Tissue Distribution of Radiolabeled 110mAg Nanoparticles in Fish: Arctic Charr (Salvelinus alpinus).

This study presents the first whole-body tissue distributions of dissolved (AgI) and 20 nm silver nanoparticles (Ag0NPs20) in fish (Arctic charr, Salvelinus alpinus). The distributions are provided for fish exposed to three different treatments: (i) intravenous (IV), (ii) dietary, and (iii) waterborne. Quantitative whole-body autoradiography (QWBA) analyses obtained on high-resolution images reveal distinct silver distribution patterns according to the treatments. The IV exposures showed that AgNPs20 were mainly located in bile and kidney after 8 d, while AgI was distributed through the whole body and reached particular tissues such as bones, eyes, skin, liver, spleen, kidney, and intestine. The Ag0NPs20 distribution with the dietary exposures suggests that some dissolution occurred within fish organs. We propose that dissolved silver could later precipitate as chloride, sulfide, or selenide and be incorporated in bones during the growth. Consequently, it is yet difficult to state if Ag0NPs20 cross biological barriers. Finally, the waterborne exposures revealed that the gills can capture Ag0NPs20, but in small quantities. This suggests that the stability of Ag0NPs20 in water is critical for the uptake via the gills.

Co-exposure to polystyrene plastic beads and polycyclic aromatic hydrocarbon contaminants in fish gill (RTgill-W1) and intestinal (RTgutGC) epithelial cells derived from rainbow trout (Oncorhynchus mykiss).

Microscopic plastic (MP) particles are a ubiquitous contaminant in aquatic environments, which may bind hydrophobic chemicals, such as polycyclic aromatic hydrocarbons (PAHs), altering their environmental fate and interactions with biota. Using rainbow trout gill (RTgill-W1) and intestinal (RTgutGC) epithelial cells we investigated the effects of polystyrene microbeads (PS-MBs; 220 nm) on the cyto- and genotoxicity of the environmental pollutants benzo[a]pyrene (BaP) and 3-nitrobenzanthrone (3-NBA) over 48 h (0, 0.1, 1 and 10 µM). The Alamar Blue bioassay, used to assess cytotoxicity, showed that both pollutants significantly decreased cell viability by 10-20% at 10 µM in both cell lines after 48 h whereas PS-MBs (5 or 50 µg mL-1) were non-toxic. Cytotoxicity in cells treated with PS-MBs together with BaP or 3-NBA were similar to those observed after exposure to BaP or 3-NBA alone. Using the formamidopyrimidine-DNA glycosylase (FPG)-modified comet assay 3-NBA, but not BaP, induced DNA damage in RTgutGC cells at 10 µM (∼10% tail DNA in the absence and ∼15% tail DNA in the presence of FPG versus ∼1% in controls), whereas PS-MBs alone showed no detrimental effects. Interestingly, comet formation was substantially increased (∼4-fold) when RTgutGC cells were exposed to PS-MBs (50 µg mL-1) and 10 µM 3-NBA compared to cells treated with 3-NBA alone. Further, using 32P-postlabelling we observed strong DNA adduct formation in 3-NBA-exposed RTgutGC cells (∼900 adducts/108 nucleotides). 3-NBA-derived DNA adduct formation was significantly decreased (∼20%) when RTgutGC cells were exposed to MB and 3-NBA compared to cells treated with 3-NBA alone. Our results show that PS-MBs impact on the genotoxicity of 3-NBA, causing a significant increase in DNA damage as measured by the comet assay in the intestinal cell line, providing proof of principle that MPs may alter the genotoxic potential of PAHs in fish cells.