VI. BIOGENESIS 359 



D-Araboflaviii (compound d) inhibits growth and increases the mortaHty 

 rate^- more than the absence of riboflavin alono. The other aral)ityl deriva- 

 tives can sustain life in rats at a cUminished growth rate if given in rela- 

 tively large amounts. 



^soribofla^■in [5,6-dimethyl-0-(D-l'-ribityl)isoalloxazine] is an isomer of 

 riboflavin which, if given to rats at levels of 2 mg. per day, will counteract 

 the growth-promoting effects of 40 7 of riboflavin. It is interesting that 

 isoriboflavin has no inhibitory effect on Laclo})acillus casei. 



Ribofla\-in tetraacetate^^ and both the mono- and diacetone derivatives^^ 

 are fully active in supporting rat growth, probably owing to hydrolysis in 

 the mammalian organism, but they are inactive for lactic acid bacteria. 

 Replacement of the D-ribityl group by a glucosidic group''* results in a total 

 loss of biological activity. The monomethylol derivative^* prepared by 

 reacting ribofla\'in with formaldehj^de retains about half the original activ- 

 ity. Riboflavin mono-, di-, tri-, and tetrasuccinates*^ vary in rat growth 

 activity as 100, 65, 21, and 0%, respectively. Substitution of a methyl 

 group in the 3 position'^ results in complete loss of vitamin activity. 



Generally speaking, the activity of esterified derivatives of riboflavin 

 may vary with the abihty of the test organism to effect hydrolysis of the 

 ester; the 3 position must remain unsubstituted, and substitution in the 

 6 or 7 position is necessary. 



When the 6 and 7 positions are not substituted, the compounds are 

 toxic. '^ A recent review by Woolley*^ has highlighted the increased interest 

 in the inhibitory analogs of the vitamins. 



VI. Biogenesis 



M. K. HORWITT 



Riboflavin is synthesized by most higher plants, yeasts, and lower fungi, 

 and by some bacteria. The tissues of higher animals are unable to synthe- 

 size this vitamin, but the gastrointestinal tract of many of these animals 

 harbor bacteria which may be capable of providing riboflavin for their host. 



= H. von Euler and P. Karrer, Helv. Chim. Acta 29, 353 (1946). 

 ' R. Kuhn, H. Rudy, and F. Weygand, Bcr. 68, 625 (1935). 

 ' R. Kuhn and K. Strobele, Ber. 70, 747 (1937). 

 ^ K. Schoen and S. M. Gordon, Arch. Biochcm. 22, 149 (1949). 

 « M. F. Furter, G. J. Haas, and S. H. Rubin, J. Biol. Chcm. 160, 293 (1945). 

 ' R. Kuhn, K. Reinemund, F. Weygand, and R. Strobele, Ber. 68, 1765 (1935). 

 ■* R. Kuhn and P. Boulanger, Z. physiol. Chem. 241, 233 (1936). 

 ' D. W. Woolley, A Study of Antimetabolites. John Wiley and Sons, New York, 

 1952. 



