Tuesday, April 10, 2012

History of Biotin

History of Biotin
1901  Wildiers discovers that yeast requires a special growth factor which he names “bios”. Over the next 30 years, bios proves to be a mixture of essential factors, one of which – bios IIB – is biotin.

1916  Bateman observes the detrimental effect of feeding high doses of raw egg white to animals.

1927  Boas confirms the findings of dermatosis and hair loss in rats fed with raw egg white. She shows that this egg white injury can be cured by a “protective factor X” found in the liver.

1931  Gy?rgy also discovers this factor in the liver and calls it vitamin H (from Haut, the German word for skin).

1933  Allison and coworkers isolate a respiratory coenzyme – coenzyme R – that is essential for the growth of Rhizobium, a nitrogen-fixing bacterium found in leguminous plants.

1935  K?gl and T?nnis extract a crystalline growth factor from dried egg yolk and suggest the name ‘biotin’.

1940  Gy?rgy and his associates conclude that biotin, vitamin H and coenzyme R are identical. They also succeed in isolating biotin from the liver.

1942  K?gl and his group in Europe and du Vigneaud and his associates in the USA establish the structure of biotin.

1942  Sydenstricker and colleagues demonstrate the need for biotin in the human diet.

1943  Total synthesis of biotin by Harris and colleagues in the USA.

1949  Goldberg and Sternbach develop a technique for the industrial production of biotin.

1956  Traub confirms the structure of biotin by X-ray analysis.

1959  Lynen’s group describes the biological function of biotin and paves the way for further studies on the carboxylase enzymes.

1971  First description of an inborn error of biotin-dependent carboxylase metabolism by Gompertz and associates.

1981  Burri and her colleagues show that the early infantile form of multiple carboxylase deficiency is due to a mutation affecting holocarboxylase synthetase activity.

1993  Wolf and coworkers suggest that late-onset multiple carboxylase deficiency results from a deficiency in biotinidase activity.

No comments:

Post a Comment