ISSUE FOCUS FEED & ADDITIVE MAGAZINE March 2024 37 on such products to understand the ability of the product to bind mycotoxins in the animal’s GIT. Aflatoxin B1 (AFB1) was the first mycotoxin to undergo such tests. A known amount of AFB1 was mixed with a known quantity of mycotoxin binder in a test tube and allowed to interact in a liquid media of pH 3 to 3.5 or 6 to 6.5. Most of the mycotoxins in the feed get released into GIT at the intestinal level and hence, the binding % at the alkaline pH was considered as the strong binding. Many times, a product would achieve a superior binding at acidic pH but show a significant desorption at alkaline pH. MYCOTOXIN BINDER IS A MISNOMER The binding mode of action (MOA) worked quite well for aflatoxins, ergot toxins and endo(bacterial) toxins. However, only a moderate binding (35 to 50%) was achieved for T-2 toxin, OTA, and ZEN. Only a maximum of 10% binding was achieved for DON. The effect of pH on FB binding was more severe. At an acidic pH, bentonite was able to bind more than 90% of FB but this was reduced to almost “zero” at alkaline pH. Such findings may be related to varying structure and polarity of mycotoxins. Since all mycotoxins can’t be bound by the socalled mycotoxin binder and the mycotoxin binder contains agents other than sequestering agents, the word “mycotoxin binder” is a misnomer. A suitable name covering all MOA of mycotoxin toxicity reduction should be employed. BEYOND MYCOTOXIN BINDING Selko® has always looked beyond binding to manage multiple mycotoxins within the animal and incorporated specific ingredients in its TOXO® product line (Figure 1). The combined MOA of these ingredients has delivered significant benefits in animals exposed to multiple mycotoxins (Figure 2). These MOAs include; 1. Use of yeast cell wall derivatives in the feed strengthens the tight junction proteins between intestinal epithelial cells to limit mycotoxin transfer into the blood circulation. This MOA has been proven both at animal and molecular levels. 2. Use of yeast beta-glucans in the feed enhances the macrophage activity. Such activity is very crucial for innate immunity, antibody-mediated immunity, and cell-mediated immunity. All beta-glucans are not the same and hence, attention should be given to the functional benefits rather than the quantity of beta-glucans in the product. 3. Use of anti-oxidants (Se, Vitamin E, Phytogenic compounds) in the feed can help to reduce the mycotoxin toxicity by reducing lipid peroxidation. Such compounds have been shown to reduce laminitis, mastitis and ruminitis in cows. 4. Various microbes and enzymes are also added to the feed to break down some of the mycotoxins into less toxic metabolites in the gastrointestinal tract (GIT). Despite some stability issues, such technologies support the concept of “beyond binding”. Figure 1. Multiple mode of action of mycotoxin risk management
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