Probiotic Lactobacillus casei Shirota (LcS) is a potential decontaminating agent of aflatoxin B1 (AFB1). However, few studies have investigated the influence of diet, especially a high protein (HP) diet, on the binding of AFB1 by probiotics. This research was conducted to determine the effect of HP diet on the ability of LcS to bind AFB1 and reduce aflatoxin M1 (AFM1) in AFB1-induced rats. Sprague Dawley rats were randomly divided into three groups: A (HP only), B (HP + 108 CFU LcS + 25 μg AFB1/kg BW), and C (HP + 25 μg AFB1/kg BW). Levels of AST and ALP were higher in all groups but other liver function's biomarkers were in the normal range, and the liver's histology showed no structural changes. The urea level of rats in group B (10.02 ± 0.73 mmol/l) was significantly lower (p < 0.05) than that of rats in group A (10.82 ± 0.26 mmol/l). The presence of carcinoma in the small intestine and colon was more obvious in group C than in group B. Moreover, rats in group B had significantly (p < 0.05) lower AFM1 concentration (0.39 ± 0.01 ng/ml) than rats in group C (5.22 ± 0.28 ng/ml). Through these findings, LcS supplementation with HP diet alleviated the adverse effects of AFB1 by preventing AFB1 absorption in the small intestine and reducing urinary AFM1.
The use of probiotic as dietary approach to prevent exposure to food contaminant, aflatoxin B1 (AFB1) has greatly increased. Several studies found that AFB1 binding to the bacterial cell wall is strain-specific. Moreover, the interaction between AFB1 and bacterial cell wall is not well-understood, thus warrants further investigation. This research was conducted to assess the ability of Lactobacillus casei Shirota (Lcs) to bind AFB1 at different concentrations and to determine AFB1 binding efficiency of different Lcs cell components including live cell, heat-treated, and cell wall. In addition, the interaction between AFB1 and Lcs was also evaluated via scanning electron microscopy (SEM) and through an animal study. The binding of AFB1 by all Lcs cell components depends on the concentration of available AFB1. Among all Lcs cell components, the live Lcs cells exhibited the highest binding efficiency (98%) toward AFB1. Besides, the SEM micrographs showed that AFB1 induced structural changes on the bacterial cell surface and morphology including rough and irregular surface along with a curve rod-shaped. In vivo experiment revealed that Lcs is capable to neutralize the toxicity of AFB1 on body weight and intestine through the binding process. The animal's growth was stunted due to AFB1 exposure, however, such effect was significantly (p < 0.05) alleviated by Lcs. This phenomenon can be explained by a significant (p < 0.05) decreased level of blood serum AFB1 by Lcs (49.6 ± 8.05 ng/mL) compared to AFB1-exposed rats without treatment (88.12 ± 10.65 ng/mL). Taken together, this study highlights the potential use of Lcs as a preventive agent against aflatoxicosis via its strong binding capability.