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

2020 ◽  
Vol 104 (5) ◽  
pp. 1531-1539
Author(s):  
Benjamin Kövesi ◽  
Csilla Pelyhe ◽  
Erika Zándoki ◽  
Miklós Mézes ◽  
Krisztián Balogh
Keyword(s):  
Common Carp ◽  
Aflatoxin B1 ◽  
Redox System ◽  
Regulatory Genes ◽  
Combined Effects ◽  
Glutathione Redox System ◽  
Glutathione Redox

scholarly journals Individual and Combined Effects of Aflatoxin B1 and Sterigmatocystin on Lipid Peroxidation and Glutathione Redox System of Common Carp Liver

Toxins ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 109
Author(s):  
Benjamin Kövesi ◽  
Szabina Kulcsár ◽  
Zsolt Ancsin ◽  
Erika Zándoki ◽  
Márta Erdélyi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Common Carp ◽  
Aflatoxin B1 ◽  
Regulatory Gene ◽  
Redox System ◽  
Glutathione Biosynthesis ◽  
Glutathione Redox System ◽  
One Year ◽  
Encoding Genes ◽  
Glutathione Redox

The purpose of the study was to evaluate the short-term effects of aflatoxin B1 (AFB1 100 µg/kg feed) and sterigmatocystin (STC 1000 μg/kg feed) exposure individually and in combination (100 μg AFB1 + 1000 μg STC/kg feed) on the parameters of lipid peroxidation and glutathione redox system both in biochemical and gene expression levels in one-year-old common carp. Lipid peroxidation parameters were slightly affected, as significant differences were observed only in conjugated diene and triene concentrations. Reduced glutathione content decreased more markedly by STC than AFB1 or AFB1+STC, but glutathione peroxidase activity did not change. Expression of gpx4a, gpx4b, gss, and gsr genes was down-regulated due to STC compared to AFB1 or AFB1+STC, while an induction was found as effect of AFB1+STC in the case of gpx4a, but down-regulation for gpx4b as compared to AFB1. Expression of the glutathione biosynthesis regulatory gene, gss, was higher, but glutathione recycling enzyme encoding gene, gsr, was lower as an effect of AFB1+STC compared to AFB1. These results are supported by the changes in the expression of transcription factors encoding genes, nrf2, and keap1. The results revealed that individual effects of AFB1 and STC on different parameters are synergistic or antagonistic in multi-toxin treatment.

scholarly journals Lack of Dose- and Time-Dependent Effects of Aflatoxin B1 on Gene Expression and Enzymes Associated with Lipid Peroxidation and the Glutathione Redox System in Chicken

Toxins ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 84 ◽  
Author(s):  
Benjámin Kövesi ◽  
Mátyás Cserháti ◽  
Márta Erdélyi ◽  
Erika Zándoki ◽  
Miklós Mézes ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Aflatoxin B1 ◽  
Control Diet ◽  
Dose Range ◽  
Thiobarbituric Acid ◽  
Redox System ◽  
Time Dependent ◽  
Treatment Groups ◽  
Glutathione Redox System ◽  
Glutathione Redox

Effects of aflatoxin B1 (AFB1) on lipid peroxidation and glutathione system were investigated in chicken liver. In a three-week feeding trial, different doses (<1.0 μg/kg (control diet), 17.0 µg (diet A1), 92.0 µg (diet A2), and 182.0 µg (diet A3) AFB1 kg/feed) were used. Markers of lipid peroxidation, conjugated dienes and trienes showed higher values in A3, while amounts of thiobarbituric acid reactive substances were increased in the A1 group at day 21. Glutathione content was lower at day 14 in Group A2. Glutathione peroxidase 4 activity was increased at days 7 and 21 in the A3 group but reduced in the A2 and A3 groups at day 14. The GPX4 gene was downregulated at day 7 in the A2 group, but overregulated at days 14 and 21, and at day 14 in the A3 group. GSS was downregulated at day 14 in the A1 group but overregulated at day 21 in A1 and A2 groups. GSR was downregulated at days 7 and 21 in all treatment groups, but on day 14, induction was observed in the A3 group. The results indicated that AFB1 did not induce dose- or time-dependent effects on the glutathione redox system and its encoding genes at the dose range used, which means that oxidative stress is not the primary effect of AFB1 toxicity.

scholarly journals Short-term effects of deoxynivalenol, T-2 toxin, fumonisin B1 or ochratoxin on lipid peroxidation and glutathione redox system and its regulatory genes in common carp (Cyprinus carpio L.) liver

2020 ◽  
Vol 46 (6) ◽  
pp. 1921-1932
Author(s):  
Benjámin Kövesi ◽  
Szabina Kulcsár ◽  
Erika Zándoki ◽  
Judit Szabó-Fodor ◽  
Miklós Mézes ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Glutathione Peroxidase ◽  
Common Carp ◽  
Fumonisin B1 ◽  
Redox System ◽  
Short Term ◽  
Initiation Phase ◽  
Glutathione Redox System ◽  
Antioxidant Defence System ◽  
Glutathione Redox

Abstract The effects of a single oral dose of 1.82 mg kg−1 bw of T-2 and HT-2 toxin (T-2), 1.75 mg kg−1 bw deoxynivalenol (DON) and 15-acetyl DON, 1.96 mg kg−1 bw fumonisin B1 (FB1) or 1.85 mg kg−1 bw ochratoxin A (OTA) were investigated in common carp juveniles on lipid peroxidation, the parameters of the glutathione redox system including the expression of their encoding genes in a short-term (24 h) experiment. Markers of the initiation phase of lipid peroxidation, conjugated dienes, and trienes, were slightly affected by DON and OTA treatment at 16-h sampling. The termination marker, malondialdehyde, concentration increased only as an effect of FB1. Glutathione content and glutathione peroxidase activity showed significantly higher levels in the T-2 and FB1 groups at 8 h, and in the DON and FB1 groups at 16 h. The expression of glutathione peroxidase genes (gpx4a, gpx4b) showed a dual response. Downregulation of gpxa was observed at 8 h, as the effect of DON, FB1, and OTA, but an upregulation in the T-2 group. At 16 h gpx4a upregulated as an effect of DON, T-2, and FB1, and at 24 h in the DON and T-2 groups. Expression of gpx4b downregulated at 8 h, except in the T-2 group, and upregulation observed as an effect of T-2 at 24 h. The lack of an increase in the expression of nrf2, except as the effect of DON at 8 h, and a decrease in the keap1 expression suggests that the antioxidant defence system was activated at gene and protein levels through Keap1–Nrf2 independent pathways.

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