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 FB_1, 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.

单次口服剂量1.82 mg kg ^-1 bw的T-2和HT-2毒素（T-2），1.75 mg kg ^-1 bw的脱氧雪腐酚（DON）和15-乙酰基DON的影响，1.96 mg kg ^-1对普通鲤鱼幼鱼的脂质过氧化作用研究了bf伏马菌素B ₁（FB ₁）或1.85 mg kg ^-1 bw och曲毒素A（OTA），谷胱甘肽氧化还原系统的参数，包括短期内它们的编码基因的表达（ 24小时）实验。在16小时的采样中，DON和OTA处理对脂质过氧化，共轭二烯和三烯的起始阶段的标记有轻微的影响。终止标记丙二醛的浓度仅作为FB ₁的作用而增加。谷胱甘肽含量和谷胱甘肽过氧化物酶活性在T-2和FB ₁组在8 h处显着升高，而DON和FB ₁组在16 h时显着升高。谷胱甘肽过氧化物酶基因（gpx4a，gpx4b）的表达表现出双重反应。由于DON，FB ₁和OTA的作用，在8 h观察到gpxa的下调，但在T-2组中上调。在16 h，gpx4a作为DON，T-2和FB ₁的作用上调_，而在DON和T-2组中的24 h。除T-2组外，gpx4b的表达在8 h下调，而在24 h上调表达为T-2。缺乏表达的增加nrf2，除了在8小时受到DON的影响外，并且keap1表达的降低表明抗氧化剂防御系统通过Keap1-Nrf2独立途径在基因和蛋白质水平上被激活。