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Journal of Nutrition Vol. 101 No. 8 August 1971, pp. 1037-1044
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Effect of Toxic Levels of Dietary Fluoride on Citrate Metabolism in the Rat1

T. R. Shearer2, J. J. Le Saouter3 and J. W. Suttie4

Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin, Madison, Wisconsin 53706

Citrate metabolism was studied in rats fed diets containing 450 or 600 ppm F. Ingestion on the high fluoride diet for 3 days caused an elevation of liver and blood citrate concentrations and a decrease in femur citrate content. After 2 weeks, liver and blood citrate concentrations returned to normal, and femur citrate remained depressed. The continuous intravenous infusion of 3 or 10 mg of citrate per day for 3 days did not cause an increase in either liver or blood citrate levels. The capacity of bone slices to incorporate 2-14C-acetate into citrate or total organic acids was not altered when the slices were prepared from rats fed the fluoride diet for 3 days. Oxidation of a tracer dose of 14C-citrate to 14CO2 was not inhibited, nor were kidney citrate concentrations affected in rats fed the fluoride-containing diet for 3 days. Although the addition of 20 ppm F to an isolated, perfused rat liver caused changes in the concentrations of glycolytic intermediates, it did not alter citrate levels. The activities of rat liver aconitase, isocitrate dehydrogenase, malate dehydrogenase, citrate-cleavage enzyme, and citrate condensing enzyme were not directly affected by fluoride ingestion for 3 or 14 days. It was concluded that the elevation of liver and blood citrate observed in rats fed a fluoride-containing diet for 3 days was caused by a specific but as yet undetermined metabolic effect of fluoride. It cannot be exclusively the result of: 1) the fluoride-induced release of citrate from bone, 2) inhibited citrate oxidation, or 3) fluoride inhibition of liver citrate metabolizing enzymes.

1 Supported in part by a research grant from the Aluminum Company of America, the Aluminum Company of Canada, Ltd., the Kennecott Copper Corporation, the Electric Reduction Company, the Monsanto Chemical Company, the Ormet Corporation, the Tennessee Valley Authority, the Stauffer Chemical Company, Reynolds Metal Company, the Kaiser Aluminum and Chemical Corporation, the Anaconda Aluminum Company, the Harvey Aluminum Company, the U. S. Steel Corporation, the Tennessee Corporation, the Intalco Aluminum Corporation, and the National Southwire Aluminum Company.

2 Present address: University of Oregon Dental School, Portland, Oregon.

3 Present address: c/o Entremont B.P.7, 56 Malestroit, France.

4 Person to whom reprint requests should be sent.

Manuscript received 13 January 1971.




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