Supplementing Silicoglycidol for the reduction of aflatoxin M1 in milk and biomarkers of liver dysfunction in dairy cows

Abstract

Aflatoxin M₁ (AFM₁) is a pathogenic metabolite 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 to 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 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 (SAS Institute Inc.). 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 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 alanine aminotransferase, aspartate aminotransferase, gamma glutamyltransferase, haptoglobin, and IgG. In summary, feeding ATX reduced the absorption and transfer of dietary AF to milk and urine.