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Department of Biological Chemistry, School of Medicine, The University of Maryland at Baltimore, 4 Baltimore, Maryland 21201
A study has been made of several factors involved in the mechanism by which 7-chloro-8-methyl-flavin produces a response in the riboflavin-deficient rat which is, for an extended period of time, indistinguishable from the response produced by the administration of riboflavin. When the riboflavin-deficient rat is given 7-chloro-8-methyl-flavin, it provides him with a stimulus which is mistaken as the stimulus he would receive from riboflavin. The animal increases his food consumption immediately, begins to grow, and begins to recover from the signs of deficiency. The ingestion of the additional food causes the intestinal bacteria to synthesize more riboflavin than is characteristic of the animal receiving no flavin. The additional riboflavin is insufficient to be solely responsible for the rapidity and the extent of the reversal of the deficiency state. Therefore, the apparent recovery of the animal must be due to a combination of the analog, a small additional quantity of riboflavin, and the consumption of food. Despite this apparent improvement in the animal's general health, it cannot avoid the lethal results of the administration of the antiriboflavin analog. A small portion of the radioactive riboflavin administered to the rat is excreted as carbon dioxide.
2 Certain portions of this work were presented before The International Symposium on Antivitamins, Zürich-Feldbach, October 1922, 1964.
3 To whom inquiries concerning this report should be sent.
4 Portions of this work were done in the Department of Physiology, University of Rochester and the Department of Biochemistry, University of Nebraska.
Manuscript received 28 January 1970.