■ Source
The discovery of vitamin A acetate dates back to the early 1900s. In 1907, a substance with potent anti-tuberculosis activity was first extracted from salmon liver and found to be a fat-soluble vitamin that could be associated with xanthine deficiency. In 1931, the British scientist Kelster succeeded in isolating yellow crystals from salmon liver, which he named vitamin A. Kelster determined the structure of vitamin A and discovered that it could be converted into an active form, retinol, in animals, thereby improving vision.
In 1948, scientists in the United States succeeded in synthesizing vitamin A acetate, a stable vitamin A derivative that is converted in the body to active retinol. Vitamin A acetate can be supplied to the body in the form of food or pharmaceutical supplements to meet the body's vitamin A needs.
■ Metabolism
Jivantid®Vitamin A acetate is hydrolyzed in the body by enzyme-catalyzed hydrolysis to form vitamin A, which is then oxidized to retinaldehyde, a photoreceptor that forms sensory cells and is involved in the formation of vision. Retinaldehyde can be further oxidized to retinoic acid. Retinoic acid is not stored in the body, but as a metabolite of vitamin A, it combines with glucuronic acid or is oxidized to other metabolites in the liver and excreted in the bile or urine.
