The aim of the present study was to evaluate the effects of Lactobacillus rhamnosus GG (LGG; ATCC 53013) on growth performance and hepatotoxicity in calves fed a single dose of aflatoxin B 1 (AFB 1) and to investigate the absorption, distribution, and elimination of AFB 1 and the hydroxylated metabolite aflatoxin M 1 (AFM 1) in rumen fluid, blood, and excretions. Twentyfour male Holstein calves were blocked for body weight and age and were randomly assigned to 1 of 3 treatment groups: (1) untreated control, (2) treated with 4.80 mg of AFB 1 (AFB 1 only), or (3) treated with 1 × 10 10 cfu of LGG suspension and 4.80 mg of AFB 1 (AFB 1 plus LGG). The calves received LGG suspension in 50 mL of phosphate-buffered saline daily via oral administration for 14 d before and on the day they received a single oral dose of AFB 1. Body weight was recorded at the beginning of the study (before LGG administration), at the day of AFB 1 administration, and at the end of the trial. Rumen fluid, blood, urine, and feces samples were collected continuously for 96 h after AFB 1 administration. Average daily gain (ADG) and plasma biochemical parameters were analyzed, and concentrations of AFB 1 and AFM 1 in the samples were determined for monitoring excretion pattern and toxicokinetics. The results showed that ADG was lower in AFB 1-treated animals; LGG administration partially mitigated the decrease in ADG (0.85 ± 0.08 vs. 0.76 ± 0.18 kg of gain/d). The AFB 1 treatment increased plasma aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase levels. Administration of LGG alleviated the AFB 1-induced increase in plasma enzymes activity. The excretion patterns of AFB 1 and AFM 1 were surprisingly regular; toxins were rapidly detected in all samples after a single oral dose of AFB 1 , and the peak of toxins concentrations was sequentially reached in rumen fluid, plasma, urine, and feces (except AFM 1 in rumen fluid), followed by an exponential decrease. The excretion curves showed that AFB 1 and AFM 1 concentrations were the highest in feces and urine, respectively. Administration of LGG decreased the concentrations of free AFB 1 and AFM 1 in rumen fluid and reduced the release of toxins into plasma and urine. Toxicokinetic parameters (except for the time of maximum concentration and the terminal half-life) were reduced by LGG administration. In conclusion, the absorption, distribution, and excretion of AFB 1 and AFM 1 were rapid in calves fed a single dose of AFB 1. Urine was the main route for the excretion of AFM 1 , and the clearance pattern from the peak of concentration was well fitted by exponential decreasing function. Administration of LGG reduced the absorption of AFB 1 in the gastrointestinal tract by increasing the excretion via the feces, thus alleviating the hepatotoxic effect of AFB 1 .
Acrylamide (AA), which is mainly found in fried foods, causes neurotoxicity, genetic toxicity, carcinogenic effects, and DNA damage. This study confirms that a strain of lactic acid bacteria (Lactobacillus plantarum ATCC8014) could alleviate the toxicity of rats by inhibiting the AA-induced oxidative damage. Forty-eight adult male SD rats were randomly divided into eight groups: control group, AA group (40 mg/kg), three different doses (1 × 10 7 CFU/ml, 1 × 10 8 CFU/ ml, 1 × 10 9 CFU/ml of Lactobacillus plantarum ATCC8014) of prevention groups and therapeutic groups, respectively. At the end of three-week experiment, AA treatment produced a significant reduction in the rate of weight gain along with the symptoms of hind limb splay and ataxia. Histological examinations revealed various degrees of injury in five tissues. Levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) in group AA rats were significantly decreased, but the level of lipid peroxidation (LPO) was significantly increased (p < 0.05). Both prevention and therapeutic groups with 1 × 10 9 CFU/ml of Lactobacillus plantarum ATCC8014 could effectively reduce the injury of AA to the body. However, reductions in both groups were not statistically significant.
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