Assessing the exposure to nanosilver and silver nitrate on fathead minnow gill gene expression and mucus production

Abstract

Silver exposure is toxic to fish due to disturbances of normal gill function. A proposed toxicity mechanism of silver nanoparticles (AgNP) is derived from the release of silver ions, similar to silver nitrate (AgNO3). However, some datasets support the fact that AgNP can have unique toxic effects that are mediated at the gill. To determine if differences between AgNO3 and AgNP toxicities exist, fathead minnows were exposed to 20 nm PVP- or citrate-coated silver nanoparticles (50.3 μg/L PVP-AgNP; 56.0 μg/L citrate-AgNP) or 3.81 μg/L AgNO3 for 96 h. These concentrations were applied to approximate the dissolved fraction of Ag in the AgNP suspensions. Mucus production in the water was measured. While mucus production was initially significantly increased in the first 4 h of exposure in all silver treatments compared to control, a decrease in mucus production was observed following 24–96 h of exposure. To determine which genes/pathways are driving this shift in mucus production, gills were dissected and microarray analysis was performed. Hierarchical clustering of differentially expressed genes revealed that all samples distinctly clustered by treatment. There were 109 differentially expressed genes shared among all Ag treatments compared to controls. However, there were 185, 423, and 615 differentially expressed genes unique to AgNO3, PVP-AgNP, and citrate-AgNP, relative to control. While functional analysis indicated several common enriched pathways, such as aryl hydrocarbon receptor signaling, this analysis also indicated some unique pathways between nanosilver and AgNO3. Our results show that AgNO3, PVP-AgNP, and citrate-AgNP exposure affected mucus production in fish gills and also lead to common and unique transcriptional changes.