Excretion of Aflatoxin M1 in Milk of Dairy Ewes Treated with Different Doses of Aflatoxin B1

Abstract

Two experiments were conducted to study the amount of aflatoxin M1 (AFM1) in milk in response to feeding aflatoxin B1 (AFB1). In experiment 1, four dairy ewes in early lactation received a single dose of pure AFB1 (2 mg). Individual milk samples were collected during the following 5 d to measure AFM1 concentration. The average excretion of AFM1 in milk followed an exponential decreasing pattern, with two intermediate peaks at 24 and 48 h. No AFM1 was detected in milk at 96 h after dosing. The mean rate of transfer of AFB1 into AFM1 in milk was 0.032%, with a high individual variability (SD = 0.017%). In experiment 2, 16 dairy ewes in midlactation were divided into four groups that received different daily doses of AFB1 (0, 32, 64, and 128 microgram for control and groups T1, T2, and T3, respectively) for 14 d. Pure AFB1 was administered to each animal divided in two daily doses. Individual milk samples were collected at 12, 24, 36, 48, 72, 96, 144, 216, and 312 h after the first AFB1 administration, during the intoxication period, and every 24 h for 7 d after the withdrawal of AFB1. AFM1 was detected in the milk of all animals of the treated groups at 12 h after the administration of AFB1. In all treated groups, milk AFM1 concentration increased from 12 to 144 h after the beginning of administration. It then decreased, reaching a stable concentration at 216 and 312 h after the first administration. No AFM1 was detected in milk 3 d after the last administration of AFB1. Milk AFM1 concentration measured at steady-state condition was significantly affected by the AFB1 dose (0.031, 0.095, and 0.166 in T1, T2, and T3 groups, respectively), with a linear relationship between AFB1 dose and milk AFM1 concentration (R2 = 77.2%). The carryover (AFM1/AFB1 ratio) was not significantly affected by treatment, and its mean value was 0.112% (SE = 0.011). The carryover was lower than that reported for dairy cattle and goats, suggesting a better ability of sheep to degrade AFB1.

Carryover of aflatoxin from feed to milk in dairy cows with low or high somatic cell counts

“…The observed plateau developed later than in previous studies, in which the steady state for AFM1 was established at 24 (Frobish et al, 1986) and 76 h (Polan et al, 1974, Diaz et al, 2004) from the initial AFB1 ingestion, but is in agreement with results reported by Battacone et al (2003) on sheep, in which the observed plateau condition was between day 9 and day 13 from the first AFB1 ingestion. However, milk AFM1 levels in the present study were lower than previously reported maximum concentrations.…”

“…Other factors that affect carryover (CO) into milk include species differences (Battacone et al, 2003), animal variability (Van Egmond, 1989;Steiner et al, 1990;Veldman et al, 1992) and mammary alveolar cell membrane health (Lafont et al, 1983).…”

Aflatoxins of type B and G affect porcine dendritic cell maturationin vitro

“…Recent data indicate that the chronic exposure of piglets to low mycotoxin levels still could affect the intestinal immune system and prolong infection with intestinal pathogens (Devriendt et al, 2009;Oswald et al, 2003). Based on the chemical structure and properties of Group B and G AF, they can easily pass through the plasma membrane of (for example) intestinal epithelial cells and rapidly appear in the blood circulation (Battacone et al, 2003;Gallo et al, 2008;Martins et al, 2007). Although the expression of major AF-metabolizing enzymes in intestinal epithelial cells is yet to be explored, detoxification of AF by these cells is minimal, and these highly carcinogenic AF can easily reach the blood stream.…”

Aflatoxin M1 in Pasteurized Market Milk in Korea

“…This somewhat unexpected result against the general assumption that some of raw milk might have higher level of residue than processed milk in plants due to the dilution effect, could be explained as the difference in sampled source of brands. In those studies, they used 1) Limit of detection at ppt ND: not described the milk from single dairy company but we used various brands of milk from supermarket.…”

“…It is produced by molds and ingested into animal body through the contaminated feedstuffs during animal breeding. Once ingested by the animal it is rapidly absorbed by the gastrointestinal tract and is transformed from AFB1 into the metabolite AFM1 (Battacone et al, 2003). It has been demonstrated that up to 6% of the ingested AFB1 is secreted into the milk as AFM1 (Van Egmond and Dragacci, 2001) and, because it is relatively resistant to heat treatments, it is almost entirely retained in pasteurized milk, powdered milk, and infant formula.…”