Department of Biosciences, Teikyo University, 1-1 Toyosatodai, Utsunomiya 320-8551, Japan.
Toxins (Basel). 2019 Feb 12;11(2):107. doi: 10.3390/toxins11020107.
Aflatoxin contamination of crops is a worldwide problem, and elucidation of the regulatory mechanism of aflatoxin production, for example relative to the oxidative⁻antioxidative system, is needed. Studies have shown that oxidative stress induced by reactive oxygen species promotes aflatoxin production. However, superoxide has been suggested to have the opposite effect. Here, we investigated the effects of the superoxide generator, paraquat, and externally added superoxide dismutase (SOD) on aflatoxin production in . Paraquat with an IC value of 54.9 µM inhibited aflatoxin production without affecting fungal growth. It increased cytosolic and mitochondrial superoxide levels and downregulated the transcription of aflatoxin biosynthetic cluster genes, including , a key regulatory protein. The addition of bovine Cu/ZnSOD to the culture medium suppressed the paraquat-induced increase in superoxide levels, but it did not fully restore paraquat-inhibited aflatoxin production because bovine Cu/ZnSOD with an IC value of 17.9 µg/mL itself inhibited aflatoxin production. Externally added bovine Cu/ZnSOD increased the SOD activity in fungal cell extracts and upregulated the transcription of genes encoding Cu/ZnSOD and alcohol dehydrogenase. These results suggest that intracellular accumulation of superoxide impairs aflatoxin production by downregulating expression, and that externally added Cu/ZnSOD also suppresses aflatoxin production by a mechanism other than canonical superoxide elimination activity.
农作物黄曲霉毒素污染是一个全球性问题，需要阐明黄曲霉毒素产生的调控机制，例如与氧化还原系统的关系。研究表明，活性氧诱导的氧化应激促进黄曲霉毒素的产生。然而，超氧阴离子被认为有相反的作用。在这里，我们研究了超氧阴离子发生器百草枯和外加超氧化物歧化酶（SOD）对. 的黄曲霉毒素产生的影响。IC 值为 54.9 µM 的百草枯抑制黄曲霉毒素的产生而不影响真菌的生长。它增加了胞质和线粒体中超氧阴离子的水平，并下调了包括. 在内的黄曲霉生物合成簇基因的转录，这是一种关键的调节蛋白。向培养基中添加牛 Cu/ZnSOD 可抑制百草枯诱导的超氧阴离子水平升高，但不能完全恢复百草枯抑制的黄曲霉毒素产生，因为 IC 值为 17.9 µg/mL 的牛 Cu/ZnSOD 本身就抑制了黄曲霉毒素的产生。外加牛 Cu/ZnSOD 增加了真菌细胞提取物中的 SOD 活性，并上调了编码 Cu/ZnSOD 和醇脱氢酶的基因的转录。这些结果表明，细胞内超氧阴离子的积累通过下调. 的表达来损害黄曲霉毒素的产生，外加 Cu/ZnSOD 也通过除经典超氧阴离子消除活性以外的机制抑制黄曲霉毒素的产生。
