Commentary
See article on page 825Alcohol and retinoid metabolism
| The first 150 words of the full text of this article appear below. |
The complex interactions between the metabolism of retinoids
and ethanol have been reported for a long time. Clinically, chronic ethanol consumption leads to vitamin A deficiency but also to enhanced
toxicity of vitamin A and beta-carotene when supplemented. Changes in
retinol metabolism due to alcohol may have a pathophysiological impact
in both alcoholic liver disease and alcohol associated cancer as
retinoic acid, the most active form of vitamin A, is an important
regulator of normal epithelial cell growth, function, and
differentiation. Under normal conditions, ingested retinol is
metabolised to retinaldehyde via cytosolic alcohol dehydrogenase (ADH),
microsomal retinol dehydrogenase (three types), and several types of
cytosolic retinol dehydrogenases, and retinaldehyde is further oxidised
to retinoic acid via aldehyde dehydrogenase (ALDH). Retinoic acid binds
to retinoic acid receptors (RAR), initiating intracellular signal
transduction leading to a cascade of events and finally to a decrease
in cell regeneration. The main molecular action of
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