, causing genetic mutations and cellular carcinogenesis, thereby accelerating cell apoptosis. Full article
(This article belongs to the Special Issue Toxicology of Anthropogenic Pollutants on Fish)
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