Aflatoxins In Feed Research Articles

Hematology of Single Comb White Leghorn Pullets Fed Aflatoxin-Contaminated and Ammonia-Treated Corn

Erythrocyte count, hemoglobin content, percent hematocrit, or mean corpuscular hemoglobin were not affected by feeding aflatoxin levels of 2.3 ppb and 500 ppb to Single Comb White Leghorn hens. Pullets fed ammoniated corn without aflatoxin and pullets fed corn containing 500 ppb aflatoxin in the finished feed had significantly reduced mean corpuscular volume.

The Effects of Short Term Feeding of Aflatoxin on Egg Production and Some Plasma Constituents of the Laying Hen ,

The effect on White Leghorn laying hens of feeding 20 p.p.m. dietary aflatoxin for seven days was investigated. During this feeding period egg production was not affected although plasma calcium, protein, cholesterol, triglycerides were decreased significantly (P < 0.05) and serum alkaline phosphatase was increased by the second day of aflatoxin treatment. At the end of the aflatoxin feeding period, the hens were returned to the control diet for recovery. The plasma calcium, protein and alkaline phosphatase values approximated the control values by the seventh day of the recovery period while plasma total lipid and cholesterol approximated control values by the tenth day. Egg production rate began to decline significantly (P < 0.05) on the first day of the recovery period and reached a minimum of 35 percent seven days later. Egg production returned to the control rate 19 days after the hens began eating the aflatoxin-free diet. These results suggest that aflatoxin impairs egg production by reducing liver synthesis and transport of yolk precursors. There is a delayed onset in the decline of egg production.

Effect of Simultaneous Feeding of Aflatoxin and Rubratoxin to Chickens

A 2 × 2 factorial experiment in broiler chicks utilizing dietary aflatoxin (2.5 p.p.m.) and rubratoxin (500 p.p.m.) failed to reveal any interaction on growth rate, relative organ weights, hemoglobin, serum cholesterol, and serum total lipid despite a previous report of an interaction of these toxins in rats.

Responses of Dairy Calves to Aflatoxin-Contaminated Feed

The purpose of this experiment was to determine the aflatoxin dose relationships, the clinical biochemical changes, and the tissue effects of feeding aflatoxin to young dairy calves. Six aflatoxin dose levels, 0.008mg B1/kg body weight per day to 0.080mg B1/kg body weight per day, were fed to six pairs of young dairy calves for six weeks. Each pair of calves was fed for a six-week pretoxin and a six-week toxin feeding period. Tissue samples were examined by light microscopy for aflatoxin-induced lesions. The young calves consumed 100% of the dose up to 0.020mg B1/kg body weight per day. At higher dose levels, smaller percentages of the aflatoxin dose were consumed. Weekly body weight changes, albumin/globulin ratios, and total serum protein were not significantly affected by aflatoxin treatment. A significant (P<.01) increase in serum alkaline phosphatase values was shown at levels of 0.020mg B1/kg body weight per day or more. Gross lesions at postmortem included loss of color in the liver and adrenal hyperplasia of the aflatoxin-treated calves. Histological examination of liver tissue indicated typical early aflatoxin bile duct and central vein proliferative changes, an accumulation of fat and a corresponding loss of glycogen, along with disorganization of the liver lobules and invasion by reticular fibers.

Studies of long term administration of aflatoxin to rats as a natural food contaminant.

AbstractThe effect of feeding aflatoxin, as a natural food contaminant, to rats over long periods of time was studied using multigeneration and longevity tests. The test animals in the multigeneration study consisted of three groups of rats fed diets containing 0, 1 and 10 ppb of aflatoxin (predominantly B1) continued over four generations, with animals of the first and fourth generation fed the diets for 104 weeks. These diets were in proper nutritional balance and included 35% ground roasted peanut products; the ration with 0 ppb aflatoxin excluded the peanuts usually discarded; the one with 1 ppb had the roasted discards returned, while the ration with 10 ppb included the discards in amount 10 times that which had been initially removed. Another longevity study was also performed in which rats were fed diets containing aflatoxin at a level of 80 ppb. In this case, the test peanuts, also fed as a simulated peanut butter at 35% concentration, consisted entirely of roasted peanut discards. Control diets provided no peanut components. Animals fed the low levels of aflatoxin grew as well and actually had a higher percentage survival at 104 weeks than did the animals on the control, aflatoxinfree diets. Organ weights, liver total lipid and cholesterol levels were comparable in all groups. Pathological abnormalities, e.g., hemorrhagic and opaque spots and mottling in some of the livers, were attributed to the aging process since the abnormalities appeared in the control as well as the experimental groups. In the animals fed the aflatoxin at 80 ppb, which has been reported by several investigators to produce well‐defined hepatomas in rats, there was liver involvement and some biochemical changes occurred that were not noted in the controls. However, no hepatomas were observed in these animals even after 21 months on this diet. The liver lesions, indicative of a toxic effect, have not been associated with the development of hepatomas. It is possible that some components of the diet used in these experiments may have protected the animal against hepatoma formation. Our studies indicate that there may be a tolerance for aflatoxin as judged by results in one species of rats when whole ground roasted peanuts provide the natural contaminant.