T-2 toxin, a type A trichothecene, is a secondary metabolite produced by Fusarium poae, Fusarium sporotrichioides, and Fusarium tricinctum. As the most toxic trichothecenes, T-2 toxin causes severe damage to multiple organs, especially to liver. However, the contamination of T-2 toxin covers a wide range of plants, including nuts, grains, fruits and herbs globally. And due to chemical stability of T-2 toxin, it is difficult to be completely removed from the food and feeds, which poses a great threat to human and animal health. Liver is the major detoxifying organ which also makes it the main target of T-2 toxin. After being absorbed by intestine, the first pass effect will reduce the level of T-2 toxin in blood indicating that liver is the main metabolic site of T-2 toxin in vivo. In this review, updated researches on the hepatotoxicity of T-2 toxin were summarized. The metabolic characteristic of T-2 toxin in vivo was introduced. The main hepatotoxic mechanisms of T-2 toxin are oxidative stress, mitochondrial damage, deoxyribonucleic acid (DNA) methylation, autophagy and apoptosis. The remission of the hepatotoxicity induced by T-2 toxin was also studied in this review followed by new findings on the detoxification of hepatotoxicity induced by T-2 toxin. The review aimed to offer a comprehensive view and proposes new perspectives in the field of hepatotoxicity induced by T-2 toxin.

T-2 毒素，一种 A 型单端孢霉烯，是由Fusarium poae、Fusarium sporotrichioides和Fusarium tricinctum产生的次级代谢产物. 作为毒性最强的单端孢霉烯，T-2毒素对多个器官造成严重损害，尤其是肝脏。然而，T-2毒素的污染涉及范围广泛的植物，包括全球范围内的坚果、谷物、水果和草药。并且由于T-2毒素的化学稳定性，很难从食品和饲料中完全去除，对人类和动物的健康构成了极大的威胁。肝脏是主要的解毒器官，这也使其成为 T-2 毒素的主要目标。被肠道吸收后，首过效应会降低血液中T-2毒素的水平，说明肝脏是T-2毒素在体内的主要代谢场所。本文综述了T-2毒素肝毒性的最新研究进展。T-2毒素在体内的代谢特征被介绍。T-2毒素的主要肝毒性机制是氧化应激、线粒体损伤、脱氧核糖核酸（DNA）甲基化、自噬和细胞凋亡。这篇综述还研究了 T-2 毒素诱导的肝毒性的缓解，以及 T-2 毒素诱导的肝毒性解毒的新发现。该综述旨在提供一个全面的观点，并在 T-2 毒素诱导的肝毒性领域提出新的观点。