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Aflatoxin biosynthesis has established a connection with oxidative stress, suggesting a prevention strategy for aflatoxin contamination via reactive oxygen species (ROS) removal. Epigallocatechin gallate (EGCG) is one of the most active and the richest molecules in green tea with well-known antioxidant effects. Here, we found EGCG could inhibit aflatoxin B1 (AFB1) biosynthesis without affecting mycelial growth in Aspergillus flavus, and the arrest occurred before the synthesis of toxin intermediate metabolites. Further RNA-seq analysis indicated that multiple genes involved in AFB1 biosynthesis were down-regulated. In addition, EGCG exposure facilitated the significantly decreased expression of AtfA which is a bZIP (basic leucine zipper) transcription factor mediating oxidative stress. Notably, KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis indicated that the MAPK signaling pathway target transcription factor was down-regulated by 1 mg/mL EGCG. Further Western blot analysis showed 1 mg/mL EGCG could decrease the levels of phosphorylated SakA in both the cytoplasm and nucleus. Taken together, these data evidently supported that EGCG inhibited AFB1 biosynthesis and alleviated oxidative stress via MAPK signaling pathway. Finally, we evaluated AFB1 contamination in soy sauce fermentation and found that EGCG could completely control AFB1 contamination at 8 mg/mL. Conclusively, our results supported the potential use of EGCG as a natural agent to prevent AFB1 contamination in fermentation industry.

Aspergillus flavus is saprophytic soil fungus that contaminates seed crops with the carcinogenic secondary metabolite aflatoxin, posing a significant threat to humans and animals. Ferrous sulfate is a common iron supplement that is used to the treatment of iron-deficiency anemia. Here, we identified an unexpected inhibitory role of ferrous sulfate on A. flavus. With specific fluorescent dyes, we detected several conidial ferroptosis hallmarks in conidia under the treatment of 1 mM Fe2+, including nonapoptosis necrosis, iron-dependent, lipid peroxide accumulation, and ROS burst. However, unlike traditional ferroptosis in mammals, Fe2+ triggered conidial ferroptosis in A. flavus was regulated by NADPH oxidase (NOXs) activation instead of Fenton reaction. Transcriptomic and some other bioinformatics analyses showed that NoxA in A. flavus might be a potential target of Fe2+, and thus led to the occurrence of conidial ferroptosis. Furthermore, noxA deletion mutant was constructed, and both ROS generation and conidial ferroptosis in ΔnoxA was reduced when exposed to Fe2+. Taken together, our study revealed an exogenous Fe2+-triggered conidial ferroptosis pathway mediated by NoxA of A. flavus, which greatly contributes to the development of an alternative strategy to control this pathogen.

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