ASSESSING THE EFFICIENCY OF PROBIOTIC BACTERIA LACTOBACILLUS ACIDOPHILUS IN DETOXIFICATION OF AFLATOXIN B1 BASED ON A SIMULATED MODEL OF DIGESTIVE SYSTEM SECRETIONS

Sayadi, M and Tajik, H (2018) ASSESSING THE EFFICIENCY OF PROBIOTIC BACTERIA LACTOBACILLUS ACIDOPHILUS IN DETOXIFICATION OF AFLATOXIN B1 BASED ON A SIMULATED MODEL OF DIGESTIVE SYSTEM SECRETIONS. The Journal of Urmia University of Medical Sciences, 29 (4). pp. 270-281.

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Abstract

Since aflatoxin contamination in food and livestock feed is considered as a serious health problem for human and animal health, this research focused on the ability of Lactobacillus acidophilus ATCC 4356 in reducing aflatoxin B1 (AFB1) in a simulated human gastrointestinal tract containing Sterilized milk. Materials & Methods: For this purpose, the bacteria count and aflatoxin concentration were adjusted to 1×1010 Cfu/ml and 5 ppm, respectively. In the simulated medium, artificial oral salivary, human small intestine and gastric secretions were inoculated. This study involved 6 treatment in the presence and absence of bacteria, sterilized milk, and gastrointestinal juice suspension. The concentration of residual aflatoxin was determined using high-performance liquid chromatography (HPLC) and purification by Immunoaffinity column. The results were statistically analyzed by SPSS 20 software. The results indicated that reduction of aflatoxin B1 at all treatments were determined using HPLC with a detection limit of 0.25mg/ml and a quantification limit of 0.75 mg/ml. The mycotoxin recovery was 89% and 94% for AFB1 Good linearity was observed for all the analytes of interest, with correlation coefficients 0.995 within their respective linear ranges. Results: The highest percentage of AFB1 removal by probiotic strain of Lactobacillus acidophilus was 70±0.022% in the absence of sterilized milk, where there was a significant difference for the six groups (P<0.05). Conclusion: The results also revealed that probiotic bacteria cell was a good biological agent for elimination or reduction of AFB1 in the human gastrointestinal tract. In addition to bacteria, gastric juice and small intestine contribute to elimination or reduction of AFB1

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