Retinol vitamin retinoic acid

Retinoids Vitamin A Carotinoids Retinylesters Retinol Retinal Retinoic acid Vitamin A acid... 

Vitamin A (retinol) and retinoic acid are carotenoid oxidation compounds that are very important for human health. The main functions of retinoids relate to vision and cellular differentiation. With the exception of retinoids, it was only about 10 years ago that other carotenoid oxidation products were first thought to possibly exert biological effects in humans and were implicated in the prevention - or promotion of degenerative diseases. A review on this subject was recently published. ... 

Van Gelder We deprive them enough. The old studies used global vitamin A depletion, which depleted retinals, retinols and retinoic acid. Survival may be a retinoic acid versus a retinal issue. The point is, how do you explain the complete loss of SCN photoresponse in Kbp (vitamin A-depleted) Cry 1 Cry2 triple mutants ... 

Vitamin A Retinol Retinal Retinoic acid p-Carotene Retinol Retinal Retinoic acid FAT-SOLUBLE Maintenance of reproduction Vision Promotion of growth Differentiation and maintenance of epithelial tissues Gene expression... 

Vitamin A (retinol, retinal, retinoic acid—the three active forms of vitamin A, and p-carotene) function in the maintenance of reproduction, vision, promotion of growth, differen tiation and maintenance of epithelial tissues, and gene expression. A deficiency of vitamin A results in impotence, night blindness, retardation of growth, and xerophthalmia. Large amounts of vitamin A are toxic and can result in an increased incidence of frac tures. 

Much recent interest has been aroused by the fact that retinoid compounds, including both retinol and retinoic acid, reduce the incidence of experimentally induced cancer. In addition, 13-czs-retinoic acid taken orally is remarkably effective in treatment of severe cystic acne. s However, both vitamin A and retinoic acid in large doses are teratogenic, i.e., they cause fetal abnormalities. The use of 13-cis-retinoic acid during early phases of pregnancy led to a high incidence of major malformations in infants born.1 11 1... 

Vitamin A-deficient experimental animals fail to grow adults are blind and sterile, with testicular degeneration in males and keratinization of the uterine epithelium in females. Although deficient female animals wUl conceive, and the fetuses will implant, formation of the placenta is impaired and the fetuses are resorbed. Epithelia in general are hyperplastic and keratinized, and there is impaired cellular immunity with increased susceptibility to infection. Both retinol and retinoic acid are required for gestation in the rat in deficient animals, retinoic acid alone will not prevent fetal resorption after about day 10 of gestation (WeUik and DeLuca, 1995 WeUik et al., 1997). 

In adults, excessive alcohol consumption reduces liver reserves of vitamin A, both as a result of alcoholic liver damage and also by induction of cytochrome P450 enzymes that catalyze the oxidation of retinol to retinoic acid (as also occurs with chronic use of barbiturates). However, chronic consumption of alcohol can also potentiate the toxicity of retinol (Section 2.5.1). 

Dickson IR, Walls J, and Webb S (1989) Vitamin A and bone formation. Different responses to retinol and retinoic acid of chick bone cells in organ culture. Biochimica et BiophysicaActa 1013,254-8. 

Retinol induces the expression of retinoic acid-binding protein (RABP) and regulates cell migration in the skin epithelium, which is vital for skin regeneration after a peel. Encapsulating retinol provides better bioavailability of the vitamin and protects the skin against oxidation. Ker-atinocytes have the enzyme tools required to convert retinol into retinoic acid (the corresponding carboxylic acid), which is the molecule ultimately responsible for the effect of vitamin A. 

Oxidation of retinol produces retinoic acid tretinoin). The reaction is irreversible. Retinoic acid enters the portal blood, is transported bound to albumin, and is not stored to any great extent. The concentration of retinoic acid in plasma is normally 3-4 ng/mL. A biologically active metabolite, 5,6-epoxyretinoic acid, has been isolated from the intestinal mucosa of vitamin A-deficient rats following administration of H-retinoic acid. Several tissues have specific cellular retinoic acid-binding proteins (CRABPs). 

Vitamin A - also called all-tra/75 -retinol, is an isoprenoid alcohol that plays a key role in vision and a role in controlling animal growth. Vitamin A must either be present in the diet, or derived from / -carotene, an isoprenoid compound prominent in carrots. See Figure 19.25 for the biosynthesis of dX -trans-xQtmo. Dehydrogenation of retinol yields the aldehyde, retinal, which has a role in vision. Another derivative of retinol is retinoic acid, which can be made by the oxidation of retinal. 

The interaction between alcohol and vitamin A is complex. They have overlapping metabolic pathways a similar 2-step process is involved in the metabolism of both alcohol and vitamin A, with alcohol dehydrogenases and acetaldehyde dehydrogenases being implicated in the conversion of vitamin A to retinoic acid. Alcohol appears to act as a competitive inhibitor of vitamin A oxidation. In addition, chronic alcohol intake can induce cytochrome P450 isoenzymes that appear to increase the breakdown of vitamin A (retinol and retinoic acid) into more polar metabolites in the liver, which can cause hepatocyte death. So chronic alcohol consumption may enhance the intrinsic hepatotoxicity of high-dose vitamin A. Alcohol has also been shown to alter retinoid homoeostasis by increasing vitamin A mobilisation from the liver to extrahepatic tissues, which could result in depletion of hepatic stores of vitamin A. ... 

Within cells, vitamin A (retinol, retinal, retinoic acid) functions mainly in vision, cellular differentiation, and embryogenesis. The adverse effects of vitamin A deficiency on complex physiological processes such as reproduction and the immvme response result primarily from defective cellular differentiation. 

A proposed hypothesis for vitamin A action should suggest experiments that will address not only the question of how vitamin A affects differentiation at the cellular level but also how the tissue specificity of this action might arise. In order to simplify our approach we have relied on two assumptions. First, because vitamin A affects ceUular differentiation, we believe it should interact in some way with the nucleus, which is the site of genomic information. Second, we have assumed that both retinol and retinoic acid are active forms of vitamin A, with separable functions in differentiation. 

Two groups of compounds, shown in Figure 11.2, have vitamin A activity retinol, retinaldehyde and retinoic acid (preformed vitamin A) and a variety of carotenes and related compounds (collectively known as carotenoids), which can be cleaved oxidatively to yield retinaldehyde, and hence retinol and retinoic acid. Those carotenoids that can be cleaved to yield retinaldehyde are known as are known as pro-vitamin A carotenoids. 

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