Polluted Environments: Effects of Chemicals and Mixtures on Fish Physiology and Biochemistry

A special issue of Animals (ISSN 2076-2615). This special issue belongs to the section "Aquatic Animals".

Deadline for manuscript submissions: 12 June 2026 | Viewed by 1482

Special Issue Editors


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Guest Editor
Department of Environment and Health, Italian National Institute of Health, 00161 Roma, Italy
Interests: ecotoxicology; emerging contaminants; environmental impacts; human and ecosystem health; zebrafish

E-Mail Website
Guest Editor
Department of Biology, University of Rome Tor Vergata, 00133 Rome, Italy
Interests: ecotoxicology; emerging contaminants; environmental impacts; human and ecosystem health; zebrafish

Special Issue Information

Dear Colleagues,

The quality and scarcity of water resources are major global concerns, as aquatic ecosystems are increasingly compromised by mixtures of chemicals, including pharmaceuticals, micro- and nanoplastics, and other emerging contaminants. Climate change and extreme events further intensify these pressures, affecting water quality and ecosystem resilience. Fish are widely recognized as bioindicators of the ecosystems’ ecological status, as they show physiological, biochemical, and behavioral responses that link environmental health to human well-being.

This Special Issue aims to highlight innovative research on emerging pollutants and their mixtures that affect fish biology across multiple levels of biological organization, from molecular and cellular mechanisms to behavioral and population-level outcomes. Particular emphasis will be placed on studies that integrate ecotoxicology, physiology, and environmental risk assessment to better understand the combined impacts of contaminants and global change.

By highlighting fish as sentinel species in their interactions with contaminants and changing environments, this Special Issue aligns closely with the journal’s scope on animal biology, welfare, and their broader ecological context. Contributions will provide novel insights into the physiological, biochemical, and behavioral responses of fish, combining fundamental research, applied perspectives, and regulatory frameworks, and promoting sustainable strategies for aquatic ecosystem protection.

For this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Ecotoxicological approaches integrating environmental risk assessment and One Health perspectives;
  • Physiological, biochemical, and molecular responses of fish to single contaminants and mixtures;
  • Behavioral assays and biomarkers linking contaminant exposure to ecological outcomes;
  • Gene expression studies and novel molecular tools for ecotoxicology;
  • Impacts of climate change and extreme events on contaminant dynamics and fish responses;
  • Methodological advances in experimental designs, assays, and modeling for aquatic toxicology;
  • Physiological, biochemical, and behavioral effects of pharmaceuticals, pesticides, plastics, and other emerging pollutants on fish health and welfare;
  • Environmental monitoring of aquatic ecosystems and integration of scientific evidence into regulatory and policy frameworks.

We look forward to receiving your valuable contributions.

Dr. Ines Lacchetti
Dr. Arnold Rakaj
Guest Editors

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Keywords

  • fish
  • aquatic animals
  • environmental risk
  • ecotoxicology
  • physiological responses
  • climate change
  • chemical contamination

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Published Papers (2 papers)

