VITAMIN A DEFICIENCY AND ISOPRENOID METABOLISM

1961 ◽  
Vol 39 (5) ◽  
pp. 855-861 ◽  
Author(s):  
W. E. J. Phillips
Keyword(s):  
Vitamin A ◽  
Guinea Pig ◽  
Vitamin A Deficiency ◽  
Metabolic Defect ◽  
Isoprenoid Metabolism ◽  
Metabolic Block ◽  
Liver Homogenates

Vitamin A deficiency in the intact rat evokes an increase in liver ubiquinone and the incorporation of mevalonate into ubiquinone and squalene. This aberration is caused by a metabolic block between squalene and cholesterol. The addition of vitamin A in vitro to vitamin A deficient liver homogenates does not influence the metabolic defect. The vitamin A deficient guinea pig does not exhibit an increase in liver ubiquinone or incorporation of mevalonate into ubiquinone or squalene, but the incorporation into sterols is enhanced.

scholarly journals Cellular basis of urothelial squamous metaplasia

2005 ◽  
Vol 171 (5) ◽  
pp. 835-844 ◽  
Author(s):  
Feng-Xia Liang ◽  
Maarten C. Bosland ◽  
Hongying Huang ◽  
Rok Romih ◽  
Solange Baptiste ◽  
...  
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Squamous Metaplasia ◽  
Culture Conditions ◽  
Growth Potential ◽  
Basal Cells ◽  
Cellular Basis ◽  
Proximal Urethra

Although the epithelial lining of much of the mammalian urinary tract is known simply as the urothelium, this epithelium can be divided into at least three lineages of renal pelvis/ureter, bladder/trigone, and proximal urethra based on their embryonic origin, uroplakin content, keratin expression pattern, in vitro growth potential, and propensity to keratinize during vitamin A deficiency. Moreover, these cells remain phenotypically distinct even after they have been serially passaged under identical culture conditions, thus ruling out local mesenchymal influence as the sole cause of their in vivo differences. During vitamin A deficiency, mouse urothelium form multiple keratinized foci in proximal urethra probably originating from scattered K14-positive basal cells, and the keratinized epithelium expands horizontally to replace the surrounding normal urothelium. These data suggest that the urothelium consists of multiple cell lineages, that trigone urothelium is closely related to the urothelium covering the rest of the bladder, and that lineage heterogeneity coupled with cell migration/replacement form the cellular basis for urothelial squamous metaplasia.

Vitamin A Status and Hepatic Drug Metabolism in the Rat

1973 ◽  
Vol 51 (1) ◽  
pp. 6-11 ◽  
Author(s):  
G. C. Becking
Keyword(s):  
Vitamin A ◽  
Drug Metabolism ◽  
Vitamin A Deficiency ◽  
Hepatic Drug Metabolism ◽  
Deficient Diet ◽  
Hepatic Drug ◽  
Vitamin A Status ◽  
Cytochrome P 450 ◽  
Liver Vitamin

The effect of vitamin A status on hepatic drug metabolism was studied in rats. Animals were fed diets with and without vitamin A for 20 and 25 days. Weight gains of control and deficient animals were not significantly different, whereas liver vitamin A levels had decreased to less than 10% of control animals after 20 days and were essentially zero after eating the deficient diet for 25 days. Aniline metabolism in vitro and aminopyrine metabolism in vitro and in vivo were significantly lower in male weanling rats fed a vitamin A deficient diet for 20 days. No alteration in in vitro p-nitrobenzoic acid metabolism was noted after 25 days on the test. Vitamin A deficiency did not alter microsomal protein levels or cytochrome c reductase activity but deficient animals did have a lower microsomal cytochrome P-450 content. Hepatic enzyme activities and cytochrome P-450 levels were restored to values approaching those found in control animals by feeding vitamin A deficient rats the vitamin A containing diet for 21 days. Liver vitamin A levels were markedly increased after re-feeding studies but were still significantly lower than control animals.

In vivo and in vitro Study of the Effects of Vitamin A Deficiency on Rat Third Molar Development

1986 ◽  
Vol 65 (12) ◽  
pp. 1445-1448 ◽  
Author(s):  
S.S. Harris ◽  
J.M. Navia
Keyword(s):  
Vitamin A ◽  
Organ Culture ◽  
Culture System ◽  
Vitamin A Deficiency ◽  
Third Molar ◽  
In Vitro Study ◽  
Organ Culture System ◽  
Vitamin A Status

We have examined the effect of in vivo vitamin A status on subsequent rat third molar formation and mineralization in an in vitro organ culture system. Vitamin A deficiency imposed during an eight-day in vitro period caused effects very similar to those of vitamin A deficiency imposed on rats in vivo. Analysis of the data also demonstrates that retinoic acid is capable of reversing the interference in mineralization of third molars induced by vitamin A deficiency in the organ culture system.

SOME BIOCHEMICAL EFFECTS OF SPORIDESMIN

1965 ◽  
Vol 43 (7) ◽  
pp. 881-888 ◽  
Author(s):  
D. E. Wright ◽  
I. T. Forrester
Keyword(s):  
Guinea Pig ◽  
Succinate Oxidation ◽  
Biochemical Effects ◽  
Sheep Liver ◽  
Liver Homogenates ◽  
Nicotinamide Coenzymes

Sporidesmin inhibits in vitro the respiration of guinea pig and sheep liver homogenates in the presence of substrates which require nicotinamide coenzymes for their oxidation. Succinate oxidation was far less sensitive. Similar results were found with mitochondria.Slight swelling and release of 260 mμ absorbing compounds from mitochondria incubated in the presence of sporidesmin were observed. These results are discussed in relation to those reported elsewhere.

