Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing wethers (mean body weight, 34.0 kg) and was evaluated for its ability to diminish the clinical signs of aflatoxicosis. The experimental design consisted of 4 treatment groups of 5 wethers each, consuming concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control; group 1); 20 g of HSCAS/kg (2.0%; group 2), 2.6 mg of AF/kg (group 3); or 20 g of HSCAS (2.0%) plus 2.6 mg of AF/kg (group 4). Wethers were maintained in indoor pens, with feed and water available ad libitum for 42 days. Lambs were observed twice daily and weighed weekly, and blood samples were obtained every 2 weeks for hematologic and serum biochemical analyses and for measurement of mitogen-induced lymphocyte-stimulation index. At the termination of the study, wethers were euthanatized and necropsied. Body weight gain was diminished significantly (P less than 0.05) by consumption of 2.6 mg of AF/kg of feed, whereas body weight of lambs consuming HSCAS plus AF did not differ from that of control wethers. The AF-alone treatment increased serum aspartate transaminase and gamma-glutamyltransferase activities, prothrombin time, and cholesterol, uric acid, and triglyceride values and decreased albumin, glucose, and urea nitrogen values, and urea-to-creatine ratio. A 27% decrease in lymphocyte stimulation index, increased spleen weight (as a percentage of body weight), and decreased liver weight were induced by AF-alone treatment. Results indicate that HSCAS may be a high-affinity sorbent for AF, that 2.6 mg of AF/kg of feed induces signs of aflatoxicosis in growing wethers, that lambs may not be as resistant to the effects of AF as previously thought, that 2.0% HSCAS can substantially reduce the toxic effects of 2.6 mg of AF/kg, and that sorbent compounds may offer a novel approach to the preventive management of aflatoxicosis in livestock.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for agricultural feeds, was added to aflatoxin (AF)-contaminated diets of 3 lactating dairy cows and evaluated for its potential to reduce aflatoxin M1 (AFM1) residues in milk. During phase I, cows were fed alternating diets that consisted of 200 microgram of AF/kg of feed for 7 days, 0.5% HSCAS plus 200 microgram of AF/kg of feed for 7 days, and feed with the HSCAS removed for a final 7 days. The AFM1 milk concentrations from the intervals with HSCAS added to diets were compared with those times when HSCAS was absent. The presence of 0.5% HSCAS in feed containing 200 microgram of AF/kg reduced AFM1 secretion into the milk by an average of 0.44 microgram/L (from pretreatment of 1.85 microgram/L to 1.41 microgram/L with HSCAS, a 24% reduction). Following a 10-day period of noncontaminated feed consumption and no AFM1 residues in the milk, phase II of the study was begun. The same experimental design as phase I was used, but the dosages of HSCAS and AF were changed to 1.0% and 100 microgram/kg of feed, respectively. The addition of 1.0% HSCAS in feed containing 100 microgram of AF/kg decreased AFM1 content in the milk by an average of 0.40 microgram/L (from a pretreatment of 0.91 microgram/L to 0.51 microgram/L when HSCAS was present, a 44% reduction). These findings suggest that HSCAS, a high-affinity sorbent compound for AF in vitro, is capable of reducing the secretion of AFM1 into milk.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing wethers (mean body weight, 34.0 kg) and was evaluated for its ability to diminish the clinical signs of aflatoxicosis. The experimental design consisted of 4 treatment groups of 5 wethers each, consuming concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control; group 1); 20 g of HSCAS/kg (2.0%; group 2), 2.6 mg of AF/kg (group 3); or 20 g of HSCAS (2.0%) plus 2.6 mg of AF/kg (group 4). Wethers were maintained in indoor pens, with feed and water available ad libitum for 42 days. Lambs were observed twice daily and weighed weekly, and blood samples were obtained every 2 weeks for hematologic and serum biochemical analyses and for measurement of mitogen-induced lymphocyte-stimulation index. At the termination of the study, wethers were euthanatized and necropsied. Body weight gain was diminished significantly (P less than 0.05) by consumption of 2.6 mg of AF/kg of feed, whereas body weight of lambs consuming HSCAS plus AF did not differ from that of control wethers. The AF-alone treatment increased serum aspartate transaminase and gamma-glutamyltransferase activities, prothrombin time, and cholesterol, uric acid, and triglyceride values and decreased albumin, glucose, and urea nitrogen values, and urea-to-creatine ratio. A 27% decrease in lymphocyte stimulation index, increased spleen weight (as a percentage of body weight), and decreased liver weight were induced by AF-alone treatment. Results indicate that HSCAS may be a high-affinity sorbent for AF, that 2.6 mg of AF/kg of feed induces signs of aflatoxicosis in growing wethers, that lambs may not be as resistant to the effects of AF as previously thought, that 2.0% HSCAS can substantially reduce the toxic effects of 2.6 mg of AF/kg, and that sorbent compounds may offer a novel approach to the preventive management of aflatoxicosis in livestock.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing barrows and was evaluated for its potential to ameliorate the clinical signs of aflatoxicosis. The experimental design consisted of 6 treatments of 5 barrows each at concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control), 5 g of HSCA/kg of feed (0.5%), 20 g of HSCAS/kg of feed (2.0%), 3 mg of AF/kg of feed, 5 g of HSCAS (0.5%) plus 3 mg of AF/kg of feed, or 20 g of HSCAS (2.0%) plus 3 mg of AF/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available ad libitum for 28 days (from the age of 7 to 11 weeks). Barrows were observed twice daily and were weighed weekly, and blood samples were obtained weekly for hematologic and serum biochemical measurements. At the termination of the study, barrows were euthanatized and necropsied. Body weight gains were diminished significantly (P less than 0.05) by consumption of 3 mg of AF/kg of feed, whereas body weight gain in barrows consuming diets containing HSCAS or HSCAS plus AF did not differ from that in control barrows. Serum enzymatic activities of alkaline phosphatase and gamma-glutamyl transferase and prothrombin time were increased in barrows consuming 3 mg of AF/kg of feed, but not in those consuming HSCAS or HSCAS plus AF. Aflatoxin alone induced decreased serum concentrations of urea nitrogen, albumin, total protein, calcium, phosphorus, cholesterol, and glucose, as well as serum total iron-binding capacity, whereas HSCAS or HSCAS plus AF did not induce such effects. Liver weight was increased in barrows of the AF-alone treatment group, compared with control barrows. Hepatic lesions in barrows of the AF-alone treatment group were charaterized as peripheral lobular lipidosis accompanied by periportal and interlobular fibrosis and bile duct hyperplasia. Hepatic lesions were not observed in barrows of the 0.5% HSCAS plus AF or 2.0% HSCAS plus AF treatment groups. These findings suggested that HSCAS can modulate the toxicity of AF in growing barrows (perhaps via sequestration and reduced bioavailability in vivo) and may offer a novel approach to the preventive management of aflatoxicosis in animals.