Abstract
T-2 toxin is a trichothecene mycotoxin produced by fusarium species, which is mainly prevalent in grain and livestock feed. One of the main effects of this toxin is immunodepression. Previous studies have shown that T-2 toxin can cause damage to immune organs and impaired immune function in animals. However, selenomethionine (SeMet) as an organic selenium source can not only promote the growth and development of the body but also effectively improve the body’s immune function. In this study, rabbits were exposed to 0.4-mg/kg T-2 toxin, and abnormal blood routine indicators were found in the rabbits. HE staining also showed obvious lesions in the spleen and thymus tissue structures, accompanied by a large number of bleeding points. In addition, rabbits showed strong oxidative stress and inflammatory response after T-2 toxin action. 0.2 mg/kg, 0.4 mg/kg, and 0.6 mg/kg organic selenium were added to the feed. However, it was found that 0.2 mg/kg selenium can effectively improve the abnormal changes of blood routine and spleen and thymus tissue of rabbits. On the other hand, it can significantly increase the expression of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and total antioxidant capacity (T-AOC) in the spleen and thymus, and downregulate the expression of reactive oxygen species (ROS) and malondialdehyde (MDA). In addition, inflammatory factors interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in blood were also significantly inhibited; the expression of proliferating cell nuclear antigen (PCNA) in the spleen and thymus was also significantly increased after low-dose selenium treatment. Surprisingly, 0.4 mg/kg and 0.6 mg/kg of selenium did not effectively alleviate the immunotoxic effects caused by T-2 toxin, and cause damage to a certain extent. In summary, our results show that 0.2 mg/kg of SeMet can effectively alleviate the immunotoxicity caused by T-2 toxin. Selenium may protect rabbits from T-2 toxin by improving its antioxidant and anti-inflammatory capabilities.
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The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.
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Funding
Financial support for this research was provided by the Henan Provincial Key Research and Development and Promotion Project (192102110077 and 202102110093) the Young Backbone Teachers Assistance Scheme of Henan Province Colleges and Universities (2019GGJS080).
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Yumei Liu, Yaolu Xu, and Ziqiang Zhang conceived and designed the study. Jiajia Wang, Hui Xie, Xueyan Sun, Xuemin Zhu, and Lan Wei performed the experiments. This paper was written by Ziqiang Zhang and Yaolu Xu. The manuscript was reviewed and edited by Yumei Liu. All authors have read and approved this manuscript.
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Ziqiang Zhang reports financial support provided by Henan Science and Technology Department. Yumei Liu reports financial support provided by Henan Science and Technology Department and by The Education Department of Henan Province. All other authors declare no conflicts of interest.
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Highlights
• Selenomethionine inhibits T-2 toxin–induced oxidative stress.
• Selenomethionine inhibits expression of inflammatory factors induced by T-2 toxin.
• Selenomethionine reduces the damage of T-2 toxin to spleen and thymus.
• Selenomethionine increases PCNA protein expression in spleen and thymus after T-2 toxin infection.
• Selenomethionine reverses abnormal changes of blood cells after T-2 toxin infection.
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Zhang, Z., Xu, Y., Wang, J. et al. Protective Effect of Selenomethionine on T-2 Toxin–Induced Rabbit Immunotoxicity. Biol Trace Elem Res 200, 172–182 (2022). https://doi.org/10.1007/s12011-021-02625-1
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DOI: https://doi.org/10.1007/s12011-021-02625-1