Mycotoxin and Gut Microbiota Interactions

Abstract

The interactions between mycotoxins and gut microbiota were discovered early in animals and explained part of the differences in susceptibility to mycotoxins among species. Isolation of microbes present in the gut responsible for biotransformation of mycotoxins into less toxic metabolites and for binding mycotoxins led to the development of probiotics, enzymes, and cell extracts that are used to prevent mycotoxin toxicity in animals. More recently, bioactivation of mycotoxins into toxic compounds, notably through the hydrolysis of masked mycotoxins, revealed that the health benefits of the effect of the gut microbiota on mycotoxins can vary strongly depending on the mycotoxin and the microbe concerned. Interactions between mycotoxins and gut microbiota can also be observed through the effect of mycotoxins on the gut microbiota. Changes of gut microbiota secondary to mycotoxin exposure may be the consequence of the antimicrobial properties of mycotoxins or the toxic effect of mycotoxins on epithelial and immune cells in the gut, and liberation of antimicrobial peptides by these cells. Whatever the mechanism involved, exposure to mycotoxins leads to changes in the gut microbiota composition at the phylum, genus, and species level. These changes can lead to disruption of the gut barrier function and bacterial translocation. Changes in the gut microbiota composition can also modulate the toxicity of toxic compounds, such as bacterial toxins and of mycotoxins themselves. A last consequence for health of the change in the gut microbiota secondary to exposure to mycotoxins is suspected through variations observed in the amount and composition of the volatile fatty acids and sphingolipids that are normally present in the digesta, and that can contribute to the occurrence of chronic diseases in human. The purpose of this work is to review what is known about mycotoxin and gut microbiota interactions, the mechanisms involved in these interactions, and their practical application, and to identify knowledge gaps and future research needs.

Assessment of Exposure to Mycotoxins in Spanish Children through the Analysis of Their Levels in Plasma Samples

“…Mycotoxins can affect the digestive tract in two ways. The first is the alteration of the gut microbiota by exerting a toxic effect on the microbes, although this effect has been observed in studies using high concentrations of mycotoxins [ 27 ]. In addition, mycotoxins have been described as altering the structures of the intestine.…”

The Ribosome-Binding Mode of Trichothecene Mycotoxins Rationalizes Their Structure—Activity Relationships

“…The C 15 -OH, C 7 -OH, and C 8 -O line one side of DON and are solvent-exposed; the groups do not make direct hydrogen bonds to 25S rRNA, but instead are likely to hydrogen bond to ordered water molecules in the binding site. Other than the above polar interactions, DON binding is also stabilized through multiple apolar interactions, including hydrophobic stacking interactions between the six-membered ring of C [6][7][8][9][10][11] in DON (ring A) and the cytosine ring of C2821 ( Figure 1). In addition, the C 9 = C 10 group in bond in DON (along with the C 16 methyl) stacks in a wedge-shaped pocket formed between a pair of successive bases-the cytosine ring of C2821 and the adenine ring of A2820.…”

“…The binding of trichothecenes (e.g., DON, T-2 and verrucarin A) to the yeast ribosome induces conformation changes in several nucleobases in 25S rRNA (Figure 4). Specifically, the uracil ring of U2821 shifted towards the C 6,7,8,9,10,11 ring (ring A) of trichothecenes to improve the hydrophobic stacking interaction between these two rings. Another uracil ring of U2875 also moved towards ring A of trichothecenes and the substituent of OCOCH 2 CH(CH 3 ) 2 at the C 8 position of T-2-toxin.…”

“…Specifically, the C 12,13 -epoxy ring, the double bond between C 9 and C 10 , and C 3 -OH in type A and B trichothecenes have been identified as key structural elements contributing to their toxicity ( Figure 1) [2,[4][5][6]. Microbial metabolism plays an important role in modifying these key structural elements, thus altering the toxicity [4,7]. For example, in ruminants, DON and NIV undergo a reductive deepoxidation of the C 12,13 epoxide ring to form de-epoxy metabolites, which display reduced cytotoxicity [8].…”

“…Although a promising means for detoxification, these conjugates may be hydrolyzed back to their parent mycotoxins in the digestive tract of mammals and, for this reason, are often referred to as masked mycotoxins. In mammals, trichothecene metabolism also involves biotransformation events by the aforementioned gut microflora as well as phase II xenobiotic detoxification involving glucuronidation at the C 3 -OH position [7,15,16]. Altogether, why and how these key structural elements, substituent groups, and biotransformed metabolites impact the toxic actions of trichothecenes has not been systematically rationalized.…”