Effects of lactic acid bacteria on the uptake and distribution of the food mutagen Trp-P-2 in mice |
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Authors: | Orrhage K M Annas A Nord C E Brittebo E B Rafter J J |
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Affiliation: | Dept. of Microbiology, Pathology and Immunology, Karolinska Institutet, Huddinge University Hospital, Sweden. |
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Abstract: | BACKGROUND: Lactic acid bacteria have been reported to have antimutagenic and anticarcinogenic properties in vivo and in vitro. Lactobacillus acidophilus and Bifidobacterium longum have earlier been shown to bind the food mutagen Trp-P-2 in vitro. METHODS: The influence of oral supplementation with L. acidophilus NCFB 1748 and B. longum BB 536 on the uptake and distribution of 14C-labelled Trp-P-2 in several mouse tissues was quantified by liquid scintillation measurements and examined by tape section autoradiography (gives an unbiased qualitative registration of differences in overall tissue distribution) in the present investigation. Furthermore, the effect of 13-naphthoflavone (BNF), a cytochrome P4501A (CYP1A)-inducing agent, on the distribution of 14C-labelled Trp-P-2 was examined. RESULTS: After oral (6 mg/kg; 5 microCi) or iv (1.2 mg/kg; 1 microCi) administration of 14C-labelled Trp-P-2, high levels of radioactivity were observed in the bile, urine and contents of the gastrointestinal tract. Lower levels were present in the liver, lung, kidney, intestines, brown fat, submaxillary salivary gland and thymus. In mice supplemented with lactic acid bacteria there was a significantly decreased level (29%-73%) of radioactivity in the lung, thymus, liver, kidney, submaxillary salivary gland and small intestine as compared with controls. In mice pretreated with BNF, a low but distinct localization of radioactivity in the lung was observed, whereas no similar localization occurred in controls. CONCLUSIONS: The results suggest that (i) there is a decreased bioavailability of the Trp-P-2 in the majority of the tissues examined in bacteria supplemented mice and (ii) there is a low but distinct CYP1A-dependent activation of Trp-P-2 in the lung of BNF-treated mice. |
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