2 research outputs found

    Effect of Ingested Tungsten Oxide (WO<sub><i>x</i></sub>) Nanofibers on Digestive Gland Tissue of Porcellio scaber (Isopoda, Crustacea): Fourier Transform Infrared (FTIR) Imaging

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    Tungsten nanofibers are recognized as biologically potent. We study deviations in molecular composition between normal and digestive gland tissue of WO<sub><i>x</i></sub> nanofibers (nano-WO<sub><i>x</i></sub>) fed invertebrate Porcellio scaber (Iosopda, Crustacea) and revealed mechanisms of nano-WO<sub><i>x</i></sub> effect <i>in vivo</i>. Fourier Transform Infrared (FTIR) imaging performed on digestive gland epithelium was supplemented by toxicity and cytotoxicity analyses as well as scanning electron microscopy (SEM) of the surface of the epithelium. The difference in the spectra of the Nano-WO<sub><i>x</i></sub> treated and control cells showed up in the central region of the cells and were related to lipid peroxidation, and structural changes of nucleic acids. The conventional toxicity parameters failed to show toxic effects of nano-WO<sub><i>x</i></sub>, whereas the cytotoxicity biomarkers and SEM investigation of digestive gland epithelium indicated sporadic effects of nanofibers. Since toxicological and cytological measurements did not highlight severe effects, the biochemical alterations evidenced by FTIR imaging have been explained as the result of cell protection (acclimation) mechanisms to unfavorable conditions and indication of a nonhomeostatic state, which can lead to toxic effects

    FTIR microscopy reveals distinct biomolecular profile of crustacean digestive glands upon subtoxic exposure to ZnO nanoparticles

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    <p>Biomolecular profiling with Fourier-Transform InfraRed Microscopy was performed to distinguish the Zn<sup>2+</sup>-mediated effects on the crustacean (<i>Porcellio scaber</i>) digestive glands from the ones elicited by the ZnO nanoparticles (NPs). The exposure to ZnO NPs or ZnCl<sub>2</sub> (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 ZnCl<sub>2</sub>, and some only upon exposure to ZnO NPs. Both the ZnO NPs and the ZnCl<sub>2</sub> increased the protein (∼1312 cm<sup>−1</sup>; 1720–1485 cm<sup>−1</sup>/3000–2830 cm<sup>−1</sup>) and RNA concentration (∼1115 cm<sup>−1</sup>). At the highest exposure concentration of ZnCl<sub>2</sub>, 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<sup>−1</sup>) and the desaturation of cell membrane lipids (∼3014 cm<sup>−1</sup>). The activation of novel metabolic pathways, as evidenced by changed proteins’ structure (at 1274 cm<sup>−1</sup>), was found only in the case of ZnO NPs. This proves that Zn<sup>2+</sup> are not the only inducers of the response to ZnO NPs. Low bioavailable fraction of Zn<sup>2+</sup> 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.</p
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