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Research

17 pages, 11118 KB  
Article
Comparative Hepatotoxicity Assessment of PFOS and Its Alternative 6:2 FTSA in Adult Female Zebrafish
by Wenying Zhang, Yunru Dong, Yanmin Jian, Yazhe Jia, Keyi Yang, Yang Chen, Yuan Cao, Lulu Guo, Shujing Zhang, Dongwu Liu, Qiuxiang Pang and Shuang Jiao
Animals 2026, 16(9), 1368; https://doi.org/10.3390/ani16091368 - 29 Apr 2026
Viewed by 318
Abstract
As an alternative to perfluorooctane sulfonate (PFOS), 6:2 fluorotelomer sulfonic acid (6:2 FTSA) has been increasingly produced and detected in aquatic environments, yet its toxicological effects in fish remain incompletely characterized. In this study, adult female zebrafish were exposed for 30 days to [...] Read more.
As an alternative to perfluorooctane sulfonate (PFOS), 6:2 fluorotelomer sulfonic acid (6:2 FTSA) has been increasingly produced and detected in aquatic environments, yet its toxicological effects in fish remain incompletely characterized. In this study, adult female zebrafish were exposed for 30 days to solvent control (CK), 50 μg/L PFOS (P50), 50 μg/L 6:2 FTSA (F50), and 500 μg/L 6:2 FTSA (F500), respectively. Histopathological analysis revealed that both compounds induced hepatic injury, with the most severe damage observed in the F500 group. Hepatic transcriptomic analysis identified 645, 191, and 85 differentially expressed genes (DEGs) in the P50, F50, and F500 groups versus CK, respectively. Functional enrichment analysis further demonstrated distinct toxic profiles: PFOS at 50 μg/L primarily disrupted pathways related to the cell cycle, DNA replication, and reproduction. In contrast, 50 μg/L 6:2 FTSA predominantly activated PPAR-mediated lipid metabolism pathways, consistent with a “metabolic toxicity” phenotype. Notably, at 500 μg/L, 6:2 FTSA induced the most severe injury accompanied by a distinct transcriptomic signature—characterized by fewer DEGs but a pronounced enrichment of endoplasmic reticulum stress pathways—suggestive of a shift from metabolic perturbation to overwhelming cellular stress. Biochemical analysis confirmed a significant increase in malondialdehyde (MDA) only in the F50 group, supporting oxidative stress-mediated metabolic toxicity. Collectively, these findings demonstrate that 6:2 FTSA is not a safe alternative to PFOS but exhibits a dose-dependent and multifaceted toxicological profile, with high-dose effects indicative of acute cellular stress. This study underscores the need for case-specific, dose-range inclusive risk assessment of emerging PFAS alternatives. Full article
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19 pages, 3983 KB  
Article
Transcriptome-Based Analysis of the Mechanism of Acute Manganese-Induced Immune Function Decline and Metabolic Disorders in Estuarine Tapertail Anchovy (Coilia nasus)
by Xiaolu Shen, Yongli Wang, Mingchun Ren, Dongyu Huang, Jiaze Gu, Leimin Zhang, Hualiang Liang and Xiaoru Chen
Animals 2026, 16(6), 974; https://doi.org/10.3390/ani16060974 - 20 Mar 2026
Viewed by 779
Abstract
To characterize the transcriptional and physiological alterations induced by manganese stress in Coilia nasus, juveniles (mean weight 5.0 ± 0.2 g) were subjected to either manganese exposure (5.50 ± 0.03 mg/L) or control (0 mg/L) for a 12 h period. Subsequently, gill [...] Read more.
To characterize the transcriptional and physiological alterations induced by manganese stress in Coilia nasus, juveniles (mean weight 5.0 ± 0.2 g) were subjected to either manganese exposure (5.50 ± 0.03 mg/L) or control (0 mg/L) for a 12 h period. Subsequently, gill tissues were excised for evaluation of antioxidant parameters and RNA-Seq analysis. A total of 753 DEGs were identified in the manganese exposure group compared to controls, comprising 287 up-regulated and 466 down-regulated genes. GO and KEGG enrichment analysis of DEGs showed that most of the DEGs were involved in immune and metabolic pathways, which disturbed the biological processes related to immunity and metabolism at the molecular level. The acute manganese stress initiated a multi-level antioxidant response to cope with oxidative stress in Coilia nasus. This finding was further supported by the significant increase in MDA content and significant decrease in GSH content and GSH-Px activity under manganese exposure, while SOD and CAT activities were significantly increased. Simultaneously, the acute manganese stress triggered profound metabolic reprogramming to cope with energy pressure in Coilia nasus, which showed that manganese exposure significantly down-regulated energy metabolism-related genes (pfkm, pgam2, eno3, pkm, aqp9, apoa1, tkt, sds); furthermore, the overall energy metabolism network was widely inhibited, while lipid metabolism-related genes (fabp3, cpt1a) were significantly up-regulated to compensatorily activate fatty acid transport and β-oxidation pathways. In addition, the acute manganese stress initiated a complex immune response pattern to cope with cell damage in Coilia nasus, which showed that manganese exposure significantly enhanced the expression of inflammatory signaling genes (mapk1, stat1, tgfb3); furthermore, certain inflammatory pathways were activated, while the expressions of immune regulatory genes (traf6, il-10) were significantly decreased. In summary, these results indicated that manganese exposure could impair immune function, disrupt metabolism, and induce oxidative stress in Coilia nasus. Full article
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