|Sarr, A - TEXAS A&M UNIVERSITY|
|Mayura, K - TEXAS A&M UNIVERSITY|
|Phillips, Timothy - TEXAS A&M UNIVERSITY|
Submitted to: Toxicology Letters
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 15, 1995
Publication Date: N/A
Interpretive Summary: Aflatoxins are poisons produced by molds and may be natural contaminants of foods and feeds. Broiler chicks are sensitive to aflatoxins and the consumption of aflatoxin-contaminated feed may cost the poultry industry millions of dollars annually. A relatively new approach to reduce the toxicity of aflatoxins is the alteration of bioavailability of the toxins by selective chemisorbents. These materials tightly bind and immobilize the toxin in the gastrointestinal tract of animals, diminishing its bioavailability and disposition to target organs. The effects of these materials on the metabolite composition and concentration is not well known. The concentration of aflatoxin metabolites in the urine were decreased when a diet containing 0.5% hydrated sodium calcium aluminosilicate (HSCAS) was fed to male rats orally dosed with aflatoxin B-1. Aflatoxin M-1 was found to be the major metabolite and, more importantly, no additional metabolites were detected. The results provide additional evidence that a stable complex is formed between aflatoxin and HSCAS in the gastrointestinal tract of animals and that no new metabolic products are formed in the process. This is important to help assure the safety of HSCAS for use in animal feeds when approved for this purpose.
Technical Abstract: The phyllosilicate clay, hydrated sodium calcium aluminosilicate (HSCAS), has been shown to prevent aflatoxicosis in farm animals by reducing the bioavailability of aflatoxin. The present study was designed to determine the effects of HSCAS on the metabolism of aflatoxin B1 (AFB1) in an aflatoxin-sensitive species. Male Fischer-344 rats were orally dosed with 1.0, 0.5, 0.25, and 0.125 mg AFB1/kg body weight alone and in combination with 0.5% HSCAS. Urine samples were collected after 6, 24, 36, and 48 h. Aflatoxin M1 (AFM1) and aflatoxin P1 (AFP1) were detected in most urine samples, with or without HSCAS. AFM1 was found to be the major metabolite. Metabolite concentrations were significantly decreased in the presence of HSCAS, and more importantly, no additional metabolites were detected. Our results suggest that the AFB1-HSCAS complex was not significantly dissociated in vivo, and support earlier findings that HSCAS tightly binds aflatoxin.