Nutrient utilization and effects of mycotoxins on the gut barrier

Based on the observation that mycotoxins reduce weight gain and feed conversion, mycotoxins were hypothesized to have a direct effect on the intestines (Li et al., 2005). A malabsorption syndrome is a common result of exposure to aflatoxins, ochratoxins or trichothecenes. Measurable signs of the malabsorption syndrome are decreased transport of soluble nutrients and (fat-soluble) vitamins. Aflatoxin Bj and ochratoxin A were the first toxins known to induce hypocarotinoedemia and reduced tissue levels of a-tocopherol (vitamin E). Comparable effects were seen in chickens, following exposure to T-2 toxin and aurofusarin. The reduced levels of vitamins with antioxidant properties are associated with an increase of reactive oxygen species and cellular oxidative stress, which impairs both normal cellular function and differentiated traits, such as intracellular killing of pathogens by cells of the immune system (see below).

Mycotoxins affect not only the transport of nutrients and vitamins, but also impair the barrier function of the gut (Bouhet and Oswald, 2005). State of the art experiments with

Caco cell monolayers and isolated segments of the intestines demonstrated that various myco-toxins, including ochratoxin A, deoxynivalenol and fumonisin Bu alter the transmembrane electric resistance (Sergent et al., 2006). These changes in membrane integrity not only contribute to the malabsorption syndrome (and hence the impaired nutrient transport), but also may increase the passage rate for bacterial toxins, including the LPS of Gram-negative bacteria and facilitate the migration of pathogens from the gut lumen into the systemic circulation. Such migration might contribute to the local inflammatory reaction in the gastrointestinal tract and the increased susceptibility of animals to bacterial and fungal infections following exposure to these mycotoxins (Islam and Pestka, 2006).

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