Physiological Actions


The retinal pigment epithelium cells (RPE) of the retina form an epithelial cell layer that takes up retinol from choroid capillaries and stores it as retinyl esters, to be used as substrate for the generation of 11-cis-retinal. In the layer of rod and cone photoreceptor cells adjacent to the RPE, 11-czs-ret-inal combines covalently with the protein opsin to generate the visual pigment rhodopsin in rods and, similarly, iodopsin in cones. Each rod outer segment is densely packed with some 108 molecules of rho-dopsin per cell. The small quantity of vitamin A stored in the retina would be inadequate to maintain vision were it not for the visual cycle, a process in which 11-ds-retinal is regenerated after photo-bleaching. The absorption of light by rhodopsin catalyzes the photoisomerization of the 11-czs-retinal moiety of rhodopsin to all-ira«s-retinal (resulting in bleaching), which induces the release of all-tra«s-retinal from opsin. The change in retinal's isomeric configuration is crucial for initiating a signal transduction cascade from the rods to nearby retinal ganglion cells, and thereafter to the optic nerve for transmission to the brain's visual cortex. For vision to continue, 11-ds-retinal must be regenerated. This is accomplished in a series of biochemical reactions constituting the visual cycle, some of which take place in the rod cell outer segment and others in the RPE. The regeneration of 11-ds-retinal (dark adaptation) is slow (on the order of minutes) compared to the photoisomerization (fractions of a second). However, normal vision continues without a period of blindness as long as retinol can be drawn from retinyl esters stored in the RPE, rapidly isomerized to 11-czs-retinol, re-oxidized to 11-cis-retinal, and passed to the rod cell outer membrane where rhodopsin is regenerated. When the supply of retinyl esters in the RPE is not adequate, there is significant slowing of the visual cycle, resulting in the condition known as night blindness, a loss of the ability to quickly dark adapt after exposure to bright light. Night blindness is often the first-detected clinical sign of vitamin A deficiency (see the article section 'Hypervitaminosis A and Vitamin A Toxicity').

Cornea The cornea, an avascular tissue, requires retinoic acid for the normal differentiation of the corneal and conjunctival epithelium. Holo-RBP, which is present in the lacrimal glands and tears, is likely to provide the substrate for the local biogenesis of retinoic acid. Retinoid deficiency results first in a loss of goblet secretory cells, which can be detected histologically. Corneal xerosis and Bitot's spots (foamy deposits) are strong signs of prolonged vitamin A deficiency (see 'Hypervitaminosis A and Vitamin A Toxicity'). Vitamin A must be administered immediately to prevent the progression of corneal xerosis to corneal ulceration, which causes life-long blindness.

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