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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 14CO2was 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.