Feeding Silicoglycidol reduces aflatoxin M1 in dairy cow milk

Abstract

Aflatoxin M1 (AFM1) is a pathogenic metabolite often transferred from feed into milk from aflatoxin (AF) B1, B2, G1, and G2; thus, it poses a human health risk. Therefore, effective mitigation strategies are needed to reduce animal and human exposure to AF. Study objectives were to evaluate a dietary adsorbent (Silicoglycidol, ATX) as a sequestering agent in AF contaminated feed and to broadly examine how AF affects liver function and the immune system. Primiparous Holstein cows (n = 12, 279 ± 88 DIM and 675 ± 19 kg BW) were used in a replicated 3 × 3 Latin square design with 21-d periods in which d 1–14 were considered adaptation and data collected on d 15 to 21 were used for analysis. Treatments were: 1) control (CON) consisting of a basal diet; 2) AF diet consisting of CON + AF challenge (100 µg of AFB1/kg dry matter intake [DMI]); and 3) AF + ATX supplemented at 0.10% of dietary DMI. Feed intake and milk yield were recorded daily, fecal samples were collected on d 20 of each period, blood and urine samples were collected on d 21 of each period, and milk samples were collected on the last 2 d of each period. Data were analyzed using the MIXED procedure of SAS. Milk yield and DMI were unaffected by treatment (26.8 ± 1.3 kg/d and 24.0 ± 0.9 kg/d, respectively). Similarly, neither milk composition nor DMI digestibility were affected by treatment. No AFM1 was detected in CON cow's milk or urine. Supplementing ATX reduced AFM1 in milk (1.57 vs. 1.14 ± 0.1 µg/L for AF and AF+ATX, respectively) and urine (9.9 vs. 5.6 ± 1.1 µg/L for AF and AF+ATX, respectively). Consuming AF did not affect biomarkers of liver health or immune activation including ALT, AST, GGT, haptoglobin (Hp), and immunoglobulin G (IgG). In summary, feeding ATX reduced the absorption and transfer of dietary AF to milk and urine.