290 °C (dec.)
The name "riboflavin" comes from "ribose" and "flavin".
Vitamin B was originally considered to have two components, a heat-labile vitamin B1 and a heat-stable vitamin B2 (1). In the 1920s, vitamin B2 was thought to be the factor necessary for preventing pellagra. In 1923, Paul Gyorgi in Heidelberg was investigating egg white injury in rats, the curative factor for this condition was called vitamin H. Since both pellagra and vitamin H deficiency were associated with dermatitis, Gyorgi decided to test the effect of vitamin B2 on vitamin H deficiency in rat. He enlisted the service of Wagner-Jauregg in Kuhan’s laboratory (1). In 1933, Kuhn, Gyorgy, and Wagner found that thiamin-free extracts of yeast, liver, or rice bran prevented the growth failure of rats fed a thiamin supplemented diet. Further, they noted that a yellow-green fluorescence in each extract promoted rat growth, and that the intensity of fluorescence was proportional to the effect on growth. This observation enabled them to develop a rapid chemical and bioassay to isolate the factor from egg white in 1933, they called it Ovoflavin. The same group then isolated the same preparation (a growth-promoting compound with yellow-green fluorescence) from whey using the same procedure (lactoflavin). In 1934 Kuhan’s group identified the structure of so-called flavin and synthesised vitamin B2 (1).
Riboflavin is not toxic when taken orally, as its low solubility keeps it from being absorbed in dangerous amounts from the gut.[4] Although toxic doses can be administered by injection,[4] any excess at nutritionally relevant doses is excreted in the urine,[5] imparting a bright yellow color when in large quantities. In humans, there is no evidence for riboflavin toxicity produced by excessive intakes. Even when 400&_160;mg/d of riboflavin was given orally to subjects in one study for three months to investigate the efficacy of riboflavin in the prevention of migraine headache, no short-term side effects were reported.[6][7]
