Combined effects of aflatoxin B1 and deoxynivalenol on the expression of glutathione redox system regulatory genes in common carp

The purpose of the present study was to evaluate the short‐term effects of aflatoxin B1 (AFB1) and deoxynivalenol (DON) exposure on the expression of the genes encoding the glutathione redox system glutathione peroxidase 4a (gpx4a), glutathione peroxidase 4b (gpx4b), glutathione synthetase (gss) and...

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Published inJournal of animal physiology and animal nutrition Vol. 104; no. 5; pp. 1531 - 1539
Main Authors Kövesi, Benjamin, Pelyhe, Csilla, Zándoki, Erika, Mézes, Miklós, Balogh, Krisztián
Format Journal Article
LanguageEnglish
Published Germany Wiley Subscription Services, Inc 01.09.2020
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Summary:The purpose of the present study was to evaluate the short‐term effects of aflatoxin B1 (AFB1) and deoxynivalenol (DON) exposure on the expression of the genes encoding the glutathione redox system glutathione peroxidase 4a (gpx4a), glutathione peroxidase 4b (gpx4b), glutathione synthetase (gss) and glutathione reductase (gsr) and the oxidative stress response‐related transcription factors Kelch‐like ECH‐associated protein 1 (keap1) and nuclear factor‐erythroid 2 p45‐related factor 2 (nrf2) in liver, kidney and spleen of common carp. During the 24‐hr long experiment, three different doses (5 µg AFB1 and 110 µg DON; 7.5 µg AFB1 and 165 µg DON or 10 µg AFB1 and 220 µg DON/kg bw) were used. The results indicated that the co‐exposure of AFB1 and DON initiated free radical formation in liver, kidney and spleen, which was suggested by the increase in Nrf2 dependent genes, namely gpx4a, gpx4b, gss and gsr. Expression of keap1 gene showed upregulation after 8 hr of mycotoxin exposure, and also upregulation of nrf2 gene was found in kidney after 8 hr of exposure, while in the liver, only slight differences were observed. The changes in the expression of the analysed genes suggest that level of reactive oxygen species reached a critical level where other signalling pathway was activated as described by the hierarchical model of oxidative stress.
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ISSN:0931-2439
1439-0396
DOI:10.1111/jpn.13343