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Retinol toxicity

II. Clinical Toxicology of Selected Retinoids A. Retinol Toxicity in Humans... [Pg.310]

These results show that retinyl esters in respiratory epithelium and in alveolar cells form a pool of vitamin A, which can be used physiologically by the tissue. The formation of retinol and at least RA from retinyl esters is strictly controlled. So far an unphysiological formation of RA and a subsequent toxicity seems not possible. Retinyl esters, however, are biochemically inert with respect to gene expression or vitamin A activity as long as they are not hydrolyzed. Consequently, the inhalative application, especially in cases of insufficient lung development, could represent a true alternative. The oral contribution is hardly successful because of the poor RBP s)mthesis of the liver and the lack of availability of a parenteral solution is currently not available. [Pg.191]

Sauer, J.-M. Sipes, I.G. (1995) Modulation of chemical-induced lung and liver toxicity by all-trans-retinol in the male Sprague-Dawley rat. Toxicology, 105, 237-249... [Pg.431]

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 Vitamin A [retinol] RDA/AI Men 900 pg/d Women 700 pg/d Physiological function Required for normal vision, gene expression, reproduction, embryonic development, and immune function Adverse Effects of Excessive Consumption Teratological effects liver toxicity... [Pg.612]

Retinoic acid (vitamin A acid), in which the alcohol group has been oxidized, shares some but not all of the actions of retinol. Retinoic acid is ineffective in restoring visual or reproductive function in certain species in which retinol is effective. Flowever, retinoic acid is very potent in promoting growth and controlling differentiation and maintenance of epithelial tissue in vitamin A-deficient animals. Indeed, all-trans-retinoic acid (tretinoin) appears to be the active form of vitamin A in all tissues except the retina, and is 10- to 100-fold more potent than retinol in various systems in vitro. Isomerization of this compound in the body yields 13-n.v-rctinoic acid (isotretinoin), which is nearly as potent as tretinoin in many of its actions on epithelial tissues but may be as much as fivefold less potent in producing the toxic symptoms of hypervitaminosis A. [Pg.617]

Synthetic 13-m-retinoic acid not only inhibited the incidence but also reduced the severity of bladder neoplasms induced by the intravesical administration of MNU of female Wister-Lewis rats [113]. In an experimental model with mice treated with TV-butyl-A -(4-hydroxybutyl)-nitrosamine (OH-BBN), retinoic acid (Re5), 13-cw-retinoic acid, and retinol acetate (Re2) show chemopreventive activity. In addition, a quite large number of synthetic -alkyl amide derivatives of Re2 have a greater activity to toxicity ratio than 13-cw-retinoic acid [113]. [Pg.110]

Neuropsychiatric changes were reported to be the earliest dose-limiting symptomatic toxicity in patients with cancer taking high doses of retinol (678). [Pg.699]

Preformed vitamin A is found only in animals and a small number of bacteria. A number of the carotenoid pigments in plants can be cleaved oxidatively to yield retinol /S-carotene is quantitatively the most important of these provitamin A carotenoids. Although preformed retinol is both acutely and chronically toxic in excess, carotene is not, because there is only a limited capacity to cleave it to retinol. [Pg.31]

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). [Pg.62]

As the intake of vitamin A increases, there is an increase in the excretion of metabolites in bile, once adequate liver reserves have been established. However, the biliary excretion of retinol metabolites reaches a plateau at relatively low levels, and it seems likely that this explains the relatively low toxic threshold (Olson, 1986). Vitamin A intoxication is associated with the appearance of both retinol and retinyl esters bound to albumin and in plasma lipoproteins, which can be taken up by tissues in an uncontrolled manner the amount of circulating retinol bound to RBP does not increase. Retinol has a membrane lytic action it was noted in Section 2.2.2.3 that one of the functions of RBP binding seems to be to protect tissues against retinol, as well as to protect retinol against oxidation (Meeks et al., 1981). [Pg.69]

The doses of retinol that are protective in animals are in the toxic range (Section 2.5.1) and are unlikely to be useful in cancer therapy or prevention. A number of synthetic retinoids have been developed, in a search for compounds that show anticancer activity, but are metabolized, stored, and transported differently, or bind to different subtypes of retinoid receptor and are less toxic. RXR-selective ligands are less toxic and more active in animal cancer models than RAR ligands (Lippman and Lotan, 2000). Fenretinamide, and possibly other retinoids that have antitumor activity, exerts at least part of its action by induction of apoptosis by a receptor-independent mechanism (Wu et al., 2001). [Pg.71]


See other pages where Retinol toxicity is mentioned: [Pg.287]    [Pg.313]    [Pg.287]    [Pg.313]    [Pg.72]    [Pg.92]    [Pg.293]    [Pg.87]    [Pg.144]    [Pg.145]    [Pg.254]    [Pg.257]    [Pg.1312]    [Pg.85]    [Pg.151]    [Pg.194]    [Pg.1312]    [Pg.417]    [Pg.841]    [Pg.383]    [Pg.140]    [Pg.278]    [Pg.71]    [Pg.763]    [Pg.40]    [Pg.43]    [Pg.46]    [Pg.64]    [Pg.68]    [Pg.40]    [Pg.43]    [Pg.46]    [Pg.64]    [Pg.68]   
See also in sourсe #XX -- [ Pg.289 , Pg.290 , Pg.291 , Pg.297 , Pg.298 , Pg.299 , Pg.310 , Pg.311 , Pg.312 ]




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