Vitamin A (Retinol)
General
Chemical formula	C20H30O
Molecular weight	? g/mol
Vitamin properties
Solubility	Fat
RDA (adult male)	900 μg/day
RDA (adult female)	700 μg/day
RDA upper limit (adult male)	3,000 μg/day
RDA upper limit (adult female)	3,000 μg/day
Deficiency symptoms
Night-blindness Pale, dry skin
Excess symptoms
Liver toxicity Teratological effects Osteoporosis (suspected, long-term)
Common sources
Liver Dairy products Darkly colored fruits Leafy vegetables

Retinol, the dietary form of vitamin A, is a fat-soluble, antioxidant vitamin important in vision and bone growth. It belongs to the family of chemical compounds known as retinoids. Retinol is ingested in a precursor form; animal sources (milk and eggs) contain retinyl esters, whereas plants (carrots, spinach) contain carotenoids. Tissue cells convert these precursors to retinol, and then to either retinal or retinoic acid. Many of the non-vision functions of vitamin A are mediated by retinoic acid, which acts at intracellular retinoic acid receptors. Retinoic acid is used medicinally as a topical treatment for acne. The other main metabolite, retinal, is used in vision.

As can be seen from the structure, retinol is derived from isoprene, and has an alcohol functional group.

During the absorption process in the intestines, retinol is incorporated into chylomicrons as the ester form, and it is these particles that mediate transport to the liver. Storage of vitamin A in liver cells (hepatocytes) is via the ester derivative, but when retinol is needed in other tissues, it is de-esterifed and released into the blood as the alcohol. Retinol then attaches to a serum carrier, retinol binding protein, for transport to target tissues. A binding protein inside cells, cellular retinoic acid binding protein, serves to store and move retinoic acid intracellularly.

Either deficiency or overdose of vitamin A can be harmful or fatal. Deficiency of vitamin A can cause night-blindness, and pale, dry skin. The body converts the dimerized form, carotene, into vitamin A as it is needed, therefore high levels of carotene are not toxic compared to the ester (animal) forms. The livers of certain animals, especially those adapted to polar environments, often contain amounts of vitamin A that would be toxic to humans. The first documented death due to vitamin A poisoning was Xavier Mertz, a Swiss scientist who died in January 1913 on an Antarctic expedition that had lost its food supplies and fell to eating its sled dogs. Mertz consumed lethal amounts of vitamin A by eating the dogs' livers. The liver of the polar bear also has enough vitamin A to kill a human being. Excess vitamin A has also been suspected to be a contributor to osteoporosis.

George Wald won the 1967 Nobel Prize in Physiology or Medicine for his work with retina pigments, including the role of vitamin A.

External links

• NIH Office of Dietary Supplements - Vitamin A (http://ods.od.nih.gov/factsheets/cc/vita.html)
• Vitamin A information (http://www.talkwellness.org/vitamina.html)
• Retinol binding protein (http://www.biochemj.org/bj/348/0481/bj3480481.htm)

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