II. CHEMISTRY 327 



It has been suggested^*' that the small vitamin B2 activity of L-arabo- 

 flavin might be due to contamination with riboflavin, formed during the 

 synthesis by an Amadori rearrangement (see p. 318). In rats receiving 10 

 Y of riboflavin per day L-araboflavin in higher doses (200 7 per day) reduces 

 the growth very shghtly.^^ 



Of the other stereoisomers of riboflavin which have been synthesized, 



OHH OH 



I I I 

 only D-xyloflavin, R — CH2 — C— C— C — CH2OH, is said to produce a slow 



H OHH 



gain of weight in vitamin B2-deficient rats.®^ 



OH OHH 



I I I 

 L-Lyxoflavin, R — CH2 — ^C — C— C — ^CH2 — OH, was isolated from hu- 



I I I 

 H H OH 



man myocardium in 1949 and has been made synthetically.^^ It is devoid 



of riboflavin activity in rats when tested by the standard assay, but in a 



rat assay for unidentified vitamins in hver and other source materials, as 



well as for Lactobacillus lactis, L-lyxoflavin has shown growth-promoting 



or vitamin activity.^"'' Lyxoflavin seems to be the first exception from the 



generally accepted rule that flavins isolated from different natural sources 



are chemically identical with n-riboflavin; but its natural existence has 



not been definitely confirmed. ^''^ 



Besides the mentioned riboflavin isomers, L-l'-ribityl-, D-l'-arabityl-, 



and D-l'-lyxitylflavin have been prepared synthetically; none of these 



substances has vitamin B2 activity. 



2. Antagonists of Riboflavin 



Diethylflavin, 6,7-diethyl-9-(D-l'-ribityl)isoalloxazine, has already been 

 mentioned as an antagonist of riboflavin in the groAving rat.^^* 



Isoriboflavin, 5,6-dimethyl-9-(D-l'-ribityl)isoalloxazine, in a daily dose 

 of 2 mg. in rats almost completely inhibits the growth-promoting effect of 

 10 7 of riboflavin per day. The inhibitory effect can be prevented entirely 



9« F. Weygand, Ber. 73, 1259, 1264 (1940). 



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



98 E. Sodi Pallares and H. Martinez Garza, Arch. Biochem. 22, 63 (1949); Arch. Inst, 

 cardiol. Mex. 19, 753 (1949) [C.A. 44, 5368 (1950)]. 



99 D. Heyl, E. C. Chase, F. Koniuszy, and K. Folkers, /. Am. Chem. Soc. 73, 3826 

 (1951). 



'O" G. A. Emerson and K. Folkers, J. Atn. Chvm. Soc. 73, 2398, 5383 (1951). Mary S. 

 Shorb, Proc. Soc. Exptl. Biol. Med. 79, 611 (1952). Compare, however, E. E. Snell, 

 O. A. Klatt, H. W. Bruins, and W. W. Cravens, Proc. Soc. Exptl. Biol. Med. 82, 583 

 (1953). 



i<" T. S. Gardner, E. Wenis, and J. Lee, Arch. Biochem. and Biophijs. 34, 98 (1951). 



