霉菌毒素可诱发细胞周期紊乱,细胞增殖,氧化应激,通过与MAPK相关的途径和细胞凋亡,JAK2/STAT3和Bcl-w/caspase-3,并引起生殖毒性,免疫毒性,和遗传毒性。以前的研究已经从DNA水平探索了霉菌毒素的毒性机制,RNA,和蛋白质,并证明霉菌毒素具有表观遗传毒性。为了探讨真菌毒素这些变化的毒性作用和机制,本文总结了DNA甲基化的变化,非编码RNA,几种常见真菌毒素诱导的RNA和组蛋白修饰(玉米赤霉烯酮,黄曲霉毒素B1,曲霉毒素A,脱氧雪腐镰刀菌烯醇,T-2毒素,等。)基于表观遗传学研究。此外,霉菌毒素诱导的表观遗传毒性在生殖细胞成熟中的作用,胚胎发育,和致癌作用被强调。总之,本综述为更好地理解霉菌毒素表观毒性的调控机制以及疾病的诊断和治疗提供了理论支持。
Mycotoxins can induce cell cycle disorders, cell proliferation, oxidative stress, and apoptosis through pathways such as those associated with MAPK, JAK2/STAT3, and Bcl-w/caspase-3, and cause reproductive toxicity, immunotoxicity, and genotoxicity. Previous studies have explored the toxicity mechanism of mycotoxins from the levels of DNA, RNA, and proteins, and proved that mycotoxins have epigenetic toxicity. To explore the toxic effects and mechanisms of these changes in mycotoxins, this paper summarizes the changes in DNA methylation, non-coding RNA, RNA and histone modification induced by several common mycotoxins (zearalenone, aflatoxin B1, ochratoxin A, deoxynivalenol, T-2 toxin, etc.) based on epigenetic studies. In addition, the roles of mycotoxin-induced epigenetic toxicity in germ cell maturation, embryonic development, and carcinogenesis are highlighted. In summary, this
review provides theoretical support for a better understanding of the regulatory mechanism of mycotoxin epigenotoxicity and the diagnosis and treatment of diseases.