EFFECT OF AMMONIATION OF AFLATOXIN B-1-CONTAMINATED COTTONSEED FEEDSTOCK ON THE AFLATOXIN M(1) CONTENT OF COWS MILK AND HEPATOCARCINOGENICITY IN THE TROUT BIOASSAY

The effectiveness of ammonia in inactivating aflatoxins in contaminate d cottonseed was investigated. Two aflatoxin-contaminated cottonseed l ots were treated separately using an atmospheric pressure, ambient tem perature ammoniation procedure (APAT) or a high pressure, high tempera ture ammoniation procedure (HPHT), and incorporated into dairy cow rat ions. Isocalorific diets containing 25% defatted, dried milk from cows fed aflatoxin-contaminated cottonseed without or with APAT or HPHT tr eatment, or an aflatoxin-free human grade commercial milk powder, were then fed for 12 months to rainbow trout (Oncorhynchus mykiss). Aflato xin M(1) (AFM(1)) concentrations in milk powders without and with seed treatment were: APAT, 85 and <0.05 pg/kg; HPHT, 32 and <0.05 mu g/kg. In the APAT experiment, trout consuming the diet containing milk from cows fed the aflatoxin-contaminated cottonseed had a 42% incidence of hepatic tumours; APAT cottonseed treatment reduced this to 2.5%. Posi tive controls were included to demonstrate trout responsiveness. AFB(1 ) fed continuously for 12 months at 4 mu g/kg resulted in a 34% tumour incidence, whereas positive controls fed 20 mu g AFB(1)/kg, 80 mu g A FM(1)/kg, or 800 mu g AFM(1)/kg for 2 wk and killed 9 months later had a 37, 5.7 and 50% incidence of tumours, respectively. These data demo nstrate that APAT ammonia treatment of aflatoxin-contaminated dairy ca ttle cottonseed feedstock abolished the detectable transfer of AFM(1) or AFB, into milk powder, and greatly reduced the carcinogenic risk po sed by any carry-over of aflatoxins or their derivatives into milk. In addition, the results confirm AFM(1) to be a lower level hepatocarcin ogen in comparison with AFB(1) in the trout carcinogenicity assay. In the separate HPHT experiment, no tumours were observed in the livers o f trout fed diets containing milk from either the ammonia-treated or u ntreated source, or the control diet containing 8 mu g AFM(1)/kg. Posi tive controls fed 64 mu g AFB(1)/kg for 2 wk exhibited a 29% tumour in cidence 12 months later. Thus in this experiment, neither AFM(1) at 8 mu g/kg nor any HPHT-derived aflatoxin derivatives that might have bee n carried over into milk, represented a detectably carcinogenic hazard to trout.