Titel
Cereulide and Deoxynivalenol Increase LC3 Protein Levels in HepG2 Liver Cells
Autor*in
Monika Ehling-Schulz
Department of Pathobiology, Institute of Microbiology, University of Veterinary Medicine
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Abstract
Food contaminants of bacterial or fungal origin frequently contaminate staple foods to various extents. Among others, the bacterial toxin cereulide (CER) and the mycotoxin deoxynivalenol (DON) co-occur in a mixed diet and are absorbed by the human body. Both toxins exert dis-tinctive mitotoxic potential. As damaged mitochondria are removed via autophagy, mitochondrial and lysosomal toxicity were assessed by applying low doses of single and combined toxins (CER 0.1–50 ng/mL; DON 0.01–5 µg/mL) to HepG2 liver cells. In addition to cytotoxicity assays, RT-qPCR was performed to investigate genes involved in lysosomal biogenesis and autophagy. CER and DON caused significant cytotoxicity on HepG2 cells after 5 and 24 h over a broad concentration range. CER, alone and in combination with DON, increased the transcription of the autophagy related genes coding for the microtubule associated protein 1A/1B light chain 3 (LC3) and sequestome 1 (SQSTM1) as well as LC3 protein expression which was determined using immunocytochemistry. DON increased LC3 protein expression without induction of gene transcription, hence it seems plausible that CER and DON act on different pathways. The results support the hypothesis that CER induces autophagy via the LC3 pathway and damaged mitochondria are therefore eliminated.
Stichwort
mitophagyFusariumBacillus cereushepatotoxicitymold
Objekt-Typ
Sprache
Englisch [eng]
Persistent identifier
Erschienen in
Titel
Toxins
Band
14
Ausgabe
2
ISSN
2072-6651
Erscheinungsdatum
2022
Publication
MDPI AG
Erscheinungsdatum
2022
Zugänglichkeit
Rechte
Rechteangabe
© 2022 by the authors
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