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United States Department of Agriculture

Agricultural Research Service

Research Project: MINIMIZING THE ADVERSE HEALTH AND ECONOMIC IMPACTS OF MYCOTOXINS AND PLANT TOXINS IN FOODS Title: Differential sensitivity of rat kidney and liver to fumonisin toxicity: Organ specific differences in toxin accumulation and sphingoid base metabolism.

Authors
item Riley, Ronald
item Voss, Kenneth

Submitted to: American Chemical Society Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: September 1, 2006
Publication Date: September 10, 2006
Citation: Riley, R.T., Voss, K.A. 2006. Differential sensitivity of rat kidney and liver to fumonisin toxicity: Organ specific differences in toxin accumulation and sphingoid base metabolism.. American Chemical Society Abstracts. September 10 - 14, 2006. San Francisco, CA.

Interpretive Summary: Abstract - no interpretive summary needed. American Chemical Society National Meeting and Exposition, San Francisco, CA, September 10-14, 2006.

Technical Abstract: Fumonisins (FB) are mycotoxins in maize and inhibitors of ceramide synthase (CS). In liver and kidney inhibition of CS results in a marked increase in the ceramide precursor sphinganine (Sa). This study was conducted to investigate the differential changes in Sa, sphingosine (So), Sa-1-phosphate (Sa-1-P) and So-1-phosphate (So-1-P) in kidney, liver, serum and heart of male Sprague-Dawley rats fed diets containing FB. The tissues were microscopically examined for the presence and severity of lesions. There was a time- and dose-dependent increase in Sa in both liver and kidney that was closely correlated with the tissue concentration of FB1 and histopathologic findings. However, the Sa and So were quickly metabolized to Sa-1-P and So-1-P in kidney. The concentration of FB1 in liver and kidney that first elicited an increase in Sa was similar in both tissues, however, over time, the kidney accumulated significantly more FB1 and total Sa (Sa plus Sa-1-P). Thus, the relative sensitivity of male Sprague-Dawley rat kidney and liver is most likely a consequence of differences in the mechanisms responsible for both FB1 uptake/clearance and Sa metabolism.

Last Modified: 10/25/2014
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