College of Veterinary Medicine, China Agricultural University, No.2 Yuanmingyuan West Road, Beijing, 100193, PR China; Beijing Key Laboratory of Detection Technology for Animal-Derived Food Safety, Beijing, 100193, PR China.
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, 75230, USA.
Food Chem Toxicol. 2022 Sep;167:113262. doi: 10.1016/j.fct.2022.113262. Epub 2022 Jul 2.
T-2 toxin is one of the most toxic and common trichothecene mycotoxins, and can cause various cardiovascular diseases. In this review, we summarized the current knowledge-base and challenges as it relates to T-2 toxin related cardiotoxicity. The molecular mechanisms and potential treatment approaches were also discussed. Pathologically, T-2 toxin-induced cardiac toxicity is characterized by cell injury and death in cardiomyocyte, increased capillary permeability, necrosis of cardiomyocyte, hemorrhage, and the infiltration of inflammatory cells in the heart. T-2 toxin exposure can cause cardiac fibrosis and finally lead to cardiac dysfunction. Mechanistically, T-2 toxin exposure-induced cardiac damage involves the production of ROS, mitochondrial dysfunction, peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling pathway, endoplasmic reticulum (ER stress), transforming growth factor beta 1 (TGF-β1)/smad family member 2/3 (Smad2/3) signaling pathway, and autophagy and inflammatory responses. Antioxidant supplementation (e.g., catalase, vitamin C, and selenium), induction of autophagy (e.g., rapamycin), blockade of inflammatory signaling (e.g., methylprednisolone) or treatment with PPAR-γ agonists (e.g., pioglitazone) may provide protective effects against these detrimental cardiac effects caused by T-2 toxin. We believe that our review provides new insights in understanding T-2 toxin exposure-induced cardiotoxicity and fuels effective prevention and treatment strategies against this important food-borne toxin-induced health problems.
T-2 毒素是最具毒性和最常见的单端孢霉烯族毒素之一，可导致各种心血管疾病。在这篇综述中，我们总结了与 T-2 毒素相关的心脏毒性的现有知识库和挑战。还讨论了分子机制和潜在的治疗方法。从病理学上看，T-2 毒素诱导的心脏毒性的特征是心肌细胞的细胞损伤和死亡、毛细血管通透性增加、心肌细胞坏死、出血以及心脏中炎性细胞的浸润。T-2 毒素暴露可导致心脏纤维化，最终导致心脏功能障碍。从机制上讲，T-2 毒素暴露引起的心脏损伤涉及 ROS 的产生、线粒体功能障碍、过氧化物酶体增殖物激活受体-γ（PPAR-γ）信号通路、内质网（ER 应激）、转化生长因子β 1（TGF-β1）/smad 家族成员 2/3（Smad2/3）信号通路以及自噬和炎症反应。抗氧化剂补充剂（例如，过氧化氢酶、维生素 C 和硒）、自噬诱导（例如，雷帕霉素）、炎症信号阻断（例如，甲基强的松龙）或 PPAR-γ 激动剂（例如，吡格列酮）的治疗可能对 T-2 毒素引起的这些有害心脏作用提供保护作用。我们相信，我们的综述为理解 T-2 毒素暴露引起的心脏毒性提供了新的见解，并为针对这种重要的食源性病原体毒素引起的健康问题的有效预防和治疗策略提供了动力。
