Aflatoxins andSaccharomyces cerevisiae: yeast modulates the intestinal effect of aflatoxins, while aflatoxin B1 influences yeast ultrastructure
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The gastrointestinal tract (GIT) is the main site where absorption of food components takes place and the first system coming into contact with mycotoxins of dietary origin. The aim of this work was to study the effect of probioticSaccharomyces cerevisiae RC016 on intestinal villi of rats exposed to aflatoxins for 60 days. Moreover, the effect ofin vitro aflatoxin B1 (AFB1) exposure on yeast cell ultrastructure was evaluated. Six treatments were applied (n=6) to inbred male Wistar rats: (1) uncontaminated feed control (F); (2) yeast control; (3) F + 40 μg/kg AFB1 + 20 μg/kg aflatoxin G1 (AFG1); (4) F + 100 μg/kg AFB1 + 50 μg/kg AFG1; (5) F + 40 μg/kg AFB1 + 20 μg/kg AFG1 + daily oral dose 108 viableS. cerevisiae cells; and (6) F + 100 μg/kg AFB1 + 50 μg/kg AFG1 + daily oral dose 108 viableS. cerevisiae cells. Morphometric measurements (villus length and width, crypt depth, quantification of goblet cells) were assessed using image analysis.S. cerevisiae RC016 cells were exposed to 20 μg/ml of AFB1 in intestinal solutions or in phosphate buffered saline and cells processed for transmission electron microscopy and high resolution light microscopy studies. Dietary exposure to the yeast did not induce significant differences in villus width but increased villus length and crypt depth. Aflatoxin-contaminated diets induced an increase in villus length, width and crypt depth and a significant decrease in the number of goblet cells which were improved by the addition ofS. cerevisiae RC016. A significant increase in the yeast cell diameter was observed when RC016 was exposed to aflatoxins, suggesting this as an advantage since a larger cell would be able to adsorb mycotoxins more efficiently. The ability of this strain to act as probiotic and aflatoxin binder makes it a candidate for the formulation of new additives to improve animal performance.
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Aflatoxins andSaccharomyces cerevisiae: yeast modulates the intestinal effect of aflatoxins, while aflatoxin B1 influences yeast ultrastructure
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The gastrointestinal tract (GIT) is the main site where absorption of food components takes place and the first system coming into contact with mycotoxins of dietary origin. The aim of this work was to study the effect of probioticSaccharomyces cerevisiae RC016 on intestinal villi of rats exposed to aflatoxins for 60 days. Moreover, the effect ofin vitro aflatoxin B1 (AFB1) exposure on yeast cell ultrastructure was evaluated. Six treatments were applied (n=6) to inbred male Wistar rats: (1) uncontaminated feed control (F); (2) yeast control; (3) F + 40 μg/kg AFB1 + 20 μg/kg aflatoxin G1 (AFG1); (4) F + 100 μg/kg AFB1 + 50 μg/kg AFG1; (5) F + 40 μg/kg AFB1 + 20 μg/kg AFG1 + daily oral dose 108 viableS. cerevisiae cells; and (6) F + 100 μg/kg AFB1 + 50 μg/kg AFG1 + daily oral dose 108 viableS. cerevisiae cells. Morphometric measurements (villus length and width, crypt depth, quantification of goblet cells) were assessed using image analysis.S. cerevisiae RC016 cells were exposed to 20 μg/ml of AFB1 in intestinal solutions or in phosphate buffered saline and cells processed for transmission electron microscopy and high resolution light microscopy studies. Dietary exposure to the yeast did not induce significant differences in villus width but increased villus length and crypt depth. Aflatoxin-contaminated diets induced an increase in villus length, width and crypt depth and a significant decrease in the number of goblet cells which were improved by the addition ofS. cerevisiae RC016. A significant increase in the yeast cell diameter was observed when RC016 was exposed to aflatoxins, suggesting this as an advantage since a larger cell would be able to adsorb mycotoxins more efficiently. The ability of this strain to act as probiotic and aflatoxin binder makes it a candidate for the formulation of new additives to improve animal performance.
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