Submitted to: Toxicology Letters
Publication Type: Peer reviewed journal
Publication Acceptance Date: 7/1/1996
Publication Date: N/A
Citation: Interpretive Summary: Mycotoxins are poisons produced by molds that can sometimes grow on grains or livestock or poultry feeds. Turkeys are extremely sensitive to many mycotoxins and the consumption of mycotoxin-contaminated feed costs the turkey industry millions of dollars annually. In the present study, turkey poults were dosed with aflatoxin (AF) and fed diets containing AF, a mycotoxin that is highly toxic to turkeys. Activated charcoal (AC) was fed or dosed simultaneously with AF to try to counteract the toxicity of AF. No beneficial effects by AC against AF toxicity were seen. This is important because if AC had worked, it could have saved the turkey industry millions of dollars. However, it is just as important to report this procedure doesn#t work because there was an existing, but misconceived notion that it did, thereby preventing further economic losses due to faulty management and production practices.
Technical Abstract: In one experiment, the effect of inorganic sorbents on the metabolic fate of aflatoxin B1 (AFB1) was studied in turkey poults. At five weeks of age, female poults were surgically colostomized and 9 days later, orally dosed with .75 mg AFB1/kg body weight. Hydrated sodium calcium aluminosilicate (HSCAS), acidic HSCAS, and activated charcoal (AC) were tested, by concomitant administration with AFB1. Urine was collected up to 48 hr post-dosing and analyzed for aflatoxin metabolites. Aflatoxin M1 (AFM1) was the major metabolite found in all treatment groups. HSCAS, AC, and acid HSCAS reduced urinary AFM1 output when orally dosed simultaneous with AFB1. A second experiment was conducted to evaluate the ability of 2 types of AC to modify aflatoxicosis when added to aflatoxin (AF)- contaminated (from culture material) diets of turkey poults. No protective effects from AF toxicity were observed in the feeding study. The adsorbents tested in this study did not modify the metabolic profile of AFB1, nor were any new metabolites identified in their presence.