Overview of current knowledge of metabolism of vitamin A and carotenoids.

Current knowledge about the metabolism of naturally occurring retinoids and carotenoids was summarized. Dietary provitamin A carotenoids are largely converted to retinol (vitamin A) during intestinal absorption in the mucosal cell. In humans, a limited amount of carotenoids can be absorbed intact, along with retinyl esters (newly synthesized or from dietary vitamin A), mainly via lymph chylomicrons. Carotenoids are stored in several tissues, particularly liver and fat. They are transported in plasma by lipoproteins (density less than 1.21 g/ml), particularly by the low-density lipoproteins. Plasma carotenoids are usually a mixture of compounds with and without provitamin A activity; beta-carotene is about 20-25% of the total. Newly absorbed vitamin A is stored in the liver as retinyl esters. Storage involves both the hepatic parenchymal cells and the nonparenchymal stellate cells. Vitamin A is mobilized from liver stores and transported in plasma as retinol bound to a specific transport protein, retinol-binding protein (RBP). Retinol mobilization is highly regulated by factors that control the rates of RBP synthesis and secretion. Much is known now about the chemical structure, metabolism, and biologic roles of RBP, RBP delivers retinol to peripheral target tissues; delivery may involve cell surface receptors for RBP. Tissues of rats, humans, and other species contain soluble binding proteins with specificity for either retinol (cellular retinol-binding protein) or retinoic acid (cellular retinoic acid-binding protein). These intracellular proteins have been purified from several tissues and partly characterized. From both immunoassay and immunocytochemical studies, information is available about their tissue distribution and levels. Retinoic acid is mainly absorbed through the portal system and transported in plasma as the anion bound to serum albumin. Nonspecific and unregulated delivery of retinoids to biologic membranes apparently leads to vitamin A (retinoid) toxicity.