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We assessed the bioavailability of Ag from Ag nanoparticles (NPs), stabilized with polyvinylpyrrolidone (PVP), to terrestrial isopods which were exposed to 10, 100 and 1000 μg Ag NPs/g of dry food. Different Ag species were determined in the NP suspension that was fed to isopods: (i) total Ag by atomic absorption spectroscopy, (ii) the sum of Ag-PVP complexes and free Ag + by anodic stripping voltammetry at the bismuth-film electrode, and (iii) free Ag + by ion-selective potentiometry. The amounts of Ag species in the consumed food were compared to the masses of Ag accumulated in the isopod digestive glands. Our results show that all three Ag species (Ag NPs, Ag-PVP complexes and free Ag + ) could be the source of bioaccumulated Ag, but to various degrees depending on the exposure concentration and transformations in the digestive system. We provide a proof that (i) Ag NPs dissolve and Ag-PVP complexes dissociate in the isopod digestive tract; (ii) the concentration of free Ag + in the suspension offered to the test organisms is not the only measure of bioavailable Ag. The type of NP stabilizer along with the NP transformations in the digestive system needs to be considered in the creation of new computational models of the nanomaterial fate. [ABSTRACT FROM AUTHOR]

Biomolecular profiling with Fourier-Transform InfraRed Microscopy was performed to distinguish the Zn2+-mediated effects on the crustacean (Porcellio scaber) digestive glands from the ones elicited by the ZnO nanoparticles (NPs). The exposure to ZnO NPs or ZnCl2(1500 and 4000 µg Zn/g of dry food) activated different types of metabolic pathways: some were found in the case of both substances, some only in the case of ZnCl2, and some only upon exposure to ZnO NPs. Both the ZnO NPs and the ZnCl2increased the protein (∼1312 cm−1; 1720–1485 cm−1/3000–2830 cm−1) and RNA concentration (∼1115 cm−1). At the highest exposure concentration of ZnCl2, where the effects occurred also at the organismal level, some additional changes were found that were not detected upon the ZnO NP exposure. These included changed carbohydrate (most likely glycogen) concentrations (∼1043 cm−1) and the desaturation of cell membrane lipids (∼3014 cm−1). The activation of novel metabolic pathways, as evidenced by changed proteins’ structure (at 1274 cm−1), was found only in the case of ZnO NPs. This proves that Zn2+are not the only inducers of the response to ZnO NPs. Low bioavailable fraction of Zn2+in the digestive glands exposed to ZnO NPs further supports the role of particles in the ZnO NP-generated effects. This study provides the evidence that ZnO NPs induce their own metabolic responses in the subtoxic range. [ABSTRACT FROM AUTHOR]