Efficacy of Silicoglycidol to bind aflatoxin in ruminants (in vitro trial)
Aflatoxin is a mycotoxin of a great concern because of its negative effects on productivity and, even more importantly, because it threatens human health, as it is a carcinogenic compound.
For these reasons, there is the need to avoid the transference of alfatoxins from contaminated feed to the milk. This prevention should be focused on avoiding the absorption of aflatoxin B1 (AFB1), which is present in feed, because, after being absorbed in the gut, it will be metabolized to aflatoxin M1 (AFM1) in the liver and excreted in the milk.
Mycotoxin binders are an effective tool to bind aflatoxin B1 (AFB1) present in feed represent a good solution to avoid the presence of AFM1 in milk. Adsorption (binding) efficacy and possible desorption are related to the physico-chemical conditions in the different parts of the GI tract. These conditions are different in ruminants and monogastrics, which means that mycotoxin binders’ efficacy should be specifically tested in ruminants GI conditions.
The objective of this trial was to evaluate the efficacy of mycotoxin binders with Silicoglycidol and other components to bind AFB1. The evaluation was conducted in vitro, simulating the conditions of a ruminant GI tract.
Materials and methods
A method that simulated the ruminant GI tract conditions (enzymes, pH…) was used.
- 300 ppb of AFB1 and the binder were added to each of the GI tract parts.
- The percent of bound and free mycotoxins was evaluated in each part.
Silicoglycidol mycotoxin binders’ efficiency was greater than the efficacy of binders based on glucomannans (yeast cell wall) and other polymers (clinoptilolite). Its efficacy was comparable to enzymes’.
In conclusion, the addition of Silicoglycidol mycotoxin binders in ruminant diets is an effective solution to prevent the presence of AFM1 in milk, as it binds a high percentage of AFB1 and the binding efficacy is not affected by the changing conditions of the GI tract. This way, Silicoglycidol avoids AFB1 hepatic metabolization to AFM1.