Effect of ammoniation of aflatoxin B1-contaminated cottonseed feedstock on the aflatoxin M1 content of cows' milk and hepatocarcinogenicity in the trout bioassay.

The effectiveness of ammonia in inactivating aflatoxins in contaminated cottonseed was investigated. Two aflatoxin-contaminated cottonseed lots were treated separately using an atmospheric pressure, ambient temperature ammoniation procedure (APAT) or a high pressure, high temperature ammoniation procedure (HPHT), and incorporated into dairy cow rations. Isocalorific diets containing 25% defatted, dried milk from cows fed aflatoxin-contaminated cottonseed without or with APAT or HPHT treatment, or an aflatoxin-free human grade commercial milk powder, were then fed for 12 months to rainbow trout (Oncorhynchus mykiss). Aflatoxin M1 (AFM1) concentrations in milk powders without and with seed treatment were: APAT, 85 and < 0.05 microgram/kg; HPHT, 32 and < 0.05 microgram/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%. Positive controls were included to demonstrate trout responsiveness. AFB1 fed continuously for 12 months at 4 micrograms/kg resulted in a 34% tumour incidence, whereas positive controls fed 20 micrograms AFB1/kg, 80 micrograms AFM1/kg, or 800 micrograms AFM1/kg for 2 wk and killed 9 months later had a 37, 5.7 and 50% incidence of tumours, respectively. These data demonstrate that APAT ammonia treatment of aflatoxin-contaminated dairy cattle cottonseed feedstock abolished the detectable transfer of AFM1 or AFB1 into milk powder, and greatly reduced the carcinogenic risk posed by any carry-over of aflatoxins or their derivatives into milk. In addition, the results confirm AFM1 to be a lower level hepatocarcinogen in comparison with AFB1 in the trout carcinogenicity assay. In the separate HPHT experiment, no tumours were observed in the livers of trout fed diets containing milk from either the ammonia-treated or untreated source, or the control diet containing 8 micrograms AFM1/kg. Positive controls fed 64 micrograms AFB1/kg for 2 wk exhibited a 29% tumour incidence 12 months later. Thus in this experiment, neither AFM1 at 8 micrograms/kg nor any HPHT-derived aflatoxin derivatives that might have been carried over into milk, represented a detectably carcinogenic hazard to trout.

Hepatocarcinogenicity of glandless cottonseeds and cottonseed oil to rainbow trout (Salmo gairdnerii).

Glandless cottonseed kernels are available for purchase and consumption by the general public. These kernels contain no gossypol but still have a full complement of naturally occurring cyclopropenoid fatty acids, which in rainbow trout are active as synergists with aflatoxins and primary liver carcinogens. Diets containing glandless cottonseed kernels or a lightly processes cottonseed oil produced significant numbers of hepatocellular carcinomas in rainbow trout after 1 year. The much greater incidence of cancer induced by the kernel than by the oil indicates that synergists or other carcinogens may be present in the kernel in addition to the cyclopropenoid fatty acids.

Reproduction and lipid composition of rats fed cyclopropene fatty acids.

The effect of cyclopropene fatty acids fed in saturated or unsaturated lipid diets on reproduction and lipid composition of progeny was determined in rats. Sterculia foetida oil (50% cyclopropene fatty acids) fed at 0.2% of the diet for three generations and 0.5% fed to first generation rats did not significantly affect breeding. Two percent S. foetida oil fed with 3% corn oil did not appreciably affect conception rate and litter size in the first litters, but reduced pup survival 36% in the first litters and 78% in the second litters. Replacement of the 3% corn oil with 3% animal fat in diet containing 2% S. foetida oil reduced litter rate from 87% to 7% in the first litter. Cyclopropene fatty acids were readily incorporated into the tissue and milk of females. Pups rapidly accumulated cyclopropene via milk from dams. Fetal tissue contained only 10% of the cyclopropene concentration of the females fed a diet containing 2% S. foetida oil and 3% corn oil; however, the level of fetal cyclopropene doubled when animal fat replaced corn oil in the diet. Unsaturated lipid in the diet enabled rats to cope with the effects of moderate levels of cyclopropene fatty acids, but the combination of cyclopropene in saturated lipid diets caused detrimental effects.