Aflatoxin B1 Degradation by a Pseudomonas Strain

Toxins

Lancine Sangare¹  Yueju Zhao¹  Yawa Minnie Elodie Folly¹  Jinghua Chang¹  Jinhan Li¹  Jonathan Nimal Selvaraj¹  Fuguo Xing¹  Lu Zhou¹  Yan Wang¹  Yang Liu¹ 

[1] Institute of Agro-products Processing Science and Technology, Chinese Academy of Agricultural Sciences, Beijing 100193, China; E-Mails:

关键词: aflatoxin;    degradation;    culture supernatant;    Pseudomonas aeruginosa N17-1;   

DOI  :  10.3390/toxins6103028

来源: mdpi

【 摘 要 】

Aflatoxin B₁ (AFB₁), one of the most potent naturally occurring mutagens and carcinogens, causes significant threats to the food industry and animal production. In this study, 25 bacteria isolates were collected from grain kernels and soils displaying AFB₁ reduction activity. Based on its degradation effectiveness, isolate N17-1 was selected for further characterization and identified as Pseudomonas aeruginosa. P. aeruginosa N17-1 could degrade AFB₁, AFB₂ and AFM₁ by 82.8%, 46.8% and 31.9% after incubation in Nutrient Broth (NB) medium at 37 °C for 72 h, respectively. The culture supernatant of isolate N17-1 degraded AFB₁ effectively, whereas the viable cells and intra cell extracts were far less effective. Factors influencing AFB₁ degradation by the culture supernatant were investigated. Maximum degradation was observed at 55 °C. Ions Mn²⁺ and Cu²⁺ were activators for AFB₁ degradation, however, ions Mg²⁺, Li⁺, Zn²⁺, Se²⁺, Fe³⁺ were strong inhibitors. Treatments with proteinase K and proteinase K plus SDS significantly reduced the degradation activity of the culture supernatant. No degradation products were observed based on preliminary LC-QTOF/MS analysis, indicating AFB₁ was metabolized to degradation products with chemical properties different from that of AFB₁. The results indicated that the degradation of AFB₁ by P. aeruginosa N17-1 was enzymatic and could have a great potential in industrial applications. This is the first report indicating that the isolate of P. aeruginosa possesses the ability to degrade aflatoxin.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.