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Retinol vitamin night blindness

A deficiency of vitamin A leads to vision defects, including a visual impairment at low light levels, termed night blindness. For the processes of vision, retinol needs to be converted first by oxidation into the aldehyde retinal, and then by enzymic isomerization to cw-retinal. c -Retinal is then bound to the protein opsin in the retina via an imine linkage (see Section 7.7.1) to give the red visual pigment rhodopsin. [Pg.40]

Since alcohol dehydrogenase is required for the conversion of retinol to retinal, excessive and prolonged ethanol ingestion can impair the physiological function of vitamin A. The decreased conversion of retinol to retinal results from competitive use of the enzyme by ethanol. Night blindness may result, since the visual cycle is a retinol-dependent physiological process. [Pg.782]

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. [Pg.501]

Vitamin A Precursor to rhodopsin, a chemical used for vision assists in inhibiting bacterial and viral infections Night blindness (retinol)... [Pg.463]

A strikingly early symptom of vitamin A deficiency is night blindness. A variety of other symptoms include dry skin and hair, conjunctivitis of the eyes, retardation of growth, and low resistance to infection. The skin symptoms are particularly noticeable in the internal respiratory passages and alimentary canal lining. About 0.7 mg/day of vitamin A is required by an adult. The content of vitamin A in foods is often expressed in terms of international units 1.0 mg of retinol equals 33331.U. [Pg.1241]

Figure S2.4 shows the structures of 11 -c/.v-retinal and its more stable isomer all-frans-retinal. The reti-nals are related to the alcohol retinol, or vitamin A,. Mammals cannot synthesize these compounds de novo but can form them from dietary carotenoids such as /3-carotene. A deficiency of vitamin A causes night blindness, along with serious deterioration of the eyes and other tissues. Figure S2.4 shows the structures of 11 -c/.v-retinal and its more stable isomer all-frans-retinal. The reti-nals are related to the alcohol retinol, or vitamin A,. Mammals cannot synthesize these compounds de novo but can form them from dietary carotenoids such as /3-carotene. A deficiency of vitamin A causes night blindness, along with serious deterioration of the eyes and other tissues.
A typical RA-receptor is the receptor fiar vitamin A (all-mtws retinol). Vitamin A is essential for pre-and postnatal development. Congenital vitamin A deficiencies are accompanied by a broad spectrum of malformations. In adult life, vitamin A is indispensable for growth, maintenance, and survival of many tissues. It is necessary for vision and reproduction. A lack of vitamin A in the adult causes night blindness and photoreceptor degeneration. But the devel-... [Pg.202]

Vitamin A (retinol) Prevents xerophthalmia, night blindness, growth retardation, bone abnormalities Visual pigments, morphogen... [Pg.19]

Hepatic depletion of vitamin A stores is caused by chronic ethanol consumption (Bonjour, 1981). Night blindness suffered by alcoholics has been attributed to a low intake of vitamin A (McClain et aL, 1979). However, Sato and Lieber (1982) have demonstrated that ethanol depletes hepatic vitamin A stores in baboons and rats even when it is administered in combination with a nutritionally adequate diet. In addition, animals consuming ethanol in marginal diets were depleted more rapidly of vitamin A. No effect of ethanol intake on retinol binding protein or on serum vitamin A levels could be detected in these studies. Leo and Lieber (1982) found that hepatic vitamin A was depleted to one-fifth of normal levels in alcoholics with only moderate liver disease. Sato and Lieber (1982) observed that retinoic acid was more rapidly metabolized by the MFO system after chronic ethanol intake, and they postulated that vitamin A depletion was the result of MFO enzyme induction. [Pg.141]

McClain, C. J., Van Thiel, D. H., Parker, S., Badzin, L. K., and Gilbert, H., 1979, Alteration in zinc, vitamin A and retinol-binding protein in chronic alcoholics A possible mechanism for night blindness and hypogonadism. Alcoholisms Clin. Exp. Res. 3 135. [Pg.149]

Night blindness can usually be cured in a half hour or so by the injection of vitamin A. It is noteworthy that both retinol and retinaldehyde are effective in the visual process, but retinoic acid has no visual function if retinoic acid is the only form of vitamin A fed to experimental animals, blindness results. [Pg.1078]

Christian P, Schulze K, Stoltzfus RJ, West KP Jr (1998) Hyporetinolemia, illness symptoms, and acute phase protein response in pregnant women with and without night blindness. Amer J Clin Nutr 67 1237-1243 Rosales FJ, Ross AC (1998) A low molar ratio of retinol binding protein to transthyretin indicates vitamin A deficiency during inflammation studies in rats and a posteriori analysis of vitamin A-supplemented children with measles. 7 Vwtr 128 1681-1687... [Pg.105]


See other pages where Retinol vitamin night blindness is mentioned: [Pg.483]    [Pg.382]    [Pg.230]    [Pg.763]    [Pg.470]    [Pg.315]    [Pg.296]    [Pg.341]    [Pg.730]    [Pg.424]    [Pg.1112]    [Pg.219]    [Pg.118]    [Pg.862]    [Pg.31]    [Pg.3]    [Pg.300]    [Pg.338]    [Pg.352]    [Pg.353]    [Pg.162]    [Pg.153]    [Pg.1078]    [Pg.34]    [Pg.73]    [Pg.98]    [Pg.570]    [Pg.365]    [Pg.430]    [Pg.443]    [Pg.220]   
See also in sourсe #XX -- [ Pg.268 ]

See also in sourсe #XX -- [ Pg.268 ]




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