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Aflatoxin degradation by Bacillus subtilis UTB1 is based on production of an oxidoreductase involved in bacilysin biosynthesis
Food Control ( IF 5.6 ) Pub Date : 2018-12-01 , DOI: 10.1016/j.foodcont.2018.03.002
Hamideh Afsharmanesh , Alejandro Perez-Garcia , Houda Zeriouh , Masoud Ahmadzadeh , Diego Romero

Abstract Aflatoxins produced by some strains of the fungal genus Aspergillus are among the most hazardous mycotoxins for humans and livestock, a reason that has forced to investigate efficient strategies of management of these fungal contaminations. Some bacterial species have been proven capable of degrading or modifying aflatoxin into less- or nontoxic derivatives. In a previous work, Bacillus subtilis UTB1 was already proposed as a good candidate to be used for degradation of aflatoxin. Aiming to deepen in this biological activity, in this study, we searched for homologous to enzymes of Mycobacterium smegmatis degrading aflatoxin within the genus Bacillus. A candidate was the gene bacC, an oxidoreductase enzyme dedicated to the production of the antimicrobial di-peptide bacilysin. bacC mutants were compromised in the inhibitory activity against A. flavus, and the degradation of aflatoxin, compared to wild type both in vitro and on pistachio fruits. Taken together, our findings led us to propose a double and complementary mechanism by which BacC contributes to the reduction of aflatoxin levels in pistachio fruits: first, by a direct antagonism towards A. flavus, presumably mediated by the peptide bacilysin, and second, by a degradative or modifying activity of aflatoxin.

中文翻译:

枯草芽孢杆菌 UTB1 的黄曲霉毒素降解基于参与杆菌素生物合成的氧化还原酶的产生

摘要 由曲霉属真菌的某些菌株产生的黄曲霉毒素是对人类和牲畜最危险的真菌毒素之一,因此不得不研究管理这些真菌污染的有效策略。一些细菌种类已被证明能够将黄曲霉毒素降解或修饰成毒性较小或无毒的衍生物。在之前的工作中,枯草芽孢杆菌 UTB1 已被提议作为用于降解黄曲霉毒素的良好候选者。为了加深这种生物活性,在本研究中,我们在芽孢杆菌属中寻找与耻垢分枝杆菌降解黄曲霉毒素的酶同源。候选者是基因 bacC,这是一种氧化还原酶,专用于生产抗菌二肽杆菌溶素。bacC 突变体在对 A. flavus 的抑制活性和黄曲霉毒素的降解方面受到损害,与体外和在开心果果实上的野生型相比。综上所述,我们的研究结果使我们提出了一种双重互补机制,通过该机制 BacC 有助于降低开心果果实中的黄曲霉毒素水平:首先,通过对黄曲霉的直接拮抗作用,大概是由肽杆菌肽介导的,其次,通过黄曲霉毒素的降解或修饰活性。
更新日期:2018-12-01
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