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ARS Home » Research » Publications at this Location » Publication #84073


item Meredith, Filmore
item Riley, Ronald
item Bacon, Charles
item Williams, David
item Carlson, David

Submitted to: Journal of Food Protection
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/23/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary: A toxic substance, named fumonisin B1 is produced by a fungus Fusarium moniliforme. This toxin is produced on corn and corn products and poses both human and animal health risks. Fumonisin B1 is a known cancer promoter in rats. Rainbow trout are a good animal to use for determining tissue changes from other toxic substances. Fumonisin B1 was added at six different concentrations to prepared diets for feeding to rainbow trout. It was not known if the fumonisin B1 would be in a form that rainbow trout could utilize. Therefore, it was necessary to determine the concentration of fumonisin B1 in the different diets. Analysis of the diets was difficult due to the fat that was present. Removal of the fat from the diet sample was carried out with a fat loving chemical solvent. The fumonisin B1 was then removed from the previously extracted diet sample with a different chemical solvent. It was found that concentrations of fumonisin B1 ranged from 12 to 81% of the calculated concentrations based on the fumonisin B1 added to the diet. The fumonisin B1 was readily absorbed and biologically active as evidenced by changes of chemicals (sphingolipids) present in the rainbow trout blood serum, liver and kidney tissue. The rainbow trout appear to be a good model for determining the effects of fumonisin B1 in a long term study.

Technical Abstract: The purpose of this study was (i) to determine whether pure fumonisin B1 could be incorporated into, recovered, and detected by HPLC chromatographic analysis from the semipurified Oregon Test Diet (OTD) used in rainbow trout feeding studies, and (ii) to determine if the incorporated fumonisin B1 was biologically available using the change in free sphingoid bases in liver, kidney, and serum as a mechanism-based biomarker. The results indicate that fumonisin is not easily quantified in OTD. Recoveries ranged from 12% to 81% of the calculated concentrations based on the fumonisin B1 added to OTD. However, the fumonisin B1 in the OTD was readily absorbed and biologically active as evidenced by marked increases in free sphinganine in liver, kidney, and serum. The magnitude of the increase in free sphinganine at 100 ppm in OTD was comparable to that known to be associated with liver toxicity in rats, pigs, and ponies.