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Response of Rats to Thalidomide as Affected by Riboflavin or Folic Acid Deficiency¹

Division of Nutrition, Bureau of Scientific Research, Food and Drug Administration, Washington, D. C.

The response of rats to thalidomide was examined under the influence of either riboflavin or folic acid deficiencies. At a level of 0.75% of the diet thalidomide depressed growth, but this was significant only for rats fed by the equalized feeding procedure, and for rats fed the riboflavin-deficient diet, ad libitum. In the former case the growth-depressing effect of thalidomide was markedly intensified by omission of riboflavin from the diet. In contrast, a riboflavin depletion-repletion regimen showed a greater degree of recovery in rats receiving thalidomide. Inclusion of thalidomide in the riboflavin-deficient diet accentuated the typical symptoms and produced a consistent leucopenia. Thalidomide had little or no specific effect on liver content or activity of riboflavin-dependent enzymes and cofactors, such as D-amino acid oxidase, FAD and flavin-mononucleotide. However, succinic dehydrogenase, but not glutamic dehydrogenase, was decreased. Centrolobular necrosis was induced by thalidomide only in the livers of rats receiving the diets used in the folic acid study which contained sulfothalidine; thalidomide also depressed growth in all rats receiving the diets with sulfothalidine.

Manuscript received 26 August 1964.