In addition, the evolution of the recommended dietary intakes of vitamin A will be discussed.
Elmer V. McCollum and M. Davis discovered vitamin A during 1912-1914. In 1913, Yale researchers, Thomas Osborne and Lafayette Mendel discoveredthat butter contained a fat-soluble nutrient soon known as vitamin A. Scientist of this era had determined that there was vitamin A activity from yellow pigmentation in plants that was similar to the yellow in butterfat. Early researchers went on to deny the possibility of a relationship between yellow coloration in plants and vitamin A activity based on findings from Palmer and Eccles, 1914. Palmer and Eccles achieved success in rearing chickens and rats up with diets almost devoid of carotene. In addition, Stephenson  found that butter fat could be completely stripped of color by charcoal without losing its retinol activity.
It was not until 1929 when the link between carotene and vitamin A activity was reestablished. Thomas Moore in 1929 continued research between carotene and vitamin A activity in rats from carrot root. In Moore's experiment test rats were fed a vitamin A restricted diet until definite signs of deficiency become obvious, Xerophthalmia (night blindness) and slowed growth. Fresh carrot root cut into pieces of 50, 100 or 200 mg. were added to the rodents daily intake. In all rats receiving 200 or 100 mg. of carrot xerophthalmia was cured and steady growth was resumed. In one rat receiving 50 mg. of carrot no response was observed.
In addition, the experiments carried out by Moore in 1929 (T, 1929) confirmed the appearance of vitamin A in liver upon the oral dose of carotene. It was assumed that conversion occurred in the liver but direct evidence to prove the fact was not known.
In 1931, the first claim of the conversion "in vitro" was brought into account from experiments by Olcott and McCann. They incubated carotene in an enzyme preparation, carotenase, for 24 hours. The product of this experiment became colorless with an absorption band at 3280 under specrspoic examination. The results of this experiment were not duplicated in subsequent procedures when the carotenase had been deactivated by heat. There was evidence that carotene went through some sort of enzymatic process but the specifics were still unknown.
Since the early 1900's much has evolved in our knowledge of how -carotene is converted into vitamin A. Olson JA in 2008 discussed the Provitamin A of carotenoids with respects to the conversion of -carotene into vitamin A. Two pathways have been suggested for the conversion of carotenoids to vitamin A in mammals, central cleavage and eccentric cleavage. -carotenoid-15-15-dioxygenase convert -carotene into two molecules of retinal in good yield. The reaction requires molecular oxygen but, is inhibited by sulphydryl-binding and iron binding reagents. This enzyme is responsible for cleavage of most provitamin A carotenoids to retinal. The excentric cleavage occurs in plants and some microorganism and might also occur in mammals. In Microcystis species, there is a highly specific and essential stochiometric conversion of -carotene to cyclocitral and to crocetin-dial. But, till this report was published no mammalian carotenoid dioxygenase with excentric bond specificity was identified and characterized. The
Vitamin A, derived form provitamin A carotenoids, mainly beta-carotene 15, 15-monooxygenases (EC 220.127.116.11). Vitamin A (retinol) is an essential nutrient needed in small amounts by humans and is necessary for vision, cellular differentiation, growth, reproduction, bone development and immune system actions…
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