Key Takeaways & Executive Findings
- •• • Chronic exposure to graphene oxide (GO) in zebrafish induces inflammation and differentially disturbs intestinal microbiota, with effects dependent on exposure duration and concentration (Jia et al., 2019). • • Polystyrene microplastics (PS-MPs) at environmentally relevant concentrations (e.g., 100 μg/L) cause gut dysbiosis and inflammation in adult zebrafish, altering microbial diversity and increasing pathogenic taxa (Jin et al., 2018). • • Nanoplastics (e.g., 50 nm PS) induce more severe gut microbiota dysbiosis and inflammation in adult zebrafish than microplastics (5 μm), highlighting size-dependent toxicity (Xie et al., 2021). • • Acute exposure to microplastics (e.g., 500 μg/L) induces metabolic disturbances and gut dysbiosis in adult zebrafish, with significant changes in metabolic pathways (Medriano & Bae, 2022).
Abstract
Non-antibiotic emerging contaminants (ECs) pose a growing threat to aquatic organisms, particularly fish, yet their impact on gut microbiota remains inadequately characterized. This systematic review synthesizes current evidence on the effects and mechanisms of non-antibiotic pharmaceuticals, pesticides, per- and polyfluoroalkyl substances (PFAS), nanomaterials, and microplastics on fish gut microbiota. Exposure to these ECs directly alters microbial composition and diversity, while indirectly disrupting host metabolism and immune function, leading to significant health impairments. Notably, EC exposure induces dysregulation of key factors such as lipopolysaccharide (LPS), compromising intestinal barrier integrity. Concurrently, gut microbiota can metabolically transform certain ECs into derivatives, establishing a complex pollutant-microbiota-host interaction network. The gut microbiota mediates EC-induced neurotoxicity, immune dysfunction, and metabolic disorders through signaling pathways such as TLR/NF-κB and metabolic homeostasis regulation. Current research predominantly addresses short-term exposure effects, leaving long-term low-dose impacts and transgenerational mechanisms poorly understood. Future investigations should employ multi-generational exposure and microbiota transplantation to elucidate gut microbiota-mediated toxicity mechanisms under non-antibiotic EC stress. This review underscores the urgent need for comprehensive risk assessment and regulatory frameworks targeting non-antibiotic ECs in aquatic environments.
1. Introduction
Non-antibiotic emerging contaminants (ECs) represent a diverse class of chemicals, including pharmaceuticals, pesticides, PFAS, nanomaterials, and microplastics, that are increasingly detected in aquatic environments. Unlike antibiotics, whose effects on fish gut microbiota are well-documented, non-antibiotic ECs have received less scrutiny despite their widespread presence and potential to disrupt microbial communities. Existing commercial water treatment and monitoring systems fail to adequately remove these contaminants, leading to chronic low-dose exposure in fish populations. This gap underscores the need for comprehensive toxicological assessments that consider the gut microbiota as a critical target and mediator of adverse outcomes.
This review addresses the bottleneck by systematically synthesizing evidence on how non-antibiotic ECs perturb fish gut microbiota and the consequent host health effects. By integrating findings from studies on graphene oxide, microplastics, and nanoplastics, we highlight the direct and indirect mechanisms, including disruption of intestinal barrier integrity and modulation of TLR/NF-κB signaling. The experimental protocols reviewed provide quantitative data on exposure concentrations and microbial changes, offering a foundation for risk assessment and regulatory action. Future research must prioritize long-term, multi-generational studies to unravel transgenerational effects and microbiota-mediated toxicity pathways.
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SU Yongsheng, GUO Xueping, YIN Daqiang (2026). Effects and Mechanisms of Non-Antibiotic Emerging Contaminants on Fish Gut Microbiota. Environmental Chemistry. https://doi.org/10.7524/j.issn.0254-6108.2025102501
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Frequently Asked Questions
What are the specific concentration thresholds for non-antibiotic ECs that induce significant gut microbiota dysbiosis in fish?
Studies indicate that polystyrene microplastics at concentrations as low as 100 μg/L can cause gut dysbiosis in adult zebrafish, while nanoplastics (50 nm) induce more severe effects at similar concentrations. For graphene oxide, chronic exposure at sub-lethal concentrations (e.g., 10 μg/L) has been shown to alter intestinal microbiota composition. These thresholds are environmentally relevant, as such concentrations are detected in polluted water bodies.
How do nanoplastics compare to microplastics in terms of gut microbiota toxicity, and what are the underlying mechanisms?
Nanoplastics (e.g., 50 nm) induce more severe gut microbiota dysbiosis and inflammation in adult zebrafish than microplastics (5 μm) at equivalent mass concentrations. This size-dependent toxicity is attributed to higher cellular uptake, greater surface area, and enhanced translocation across intestinal barriers, leading to stronger oxidative stress and immune responses.
What are the long-term ecological risks of chronic low-dose exposure to non-antibiotic ECs on fish populations?
Chronic low-dose exposure to non-antibiotic ECs can lead to persistent gut dysbiosis, metabolic disorders, and immune dysfunction, potentially reducing fish fitness and reproductive success. Transgenerational effects are plausible, as gut microbiota perturbations can be inherited, but current data are limited. Multi-generational studies are needed to assess population-level impacts.
Can gut microbiota metabolically transform non-antibiotic ECs, and what are the implications for toxicity?
Yes, gut microbiota can metabolize certain ECs, such as pharmaceuticals and pesticides, into derivatives that may be more or less toxic than the parent compounds. This metabolic transformation can alter the bioavailability and toxicity of ECs, potentially leading to bioaccumulation of harmful metabolites. Understanding these pathways is crucial for accurate risk assessment.
What are the key signaling pathways mediating gut microbiota-host interactions under non-antibiotic EC stress?
The TLR/NF-κB pathway is a central mediator, as EC-induced dysbiosis can increase LPS production, activating TLR4 and downstream NF-κB signaling, leading to inflammation. Additionally, gut microbiota influence host metabolic homeostasis through short-chain fatty acid production and regulation of metabolic genes, contributing to metabolic disorders.
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