The Guangdong Province Key Laboratory for Aquatic Economic Animals, School of Life Science, Sun Yat-sen University, Guangzhou 510275, China.
Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI 53706, USA.
Toxins (Basel). 2018 Jul 3;10(7):270. doi: 10.3390/toxins10070270.
Aflatoxin biosynthesis is correlated with oxidative stress and is proposed to function as a secondary defense mechanism to redundant intracellular reactive oxygen species (ROS). We find that the antioxidant gallic acid inhibits aflatoxin formation and growth in in a dose-dependent manner. Global expression analysis (RNA-Seq) of gallic acid-treated showed that 0.8% (/) gallic acid revealed two possible routes of aflatoxin inhibition. Gallic acid significantly inhibited the expression of , encoding a transcription factor that participates in peroxisomal fatty acid β-oxidation, a fundamental contributor to aflatoxin production. Secondly, the carbon repression regulator encoding gene, , was significantly down regulated by gallic acid treatment. CreA is necessary for aflatoxin synthesis, and aflatoxin biosynthesis genes were significantly downregulated in ∆ mutants. In addition, the results of antioxidant enzyme activities and the lipid oxidation levels coupled with RNA-Seq data of antioxidant genes indicated that gallic acid may reduce oxidative stress through the glutathione- and thioredoxin-dependent systems in .
黄曲霉毒素的生物合成与氧化应激有关，被认为是一种冗余的细胞内活性氧（ROS）的次级防御机制。我们发现抗氧化剂没食子酸以剂量依赖的方式抑制黄曲霉毒素的形成和生长。经没食子酸处理后的的全局表达分析（RNA-Seq）表明，0.8%（/）没食子酸揭示了两种可能的黄曲霉毒素抑制途径。没食子酸显著抑制了参与过氧化物体脂肪酸β-氧化的转录因子编码基因 的表达，过氧化物体脂肪酸β-氧化是黄曲霉毒素产生的一个基本贡献因素。其次，碳抑制调节剂编码基因 的表达也被没食子酸处理显著下调。CreA 是合成黄曲霉毒素所必需的，而在 ∆突变体中，黄曲霉毒素合成基因的表达显著下调。此外，抗氧化酶活性的结果以及与抗氧化基因的 RNA-Seq 数据相结合表明，没食子酸可能通过谷胱甘肽和硫氧还蛋白依赖系统来减轻 中的氧化应激。
