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Journal of Nutrition Vol. 101 No. 6 June 1971, pp. 819-829
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Induction of a Specific Enzyme Inadequacy in Infant Rats by the Use of a Homologue of Riboflavin1,2,

Yoom Soo Kim3 and John P. Lambooy4

Department of Biochemistry, University of Nebraska, College of Medicine, Omaha, Nebraska 68105, and Department of Biological Chemistry, University of Maryland School of Medicine, Baltimore, Maryland 21201

The riboflavin homologue 7-ethyl-8-methyl-flavin can replace riboflavin in the metabolism of the rat with respect to growth, survival, physical appearance and efficient food utilization. Female rats fed a diet containing this flavin from weaning to adulthood can breed and produce normal-appearing young, but these young do not survive. If under identical circumstances the diet contains a mixture of homologue (93%) and riboflavin (7%), young which are born survive. Since a small proportion of the total biologically active flavin as riboflavin corrected the survival defect, an enzyme inadequacy was suggested. Females fed diets containing either riboflavin, homologue or a mixture of these two flavins, until adulthood, were bred. The hearts, kidneys and livers of the females and their litters were assayed for succinic acid dehydrogenase (SDH) and flavin content. The flavin concentration in the tissues was found not to be limiting. The SDH activities of the hearts and kidneys of homologue young were depressed far below normal. The SDH associated with only homologue flavin-adenine dinucleotide does not appear to provide sufficient catalysis for efficient production of energy in these fetal tissues. Electron transport-linked diphosphopyridine nucleotide dehydrogenase in the mitochondria of these tissues in the female utilizes the homologue as well as riboflavin.


1 Supported in part by the National Institute of Child Health and Human Development Grants no. HD 01306 and HD 04618, and by the National Institute of Arthritis and Metabolic Diseases Grant no. AM 11034.

2 Certain portions of this work were presented before the First Korean International Biochemical Conference, Seoul, Korea, August 28, 1967.

3 Present address: Department of Biochemistry, Yonsei University School of Medicine, Seoul, Korea.

4 To whom inquiries concerning this report should be sent at the University of Maryland.

Manuscript received 4 November 1970.





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