“…It seems reasonable to assume a relatively constant tissue requirement for vitamin A and that it is supplied through a release of vitamin A alcohol into the blood from the liver. However, the rate of loss from the liver is related to the magnitude of liver reserves and an animal does not appear always to use its vitamin A reserves, particularly when they are high, to the best advantage (Moore, 1957); the vitamin may be destroyed in the Kupffer cells (Popper & Brenner, 1942) or released into the body for destruction elsewhere. In the latter connexion the persistence of high levels of vitamin A ester in the blood, long after dosing with vitamin A had ceased, of a patient suffering from hypervitaminosis A (Gerber, Raab & Sobel, 1954) is most interesting.…”