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.

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 effect of T-2 and HT-2 toxin using different doses in the starter (0-21 days: 1.04 mg T-2 toxin and 0.49 mg HT-2 toxin·kg -1 feed), and finisher diets (22-39 days: 0.12 mg T-2 toxin and 0.02 mg HT-2 toxin·kg -1 feed) was investigated in broiler chickens. Birds were divided into two groups fed with control and T-2 and HT-2 toxin contaminated diets. Pathological signs of toxicity were investigated on days 21 and 39 of the trial, individual liveweight was measured weekly. Five birds from each group were sacrificed on the 21 st and 39 th days of treatment, when blood plasma, red blood cell, liver and kidney samples were taken, in which malondialdehyde and reduced glutathione concentration and glutathione-peroxidase activity were determined.Pathological signs (lesions in the oral cavity and on the tongue, inflammation in the small intestine) were found in the group fed T-2 and HT-2 toxin contaminated feed on day 21 compared to control. Body weight was significantly lower as a result of feeding T-2 and HT-2 toxin contaminated diet. However, the contamination did not cause a significant increase of malondialdehyde content in the analysed tissues. Reduced glutathione content was significantly lower in the liver homogenate on day 39 than that of the control. Glutathione peroxidase activity also did not differ significantly in blood plasma, red blood cell haemolysates and kidney homogenates, while it was significantly higher in the liver homogenates of the mycotoxin-challenged birds.In conclusion, it can be stated that T-2 and HT-2 toxin exposure has long-term effects in broiler chickens. malondialdehyde, glutathione, glutathione peroxidase, chicken T-2 toxin,

The purpose of this study was to investigate the short-term effects of T-2 toxin exposure (3.09 mg/kg feed) on lipid peroxidation and glutathione redox system of broiler chicken. A total of 54 Cobb 500 cockerels were randomly distributed to two experimental groups at 21 days of age. Samples (blood plasma, red blood cell, liver, kidney and spleen) were collected every 12 h during a 48-h period. The results showed that the initial phase of lipid peroxidation, as measured by conjugated dienes and trienes in the liver, was continuously, but not significantly higher in T-2 toxin-dosed birds than in control birds. The termination phase of lipid peroxidation, as measured by malondialdehyde, was significantly higher in liver and kidney as a result of T-2 toxin exposure at the end of the experimental period (48th hour). The glutathione redox system activated shortly after starting the T-2 toxin exposure, which is supported by the significantly higher concentration of reduced glutathione and glutathione peroxidase activity in blood plasma at 24 and 48 h, in liver at 12, 24 and 36 h, and in kidney and spleen at 24 h. These results suggest that T-2 toxin, or its metabolites, may be involved in the generation of reactive oxygen substances which causes an increase in lipid peroxidation, and consequently activates the glutathione redox system, namely synthesis of reduced glutathione and glutathione peroxidase.

The purpose of the present study was to evaluate the effects of different dietary concentrations of T-2 toxin on blood plasma protein content, lipid peroxidation and glutathione redox system of pheasant (Phasianus colchicus). A total of 320 one-day-old female pheasants were randomly assigned to four treatment groups fed with a diet contaminated with different concentrations of T-2 toxin (control, 4 mg/kg, 8 mg/kg and 16 mg/kg). Birds were sacrificed at early (12, 24 and 72 hr) and late (1, 2 and 3 weeks) stages of the experiment to demonstrate the effect of T-2 toxin on lipid peroxidation and glutathione redox status in different tissues. Feed refusal and impaired growth were observed with dose dependent manner. Lipid-peroxidation was not induced in the liver, while the glutathione redox system was activated partly in the liver, but primarily in the blood plasma. Glutathione peroxidase activity has changed parallel with reduced glutathione concentration in all tissues. Based on our results, pheasants seem to have higher tolerance to T-2 toxin than other avian species, and glutathione redox system might contribute in some extent to this higher tolerance, in particular against free-radical mediated oxidative damage of tissues, such as liver.