4.6 Article

Metabolomics of V2O5 nanoparticles and V2O5 nanofibers in human airway epithelial BEAS-2B cells

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TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 459, 期 -, 页码 -

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ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2022.116327

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Lung metabolism; Metabolic disruption; Nanofiber; Nanoparticles; Nanotoxicity; Risk assessment; Vanadium

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This study assessed the effects of two V2O5 nanomaterials on human airway epithelial cells using high-resolution metabolomics. The results showed dose-response effects of the nanomaterials on various metabolic pathways, as well as evidence of mitochondrial stress and increased lysosome fusion. These findings suggest that V2O5 nanomaterials may impact major metabolic pathways associated with lung diseases and highlight the potential of toxico-metabolomics in evaluating health risks.
Vanadium is a toxic metal listed by the IARC as possibly carcinogenic to humans. Manufactured nanosize va-nadium pentoxide (V2O5) materials are used in a wide range of industrial sectors and recently have been developed as nanomedicine for cancer therapeutics, yet limited information is available to evaluate relevant nanotoxicity. In this study we used high-resolution metabolomics to assess effects of two V2O5 nanomaterials, nanoparticles and nanofibers, at exposure levels (0.01, 0.1, and 1 ppm) that did not cause cell death (i.e., non-cytotoxic) in a human airway epithelial cell line, BEAS-2B. As prepared, V2O5 nanofiber exhibited a fibrous morphology, with a width approximately 63 +/- 12 nm and length in average 420 +/- 70 nm; whereas, V2O5 nanoparticles showed a typical particle morphology with a size 36 +/- 2 nm. Both V2O5 nanoparticles and nanofibers had dose-response effects on aminosugar, amino acid, fatty acid, carnitine, niacin and nucleotide metabolism. Differential effects of the particles and fibers included dibasic acid, glycosphingolipid and glycer-ophospholipid pathway associations with V2O5 nanoparticles, and cholesterol and sialic acid metabolism asso-ciations with V2O5 nanofibers. Examination by transmission electron microscopy provided evidence for mitochondrial stress and increased lysosome fusion by both nanomaterials, and these data were supported by effects on mitochondrial membrane potential and lysosomal activity. The results showed that non-cytotoxic exposures to V2O5 nanomaterials impact major metabolic pathways previously associated with human lung diseases and suggest that toxico-metabolomics may be useful to evaluate health risks from V2O5 nanomaterials.

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