Published online by Cambridge University Press: 09 March 2007
1. Riboflavine given orally to sheep, calves, goats and ruminating kids gave rise, in milk and urine, to extra riboflavine accompanied by hydroxyethylflavine, by formylmethylflavine and by other as yet unidentified metabolites, but subcutaneous injection of riboflavine caused prolonged excretion of riboflavine in urine and milk unaccompanied by metabolites.
2. Placement of riboflavine by means of fistulas into the rumen, the abomasum or the caecum and abstraction of samples from the rumen or caecum showed that the rumen was the site of origin of the metabolites, thus accounting for the lapse of time of several hours between the ingestion of riboflavine and the appearance of hydroxyethylflavine in the urine and the absence of metabolites after subcutaneous injection of riboflavine.
3. Kids in which rumination had not yet become established could not produce metabolites from ingested riboflavine although, when fed milk containing the metabolites, they readily excreted them in their urine.
5. Incubation in vitro of kidney or liver tissue from cattle or goats with riboflavine did not give rise to metabolites, but these tissues could both reduce formylmethylflavine to hydroxyethylflavine in vitro.
6. Post-mortem examination of animals to which riboflavine had been fed showed the presence of metabolites only in gut contents, in the urinary bladder and in the bile. When injected, riboflavine reached the bile but no metabolites were produced.
7. Metabolites were found to occur naturally in the urine of ruminants in small amounts. Hydroxyethylflavine was readily demonstrable in the urine of the rabbit, but in the urine of the dog metabolites could not be found.
8. From these and earlier and later experiments the conclusion is drawn that riboflavine metabolites arise in the ruminant from the degradation of riboflavine by rumen bacteria.