Short-term effects of T-2 toxin or deoxynivalenol on lipid peroxidation and the glutathione system in common carp

• Published in: Acta veterinaria Hungarica (Budapest. 1983) Vol. 64; no. 4; p. 449
• Main Authors: Pelyhe, Csilla, Kövesi, Benjámin, Zándoki, Erika, Kovács, Balázs, Szabó-Fodor, Judit, Mézes, Miklós, Balogh, Krisztián
• Format: Journal Article
• Language: English
• Published: Hungary 01.12.2016
• Subjects: Animal Feed - analysis; Animals; Carps - metabolism; Food Contamination; Gene Expression Regulation, Enzymologic - drug effects; Glutathione - metabolism; Glutathione Peroxidase - genetics; Glutathione Peroxidase - metabolism; Lipid Peroxidation - drug effects; T-2 Toxin - toxicity; Trichothecenes - toxicity; Common carp; T-2 toxin; deoxynivalenol; gpx genes; glutathione peroxidase
• ISSN: 0236-6290
• DOI: 10.1556/004.2016.042

The purpose of this study was to investigate the short-term effects of a single oral dose of T-2 and HT-2 toxin at 0.15, 0.33 and 1.82 mg kg body weight, or deoxynivalenol (DON) and 15-acetyl-DON at 0.13, 0.31 and 1.75 mg kg body weight in common carp. Conjugated dienes and trienes (the early markers of lipid peroxidation) were elevated in all DON-treated groups at the 16th hour, while thiobarbituric acid reactive substances (TBARS; termination marker) were increased at the highest dose of DON at the 16th and 24th hours. T-2 toxin did not cause changes in these parameters. Glutathione content and glutathione peroxidase activity showed higher levels at the 16th hour as the effect of both mycotoxins. The expression of glutathione peroxidase (GPx4) genes (gpx4a and gpx4b) revealed a dual response. Downregulation was observed at the 8th hour, followed by an induction at the 16th hour, at the lowest dose of both mycotoxins. Higher doses revealed long-drawn emergence and an elevation was observed only at the 24th hour. However, at the lowest and highest doses of DON or T-2 toxin the changes in gene expression were delayed, which may be related to the low oxidative stress response, as suggested by the expression profiles of the nrf2, keap1, gpx4a and gpx4b genes.