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Thiel, A.* ; Drews, F.* ; Pirritano, M.* ; Schumacher, F.* ; Michaelis, V.* ; Schwarz, M.* ; Franzenburg, S.* ; Schwerdtle, T.* ; Michalke, B. ; Kipp, A.P.* ; Kleuser, B.* ; Simon, M.* ; Bornhorst, J.*

Transcriptomics pave the way into mechanisms of cobalt and nickel toxicity: Nrf2-mediated cellular responses in liver carcinoma cells.

Redox Biol. 75:103290 (2024)
Verlagsversion DOI PMC
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Creative Commons Lizenzvertrag
Cobalt (Co) and Nickel (Ni) are used nowadays in various industrial applications like lithium-ion batteries, raising concerns about their environmental release and public health threats. Both metals are potentially carcinogenic and may cause neurological and cardiovascular dysfunctions, though underlying toxicity mechanisms have to be further elucidated. This study employs untargeted transcriptomics to analyze downstream cellular effects of individual and combined Co and Ni toxicity in human liver carcinoma cells (HepG2). The results reveal a synergistic effect of Co and Ni, leading to significantly higher number of differentially expressed genes (DEGs) compared to individual exposure. There was a clear enrichment of Nrf2 regulated genes linked to pathways such as glycolysis, iron and glutathione metabolism, and sphingolipid metabolism, confirmed by targeted analysis. Co and Ni exposure alone and combined caused nuclear Nrf2 translocation, while only combined exposure significantly affects iron and glutathione metabolism, evidenced by upregulation of HMOX-1 and iron storage protein FTL. Both metals impact sphingolipid metabolism, increasing dihydroceramide levels and decreasing ceramides, sphingosine and lactosylceramides, along with diacylglycerol accumulation. By combining transcriptomics and analytical methods, this study provides valuable insights into molecular mechanisms of Co and Ni toxicity, paving the way for further understanding of metal stress.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Cobalt ; Metal Interactions ; Nickel ; Nrf2 Signaling ; Sphingolipid Metabolism ; Transcriptomic Analysis; Stem-cells; Hypoxia; Cancer; Metabolism; Autophagy; Chloride; Talk; Gene
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 2213-2317
e-ISSN 2213-2317
Zeitschrift Redox Biology
Quellenangaben Band: 75, Heft: , Seiten: , Artikelnummer: 103290 Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit BioGeoChemistry and Analytics (BGC)
POF Topic(s) 30202 - Environmental Health
Forschungsfeld(er) Environmental Sciences
PSP-Element(e) G-504800-002
Förderungen DFG Research Infrastructure NGS_CC as part of the Next Generation Sequencing Competence Network
University of Wuppertal and the Faculty of Mathematics and Natural Sciences
DFG Research Unit TraceAge (FOR 2558)
DOI 10.1016/j.redox.2024.103290
WOS ID 001286472500001
Scopus ID 85199895185
PubMed ID 39088892
Erfassungsdatum 2024-08-02
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