Genotoxicity of beauvericin.

Autor: Knutsen, Helle Katrine (AUTHOR), Åkesson, Agneta (AUTHOR), Bampidis, Vasileios (AUTHOR), Bodin, Laurent (AUTHOR), Chipman, James Kevin (AUTHOR), Degen, Gisela (AUTHOR), Hernández‐Jerez, Antonio (AUTHOR), Hofer, Tim (AUTHOR), Hogstrand, Christer (AUTHOR), Landi, Stefano (AUTHOR), Leblanc, Jean‐Charles (AUTHOR), Machera, Kyriaki (AUTHOR), Ntzani, Evangelia (AUTHOR), Rychen, Guido (AUTHOR), Sand, Salomon (AUTHOR), Schwerdtle, Tanja (AUTHOR), Vejdovszky, Katharina (AUTHOR), Viviani, Barbara (AUTHOR), Corsini, Emanuela (AUTHOR), Le Hégarat, Ludovic (AUTHOR)
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Zdroj: EFSA Journal. Oct2024, Vol. 22 Issue 10, p1-23. 23p.
Abstrakt: The European Commission (EC) asked EFSA to assess the genotoxicity of beauvericin (BEA). Relevant information, including that which has become available since the 2014 Scientific Opinion on the risks to human and animal health related to the presence of BEA and enniatins in food and feed, was reviewed. In the previous Opinion the Panel concluded that in vitro genotoxicity data were equivocal and there were no in vivo genotoxicity data available. New in vitro studies in mammalian cell lines provided no convincing evidence for induction of chromosomal damage by BEA as measured by micronucleus and chromosome aberration tests or an increase of DNA strand breaks as assessed by the Comet assay. In these studies, no concentration‐dependent effects or potential for interference from associated cytotoxicity were observed. In addition, DNA double‐strand breaks as measured by γ‐H2AX analysis were only observed following exposure to highly cytotoxic BEA concentrations. In vivo studies (Comet and Pig‐a assays, micronucleus test) with BEA were negative. In vitro gene expression studies showed no indication of a DNA damage response and (quantitative) structure activity relationship analysis was also not indicative of genotoxic potential. Some effects of BEA might play an indirect role in the formation of DNA strand breaks. These include increased reactive oxygen species, induction of cell cycle arrest and apoptosis, associated with interference in mitochondrial function and cell signalling. There was no compelling evidence of inflammatory and immunosuppressive effects. Taken together, the available data indicate that BEA is devoid of genotoxic potential. [ABSTRACT FROM AUTHOR]
Databáze: GreenFILE
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