The purpose of study was to investigate the effects of T-2 toxin (4.11 mg T-2 toxin and 0.45 mg HT-2 toxin kg(-1) feed) and deoxynivalenol (5.96 and 0.33 mg 15-acetyl deoxynivalenol (DON) kg(-1) feed) in 1-year-old common carp juveniles in a 4-week feeding trial. The exposure of mycotoxins resulted in increased mortality in both groups consuming mycotoxin-contaminated diet. Parameters of lipid peroxidation were not affected during the trial, and antioxidant defence also did not show response to oxidative stress; however, glutatione peroxidase activity slightly, but significantly, decreased in the T-2 toxin group. Glutathione S-transferase activity showed moderate decrease as effect of T-2 toxin, which suggests its effect on xenobiotic transformation. Reduced glutathione concentration showed moderate changes as effect of DON exposure, but T-2 toxin has no effect. Expression of phospholipid hydroperoxide glutathione peroxidase (GPx4) genes showed different response to mycotoxin exposure. T-2 toxin caused dual response in the expression of gpx4a (early and late downregulation and mid-term upregulation), but continuous upregulation was found as effect of deoxynivalenol. Expression of the other gene, gpx4b, was upregulated by both trichothecenes during the whole period. The results suggested that trichothecenes have some effect on free radical formation and antioxidant defence, but the changes depend on the duration of exposure and the dose applied, and in case of glutathione peroxidase, there was no correlation between expression of genes and enzyme activity.

Authors studied the effect of sterigmatocystin from infected corn (STC), purified sterigmatocystin (PSTC), and aflatoxin B1 from infected corn (AFB1) on lipid peroxidation and glutathione redox parameters, including the expression of their encoding genes in a sub-chronic (14 days) trial. A total of 144 three-week-old cockerels was divided into four experimental groups (n = 36 in each). Control feed was contaminated with STC or PSTC (1590 µg STC/kg or 1570.5 µg STC/kg feed), or with AFB1 (149.1 µg AFB1/kg feed). Six birds from each group were sampled at day 1, 2, 3, 7 and 14 of mycotoxin exposure. As parameters of lipid peroxidation, conjugated dienes (CD) and trienes (CT) were measured in the liver, while malondialdehyde (MDA) concentration was determined in blood plasma, red blood cell hemolysate and liver. Reduced glutathione (GSH) concentration and glutathione peroxidase (GPx) activity were determined in the same samples, and expression of glutathione peroxidase 4 (GPX4), glutathione synthetase (GSS) and glutathione reductase (GSR) genes was measured by RT-PCR in the liver. STC, PSTC or AFB1 caused a slight, but not significant, increase in CD and CT levels; however, in the case of MDA, no increase was found in the liver. Glutathione redox system was activated in the liver by AFB1, but less markedly by STC/PSTC. PSTC and AFB1 resulted in a higher expression of GPX4, while GSS expression was down-regulated by AFB1 on day 1, but up-regulated by STC on day 2 and by both mycotoxins on day 7. However, on day 14, GSS expression was down-regulated by PSTC. Expression of GSR was low on day 1 in AFB1 and PSTC groups, but later it was up-regulated by AFB1. The observed changes regarding gene expression strengthen the hypothesis that the mild oxidative stress, caused by the applied STC doses, activates the glutathione redox system of broiler chickens.

No abstract

It has been proven by several studies that Fusarium mycotoxins induce oxidative stress in animals, consequently inducing lipid peroxidation, which the glutathione system can neutralize. A short-term (3-day) in vivo feeding trial was performed with laying hens using a double dose of the EU recommendation for mycotoxin contamination (T-2 toxin 0.5 mg/kg feed; deoxynivalenol (DON) 10 mg/kg feed; fumonisin B1 (FB1) 40 mg/kg feed). Some lipid peroxidation and glutathione redox system parameters and gene expression levels were measured in the liver. The results show that FB1 significantly decreased the reduced glutathione (GSH) content and the activity of glutathione peroxidase (GPx) compared to the control and the two other mycotoxin-treated groups on day 3. Lipid peroxidation was affected by all three mycotoxins. Significantly lower values were observed in the case of conjugated dienes for all of the three mycotoxins and malondialdehyde concentration as an effect of DON on day 3. T-2 toxin and DON upregulated the expression of the GPX4 gene. The results show that Fusarium mycotoxins had different effects at the end of the trial. The FB1 exposure caused a decrease in the glutathione redox markers, while DON decreased the formation of malondialdehyde. The results suggest that the Fusarium mycotoxins investigated individually differently activated the antioxidant defense and caused low-level oxidative stress at the dose applied.

The purpose of this study was to evaluate the effect of three-weeks ochratoxin A (OTA) exposure on some lipid peroxidation parameters, reduced glutathione concentration and glutathione-peroxidase activity, as well as expression of oxidative stress response-related (KEAP1, NRF2) and glutathione system (GPX3, GPX4, GSS, GSR) genes in chickens. Three levels of exposure (106, 654 and 1126 μg/kg feed) were applied. The results showed that OTA initiated free radical formation, which was suggested by the increase in the malondialdehyde content in the liver and kidney, which was more marked in the liver, depending on the length of exposure and dose. Reduced glutathione concentration increased as an effect of the highest OTA dose in blood plasma and in liver, but not in red blood cell hemolysates and the kidney. Glutathione peroxidase activity did not change in the blood and showed increasing tendency in the liver, and significant increase in the kidney. Expression of KEAP1 gene showed up-regulation in the liver, and down-regulation in the kidney, but overexpression of NRF2 gene was found in the liver and kidney at the highest dose. However, down-regulation of Nrf2 dependent genes, GPX3, GPX4, GSS and GSR, suggested an improper antioxidant response at the protein level, thus oxidative stress occurred, even at the dose of the EU regulatory limit for poultry diets.