INTERRELATIONSHIP OF VITAMINS A AND C ON TISSUE UBIQUINONES AND STEROLS OF RATS AND GUINEA PIGS

1967 ◽  
Vol 45 (6) ◽  
pp. 749-756 ◽  
Author(s):  
W. E. J. Phillips
Keyword(s):  
Ascorbic Acid ◽  
Vitamin A ◽  
Vitamin C ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Vitamin A Deficiency ◽  
Secondary Effect ◽  
Vitamin C Deficiency ◽  
Vitamins A And C ◽  
Combined Deficiency

The effect of administration of ascorbic acid to normal or vitamin A-deficient rats was studied in relation to hepatic levels of ubiquinones and sterols. Similar studies were made on tissues from guinea pigs deficient in vitamin C, vitamin A, or both. Vitamin A deficiency increased the concentration of liver ubiquinones in the rat. Administration of ascorbate did not influence tissue levels of ubiquinones or sterols. Vitamin C deficiency increased the concentration of sterols but not of ubiquinones in the liver of the guinea pig. Vitamin A deficiency did not increase ubiquinones nor did a combined deficiency of vitamins A and C. A secondary effect of vitamin C deficiency in the vitamin A-deficient rat is not the cause of increased ubiquinone levels.

Effect of vitamin a deficiency on guinea pig peyer's patches

1987 ◽  
Vol 7 (5) ◽  
pp. 539-545 ◽  
Author(s):  
M.S.I. Majumder ◽  
A.K.M. Abdus Sattar ◽  
Md. Mohiduzzaman
Keyword(s):  
Vitamin A ◽  
Guinea Pig ◽  
Vitamin A Deficiency ◽  
Peyer's Patches ◽  
Peyer’S Patches

The Effects of Vitamin A and Citral on Epithelial Differentiation in vitro 1. The Chick Tracheal Epithelium

Development ◽  
1963 ◽  
Vol 11 (1) ◽  
pp. 279-291
Author(s):  
Margaret B. Aydelotte
Keyword(s):  
Vitamin A ◽  
Vitamin A Deficiency ◽  
Epithelial Differentiation ◽  
Tracheal Epithelium ◽  
Careful Study ◽  
Histological Changes ◽  
Mucous Membranes ◽  
High Concentrations

In many animals the tracheal epithelium is one of the first tissues to respond to deficiency of vitamin A. Mori (1922a, b) in a careful study of the histological changes in vitamin A deficient rats, showed that the secretion of mucus from the tracheal epithelium and many other mucous membranes and glands was reduced, and that the secretory epithelia were gradually replaced by thicker, drier, keratinized membranes. Similar changes have been demonstrated in many other vitamin A deficient animals, including chickens (Beach, 1923; Seifried, 1930; Jungherr, 1943). Though vitamin A deficiency appears to have relatively little effect on skin and other epithelia that are normally keratinized, these epithelia change with high concentrations of vitamin A. When the vitamin was applied locally to the skin of rats (Sabella, Bern & Kahn, 1951) or administered orally in very large doses (Studer & Frey, 1949), the skin failed to keratinize normally, while the immature, non-keratinized cells proliferated rapidly and formed a thick epithelium.

scholarly journals Vitamin A and the biosynthesis of sulphated mucopolysaccharides. Experiments with rats and cultured neoplastic mast cells

1969 ◽  
Vol 111 (4) ◽  
pp. 407-412 ◽  
Author(s):  
D. B. Thomas ◽  
C A Pasternak
Keyword(s):  
Growth Rate ◽  
Mast Cells ◽  
Vitamin A ◽  
Uronic Acid ◽  
Vitamin A Deficiency ◽  
Horse Serum ◽  
Vitamin A Status ◽  
Uronic Acid Content

1. The uptake and incorporation of [35S]sulphate into mucopolysaccharides by colon and duodenum in vitro are unaffected by the vitamin A status of the animals. 2. Uptake and incorporation in vivo are unaffected at 4hr. after injection of [35S]sulphate, but at later times are decreased in some tissues of vitamin A-deficient animals. 3. The rate of removal of 35S from blood, its rate of appearance in urine, the plasma concentration of sulphate and the uronic acid content of several tissues are not significantly altered in vitamin A deficiency. 4. These results, and direct measurement of 35S in mucopolysaccharides at various times after injection of [35S]sulphate, suggest that the synthesis of mucopolysaccharides is unaffected but that their turnover is increased in vitamin A deficiency. 5. Neither the growth rate of, nor the incorporation of [35S]sulphate into heparin by, P815Y and HC cultured neoplastic mast cells is decreased when the horse serum necessary for growth is treated with ultraviolet light or is replaced by serum from vitamin A-deficient rats. 6. The addition of citral is no more toxic to growth rate or to incorporation of 35S than is the addition of vitamin A itself. 7. It is concluded that neoplastic mast cells in culture do not require vitamin A for growth or for the synthesis of heparin. 8. None of these results is compatible with the view that vitamin A or a derivative is directly involved in the biosynthesis of sulphated mucopolysaccharides.

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