The review followed the PRISMA-ScR reporting guidelines for scoping reviews, searching five databases between January 2010 and February 2026 for studies that exposed freshwater fish to silver nanoparticles through water and compared at least two surface conditions under equivalent circumstances. Twenty-one studies met those strict criteria, and together they paint a picture of a field dominated by a handful of model organisms. Zebrafish, Danio rerio, appears in virtually every endpoint category examined, from lethality and malformations to oxidative stress, DNA damage, neurobehavioral changes, histopathology and gene expression. Japanese medaka, Oryzias latipes, is the second most represented species, while rainbow trout and a few neotropical fish round out the dataset. Across all of these species, oxidative stress and silver bioaccumulation were the most broadly assessed endpoints, while genotoxicity and behavioral effects remained largely confined to the two main laboratory models.

To understand why surface chemistry matters so much, it helps to grasp what happens to a silver nanoparticle the moment it enters freshwater. Unlike seawater, where high ionic strength screens the electrostatic repulsion between particles and triggers almost instant agglomeration, freshwater allows nanosilver to remain colloidally stable for longer periods. That stability keeps the particles suspended in the water column where pelagic fish encounter them, but it also means the particles continue to oxidize and release silver ions, the single most important driver of nanosilver toxicity. Over time, agglomeration and sedimentation progressively shift the particles toward the benthic compartment, transferring the exposure burden from open-water fish to bottom-dwelling organisms. Temperature, fluctuating water levels and algal exudates have all been shown to accelerate ion release, while sulfidation and chlorination in natural waters lock silver into far less soluble compounds such as silver sulfide and silver chloride.

Manufacturers fight this instability by wrapping particles in capping agents, and the choice of wrapper turns out to be a decisive toxicological variable. The most common coatings in chemically synthesized nanosilver are citrate, polyvinylpyrrolidone, polyethylene glycol, gum arabic, silicate and polyethyleneimine, with citrate, PVP and PEI dominating the fish literature. The comparative evidence reveals a striking lack of consistency about which coating is worst. In zebrafish embryos, one study of five differently stabilized formulations concluded that the toxicity mechanism depends entirely on the stabilizer: in some cases the coating itself was the poison, in others the nanoparticle, and in others a combination of both. Another zebrafish study found that adding a coating actually increased toxicity compared with naked particles, because a positively charged hydroxyethylcellulose shell reacted more strongly with the negatively charged chorion surrounding the embryo. A third investigation of fourteen different preparations ranked PVP-coated particles as the most toxic, largely because PVP and thiol coatings released the most silver ions.

Rainbow trout told a different story. When researchers compared citrate, branched PEI, PVP and silicate coatings at an environmentally realistic concentration of 50 micrograms per liter, PVP proved the most bioavailable but not the most toxic. Instead, citrate and branched PEI, both charged coatings, produced the greatest genotoxicity and inflammation, reinforcing surface charge as a primary driver of biological damage. In Japanese medaka, gum arabic-coated particles were the most lethal despite releasing little ionic silver, pointing to a genuinely particle-specific toxicity pathway. A follow-up study with ten formulations confirmed gum arabic as the most dangerous coating and traced the mechanism to disruption of sodium regulation through inhibition of the Na+/K+-ATPase pump at the ionocytes of the gill epithelium, rather than to oxidative stress. The same coating can therefore occupy entirely different positions in a toxicity ranking depending on the species, life stage and endpoint being measured.

Particle size compounds the picture. In adult zebrafish exposed to citrate- or PVP-coated particles of 20 and 100 nanometers, size contributed more to toxicity than coating type, with smaller particles consistently more damaging. Yet even here the coating mattered: at equivalent sizes, citrate-coated particles outperformed PVP-coated ones across oxidative stress, DNA damage and apoptosis endpoints, even though PVP-exposed fish accumulated more silver in their tissues. That dissociation between internalized silver and harm is one of the review’s most important insights, because it demonstrates that total tissue burden is a poor proxy for toxicological risk. What matters is not how much silver enters the fish but in what chemical form, released where, and at what rate, a conclusion that challenges the assumptions underlying many standard hazard assessments.

Once nanosilver enters a natural water body, its synthetic coating is almost immediately overlaid by a second layer of adsorbed molecules, the eco-corona, composed of humic and fulvic substances, proteins, carbohydrates and extracellular polymeric substances. This environmental corona resets the particle’s biological interface, typically increasing its hydrodynamic diameter, rendering its surface more negative and blocking the oxidation sites where silver ions are generated. The review found that natural organic matter, especially humic acid, consistently mitigates nanosilver toxicity in fish. In zebrafish larvae, humic acid reduced mortality in a concentration-dependent manner by acting as a barrier to ion release. In adult zebrafish, humic acid actually increased dissolved silver over time by complexing ions through its carboxylic groups, yet mortality and behavioral impairments were still alleviated, showing that toxicity mechanisms extend well beyond simple ion release. An ex vivo gill model in two neotropical species confirmed reduced bioaccumulation, oxidative stress and ion release in the presence of humic acids, extending the protective effect beyond standard laboratory models.

Environmental transformations over time add further layers of complexity. Aged silver nanoparticles proved significantly more toxic than freshly prepared ones in medaka embryos, because ten days of aging increased ionic silver release in linear proportion to mortality. Humic acid counteracted this effect, but only when it had been pre-incubated with the particles, highlighting that contact time is essential for eco-corona formation and its protective action. Sulfidation, the natural conversion of particle surfaces to silver sulfide, acted as what one research team called a natural antidote: mortality in zebrafish embryos decreased progressively with increasing sulfidation levels, and sulfidated particles alleviated hepatic oxidative stress and brain acetylcholinesterase suppression in adult fish. Even the absence of a coating proved informative, as uncoated particles aggregated on the outer chorion surface without penetrating the embryo, yet still caused harm through ions generated at the chorion surface, confirming that the embryonic envelope functions as a filter for particles but not for dissolved silver.

The review closes with a candid assessment of the field’s blind spots. Most studies employed concentrations in the milligram-per-liter range, far above reported environmental levels, and only one included study used a genuinely environmentally relevant concentration of 20 micrograms per liter. The assumption that green-synthesized nanoparticles, made with plant extracts as reducing and capping agents, are inherently safer was directly contradicted by a zebrafish study in which green-synthesized particles were markedly more toxic than PVP-coated counterparts, releasing more ionic silver despite similar sizes, while a comparison in silver carp was confounded by lead contamination in the chemical reference material. Taxonomic coverage remains narrow, dominated by zebrafish and medaka, and endpoints skew toward embryo lethality rather than reproduction, neurobehavior or histopathology. The author argues that hazard assessments based solely on pristine, as-synthesized nanoparticles likely overestimate environmental risk, and that future experiments must track surface transformations dynamically, use realistic exposure levels and broaden both species and endpoints if protective water quality criteria for this emerging nanopollutant are to rest on solid ground.

Subject of Research: How surface coatings, eco-corona formation and environmental transformations modulate silver nanoparticle toxicity in freshwater fish

Article Title: Surface coatings and eco-corona as modulators of silver nanoparticle toxicity in freshwater fish

Article References: Ale, A. (2026). Surface coatings and eco-corona as modulators of silver nanoparticle toxicity in freshwater fish. Discover Toxicology, 3(1), Article 14. https://doi.org/10.1007/s44339-026-00060-2

Image Credits: AI Generated

DOI: 10.1007/s44339-026-00060-2

Keywords: silver nanoparticles, nanotoxicology, freshwater fish, eco-corona, surface coatings, zebrafish, humic acid, sulfidation, oxidative stress, silver ion release, green synthesis, ecotoxicology