Deoxynivalenol (DON) is a mycotoxin that seriously pollutes feed and the environment at a high risk to livestock and fish. Excessive DON could trigger oxidative stress and cause toxicity in non-target organisms. However, the impact of various concentrations of DON exposure on immune cells and the mechanism in it remain unknown. In the present test, the carp was a study object, the neutrophils were isolated and treated with different concentrations of DON (0, 20, 40 and 80 μg/mL). Cell death analysis found that an obvious increase of the apoptosis and necrosis rates exposed to DON, and aggravation in a dose-dependent manner. Moreover, DON exposure induced the expression of Cytochrome P450 (CYP450) family genes and triggered oxidative stress, including increased levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA), reduced the catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px)’s activities and glutathione (GSH) contents. Besides, inhibited PI3K/AKT signal and activated BCL2/BAX/Cyt-c/Caspase-3 and RIP1/RIP3/MLKL pathway were obvious and in a DON dose-dependent manner. In summary, the results indicate DON exposure could cause neutrophil death via activating CYP450s/ROS signal, inhibiting RI3K/AKT pathway, and inducing apoptosis and necroptosis. These data provide new insights for revealing the toxicological effects of mycotoxin.

脱氧雪腐镰刀菌烯醇 (DON) 是一种严重污染饲料和环境的真菌毒素，对牲畜和鱼类具有高风险。过量的 DON 会引发氧化应激并导致非目标生物体中毒。然而，不同浓度的 DON 暴露对免疫细胞的影响及其机制尚不清楚。在本试验中，以鲤鱼为研究对象，分离中性粒细胞并用不同浓度的 DON（0、20、40 和 80 μg/mL）处理。细胞死亡分析发现DON暴露后细胞凋亡和坏死率明显增加，并呈剂量依赖性加重。此外，DON 暴露诱导细胞色素 P450 (CYP450) 家族基因的表达并引发氧化应激，包括细胞内活性氧 (ROS) 和丙二醛 (MDA) 水平升高，降低过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD) 和谷胱甘肽过氧化物酶 (GSH-Px) 的活性和谷胱甘肽 (GSH) 含量。此外，抑制PI3K/AKT信号和激活BCL2/BAX/Cyt-c/Caspase-3和RIP1/RIP3/MLKL通路是明显的，并且呈DON剂量依赖性。总之，结果表明 DON 暴露可通过激活 CYP450s/ROS 信号、抑制 RI3K/AKT 通路、诱导细胞凋亡和坏死性凋亡导致中性粒细胞死亡。这些数据为揭示霉菌毒素的毒理学作用提供了新的见解。结果表明，DON 暴露可通过激活 CYP450s/ROS 信号、抑制 RI3K/AKT 通路、诱导细胞凋亡和坏死性凋亡导致中性粒细胞死亡。这些数据为揭示霉菌毒素的毒理学作用提供了新的见解。结果表明，DON 暴露可通过激活 CYP450s/ROS 信号、抑制 RI3K/AKT 通路、诱导细胞凋亡和坏死性凋亡导致中性粒细胞死亡。这些数据为揭示霉菌毒素的毒理学作用提供了新的见解。