Vitamin A and Keratinization

Logan, William

doi:10.1001/archderm.1972.01620080072021

Cited by 58 publications

(9 citation statements)

References 62 publications

(11 reference statements)

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“…Table 2 shows the epithelial response in normal and stressed hamster cheek pouch mucosa in this study. Epithelial changes prodticed by excess of vitamin A on rodent epi- dermi.s Include hyperplasia, differentiation, keratinization and mucous metaplasia (Fell 1956, Lawrence et al 1960, Rothberg 1967, Logan 1972, Chopra & Flaxman 1975, Wong 1975. Table 2 emphasizes the hyperplastic epithelium and anomalous keratinization patterns seen in the animals treated with vitamin A. Epithelial hyperplasia is often a non-specific response to trauma in the hamster cheek pouch and occurs even on exposure of the cheek poueh mucosa to the external environment (Butcher & Johnson 1959).…”

Section: Discussionmentioning

confidence: 99%

Changes in vitamin A conditioned hamster cheek pouch epithelium on exposure to commercial shell lime (calcium hydroxide) and tobacco I — Optical histopathology

Kandarkar

Sirsat

1977

J Oral Pathology Medicine

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Epidcmiologically a high incidence of oral cancer and addiction to tobacco, singly or in combination with other ingredients of the betel quid, arc closely correlated. Attempts at the induction of malignancy in laboratory animals on exposure to these ingredients have hitherto failed. Studies are reported on check pouch epithelium of 152 Syrian golden hanLstcrs exposed to commercial shell lime (calcium hydroxide) and tobacco, singly and in combination, with parallel conditioning by Vitamin A palmilatc. The abnormal changes found especially iu lime and limc-plus-tobacco treated epithelia arc massive hypcrplasia, keratinization anomalies, maikcd edema and dysplasia. The most significant findings are (I) greater epithelial alteration caused by lime, lime plus vitamin A, tobacco plus vitamin A, lime plus tobacco and lime plus tobacco and vitamin A, than by tobacco alone;(2) increasing epithelial dysplasia in response to longer periods of exposure to the test substatices; and (3) enhancement of tissue changes in the presence of vitamin A.

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Section: Discussionmentioning

confidence: 99%

Changes in vitamin A conditioned hamster cheek pouch epithelium on exposure to commercial shell lime (calcium hydroxide) and tobacco I — Optical histopathology

Kandarkar

Sirsat

1977

J Oral Pathology Medicine

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“…Vitamin A is also needed for normal skeletal development and reproduction (2). That the vitamin is necessary for normal differentiation of epithelial tissues is also well established (3)(4)(5), although the mechanism(s) by which cytodifferentiation is regulated remain obscure. There is, however, increasing evidence that protein synthesis and RNA metabolism are affected in deficient animals.…”

mentioning

confidence: 99%

In Vitro Binding of Retinol to Rat-Tissue Components

Bashor

Toft

Chytil

1973

Proc. Natl. Acad. Sci. U.S.A.

183

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The high-speed supernatant fraction of rat liver, lung, kidney, testis, and intestinal mucosa contains a component capable of binding [ 3 H]retinol in vitro when binding is analyzed by sucrose density gradient centrifugation or gel filtration. This binding component can be distinguished from one identified in rat serum. Whereas the tissue component sediments in the 2S region of sucrose gradients, the serum component sediments in the 4.6S region. Molecular weight estimations by gel filtration indicate molecular weights of 16,000 and 67,000 for the tissue and serum binding components, respectively. Unlabeled retinol, but not retinoic acid, competes for the binding of [ 3 H]retinol in tissue cytosols. Competition for the binding of [ 3 H]retinol by unlabeled retinal has also been observed in tissue cytosols, but may result from the in vitro reduction of retinal to retinol. Unlabeled retinol, retinal, and retinoic acid fail to compete for the binding of [ 3 H]retinol in serum under the conditions used. The tissue binding component (testis) is sensitive to digestion with Pronase, but not with RNase or DNase, indicating a protein nature for this component.

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“…The physiologic and pharmacologic ef fects of vitamin A and its derivatives on the epidermis are still incompletely understood because of both sharp species variability [8] and differences between in vivo and in vitro data [14]. Although topical RA increases the uptake of tritiated thymidine in human epidermis and pilosebaceous follicles [16], others have noted decreases numbers of mitotic figures after oral administration of vitamin A [17], suggesting that nonspecific irritancy may explain the increased labeling index from topical RA.…”

Section: Pathophysiology O F Retinoid Action On Epidermismentioning

confidence: 99%

“…Conversely, vitamin A deficiency leads to squamous metaplasia, but in all of these models the initial effects are focal and reversible, selectively altering the differenti ation of germinative layers of epithelia [reviewed in 7]. Although mucous metapla sia, i.e., a shift in differentiation away from normal cornification toward a mucoussecretory epithelium, is common in em bryonic and neoplastic tissues [8], it is de batable whether this process occurs in postembryonic mammalian skin [7][8][9][10]. Thus, the dramatic clinical impact of vit amin A and its synthetic analogues (reti noids) on postembryonic skin must be ascribed to other mechanisms, to be dis cussed below.…”

Section: Introductionmentioning

confidence: 99%

Retinoid Effects on the Epidermis

Elias

1987

Dermatology

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Since metaplasia and gap junction stimulation are prominent features of retinoid activity in embryonic and neoplastic epidermis, it is ironic that the mechnism(s) of retinoid action in postnatal tissues, where these drugs are employed clinically, appears to be different. Histologic studies in both animals and man with both topical and systemic retinoids demonstrate acanthosis, hypergranulosis, and changes in the thickness and organization of the stratum corneum, due to a boost in cell turnover. On an ultrastructural level, desmosomes are actively shed at the level of the spinous layer, leading to many new attachment points along the cell membranes of the outer epidermis. This change coupled with decreased tonofilaments, enhanced keratinocyte autolysis, and intercellular deposition of glycoconjugates (not mucin by standard histochemistry and lectin binding) lead to loosening and fragility of the stratum corneum. The biochemical basis of retinoid activity (in addition to increased cell turnover) appears to be global enhancement of glycoconjugate synthesis and the generation of less mature keratins. These epidermal effects of retinoids can be exploited therapeutically: (1) to cause loosening of thickened stratum corneum, e.g., in psoriasis or ichthyosis; (2) to enhance penetration of pharmacologic agents, e.g., 5-FU, across hyper-trophic actinic keratoses; and finally (3) in neoplastic epidermis, where mucous metaplasia and gap junction proliferation occur, retinoids can normalize differentiation.

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Vitamin A and Keratinization

Cited by 58 publications

References 62 publications

Changes in vitamin A conditioned hamster cheek pouch epithelium on exposure to commercial shell lime (calcium hydroxide) and tobacco I — Optical histopathology

Changes in vitamin A conditioned hamster cheek pouch epithelium on exposure to commercial shell lime (calcium hydroxide) and tobacco I — Optical histopathology

In Vitro Binding of Retinol to Rat-Tissue Components

Retinoid Effects on the Epidermis

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