To evaluate the effect of exogenous testosterone on the development of T-2 toxin-induced necrosis of adrenal glands, mice were allotted to 3 treatment groups. Each treatment group contained castrated male, and castrated and sexually intact female mice. Each mouse in group 1 was given 0.16 mg testosterone propionate at 48-hour intervals for a total of 12 infections, group-2 mice were given similar injections of only the vehicle, and group-3 mice were given no treatment. Twenty-four hours after the last injection, the mice in all 3 groups were exposed for 10 minutes to an aerosol of T-2 toxin. All mice alive at 24 hours after exposure were euthanatized and the adrenal glands and thymuses were examined histologically. Necrosis of the adrenal cortex was not found in any of the mice given preexposure treatment with exogenous testosterone, whereas all mice given vehicle only or no treatment had T-2 toxin-induced necrosis of the inner portion of the adrenal cortex. Lymphocytolysis in the cortex of the thymus confirmed that each mouse of all 3 treatment groups had experienced systemic mycotoxicosis. The uniform severity of the lesion in all mice suggests that the thymus was not protected by exogenous testosterone administration or by the castration status of the mice. We propose that T-2 toxin-induced adrenal necrosis in mice is prevented by the presence of testosterone.

The relationship of serum complement activity and bacteriostatic activity was investigated in male guinea pigs given aflatoxin and/or rubratoxin. In experiment 1, guinea pigs were given 0.6 mg of aflatoxin/kg of body weight, PO, once. In experiment 2, guinea pigs were given 0.02 mg of aflatoxin/kg, PO, and/or 8 mg of rubratoxin, PO, 11 times. Aflatoxin (0.02 mg/kg) had no effect given alone, but potentiated the effect of rubratoxin. In both experiments, changes in complement activity were accompanied by similar but not always significant (P less than 0.05) changes in bacteriostatic activity of serum. Guinea pigs given 0.06 mg of aflatoxin/kg had significant (P less than 0.05) changes in complement titers and in serum alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase activities. Guinea pigs given repeated oral doses of aflatoxin and/or rubratoxin had changes in complement titers, bacteriostasis, and alkaline phosphatase and aspartate aminotransferase activities, but not in alanine aminotransferase activities. Significant differences were detected only when average values for all guinea pigs given rubratoxin or rubratoxin with aflatoxin were compared with average values for guinea pigs not given rubratoxin.

Diacetoxyscirpenol (DAS) was given IV to pigs (0, 0.5, and 1.0 mg/kg of body weight), cattle (0 and 0.5 mg/kg), and dogs (0 and 0.5 mg/kg). Blood was collected and hemograms were done at 0.5-hour intervals for 8 hours. The animals were euthanatized at 8 hours after treatment, and bone marrow samples were taken and examined by light microscopy. Moderate to severe necrosis of bone marrow hematopoietic elements was found in animals given DAS. The sequential increase in the type and number of abnormal cells in the blood suggested a successive destruction of the hematopoietic elements. A marked left shift in the neutrophil population was found in animals given DAS. Metarubricytes and large platelets were found in the blood of animals given DAS. Lymphocytes were replaced with immature cells. Pathologic changes were most severe in the pigs given a dosage of 1.0 mg of DAS/kg. The order of species sensitivity to DAS was pigs greater than dogs much greater than cattle.