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Title: FUMONISIN B1 PROMOTES AFLATOXIN B1 AND N-METHYL-N'-NITRO-NITROSOGUANIDINE INITIATED LIVER TUMORS IN RAINBOW TROUT

Author
item Riley, Ronald
item CARLSON, D - PENN STATE UNIVERSITY, PA
item WILLIAMS, D - OREGON STATE UNIV., OR
item SPITSBERGEN, J - OREGON STATE UNIV., OR
item ROSS, P - APHIS/NVSL/USDA, AMES, IA
item Bacon, Charles
item Meredith, Filmore

Submitted to: Toxicologist
Publication Type: Abstract Only
Publication Acceptance Date: 1/15/2001
Publication Date: 3/1/2001
Citation: N/A

Interpretive Summary: No Interpretive Summary Required. Abstract presented at the 40th Annual Meeting of the Society of Toxicology, San Francisco, California, March 25-29, 2001.

Technical Abstract: Laboratory studies have described the caracinogenicity of FB1 in rodents and epidemiological evidence suggests an association between fumonisin B1 (FB1) (a mycotoxin produced by Fusarium moniliforme = F. verticillioides) and esophageal cancer in humans. This study was designed to reveal in rainbow trout, a species with very low spontaneous tumor incidence, if FB1 was (i) a complete carcinogen in the absence of an initiator; (ii) a promoter of liver tumors in AFB1 initiated fish; and, (iv) a promoter of liver, kidney, stomach, or swim bladder tumors in fish initiated with N-methyl-N'-nitro- nitrosoguanidine (MNNG). FB1 was not a complete carcinogen in trout. No tumors were observed in any tissues of fish fed FB1 for 34 weeks in the absence of a known initiator. FB1 promoted AFB1 initiated liver tumors in a dose-dependent manner in fish fed 5, 25, or 100 ppm FB1 for 42 weeks. Liver tumor incidence in AFB1 initiated fish correlated with dose-dependent alterations in sphingolipid metabolism, as measured by free sphingosine (So) and sphinganine (Sa) ratios. In MNNG initiated fish, liver tumors were promoted in 100 ppm FB1 treatments (42 weeks), but FB1 did not promote tumors in any other tissues. Tumor incidences decreased in kidney and stomach in 100 ppm FB1 treatments of MNNG initiated trout. A one-week pre-treatment of FB1 did not alter the amount of liver [3H]-AFB1 DNA adducts, which suggested that FB1 promotion of AFB1 did not involve Phase I or Phase II metabolism of AFB1. We hypothesize that FB1 promotion of hepatocarcinogenesis was due to changes in cellular signaling, possibly through disruption of sphingolipid mediated pathways.