生物转化
黄曲霉毒素
乳酸
细菌
化学
食品科学
生物化学
微生物学
生物
酶
遗传学
作者
Jenna M. Lemmetty,Youngsun Lee,Tiina Laitila,Swantje Bredehorst,Rossana Coda,Kati Katina,Ndegwa Henry Maina
标识
DOI:10.1016/j.foodres.2024.115351
摘要
• Lactic acid bacteria (LAB) used in this study were able to bind aflatoxin B1 (AFB1). • Viable cells bound 16–50 %, whereas non-viable cells bound 30–66 % AFB1. • The reduction of AFB1 was lower (0–18 %) when incubating the LAB and AFB1 in growth media. • The main AFB1 reduction mechanism by LAB was binding rather than biotransformation. Climate change has introduced new challenges to food safety by altering the occurrence and distribution of fungi leading to increased mycotoxin contamination in crops. Among these mycotoxins, aflatoxin B1 (AFB1) stands out as a potent carcinogen, posing significant health risks to consumers. Methods for AFB1 decontamination have been intensively investigated and lactic acid bacteria (LAB) have gained increasing interest for their potential in AFB1 detoxification. The present study aimed to evaluate the potential of various LAB strains for reducing AFB1. A simple binding assay was used to evaluate the AFB1 binding by LAB. The ability of LAB to biotransform AFB1 was studied by simultaneous incubation of LAB and AFB1 in growth media and the biotransformation products were evaluated using liquid chromatography quadrupole time-of-flight mass spectrometry. Furthermore, the main reduction mechanism was investigated by conducting the binding assay using the same cell concentration used in the biotransformation experiment. The binding assay demonstrated a substantial reduction of AFB1 (16–71 %) depending on the strain, cell viability and pH. The binding capacity was shown to be strain-specific and improved when using non-viable cells. On the other hand, biotransformation exhibited much lower reduction of AFB1 (0–18 %). The reduction was also strain-specific and increased with longer incubation time. Additionally, no biotransformation products were found. The experiment on AFB1 reduction mechanism revealed binding as the primary mechanism of LAB for reducing AFB1, surpassing potential enzymatic degradation routes.
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