Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02003 (NBT)
 1,323 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the presence of vitamin A, NBT II cells, derived from a carcinoma of rat bladder, grew as a monolayer with diminished piling up. Keratinization, which normally appeared within stratified cells in postconfluent cultures, was inhibited. A "wounding" technique suitable for quantitative analysis of cell migration was developed for confluent cultures grown on glass coverslips. Vitamin A treatment enhanced the migration of cells from the wound edge. In dense postconfluent monolayer cultures, vitamin A treatment maintained a higher percentage of cells in DNA synthesis than in the control cultures, as determined by 3H-TdR uptake and autoradiography. In contrast, in sparse cultures vitamin A did not stimulate DNA synthesis or increase the mitotic index. This stimulatory effect, limited to dense cultures, may be attributable to vitamin A causing viable cells to be shed into the medium, thereby maintaining the monolayer just at confluence. Thus vitamin A inhibits squamous cell differentiation, enhances migration, and maintains the culture in the proliferative phase. In a different system of high cell density, NBT II aggregates cultured in a combined matrix of chick plasma clot and collagen-coated sponge, vitamin A also enhanced the migration of cells. These results may explain, in part, the failure of vitamin A to inhibit completely the growth of some established tumors.
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PMID:The effect of vitamin A on the migration and DNA synthesis of rat bladder tumor cell line NBT II in culture. 44 81

A 74 year-old woman, who had been diagnosed as AML (M3) in poor condition, was treated with Retinol Palmitate (Chocola-A, 150,000 unit/m2 per os, after informed consent. An increase of white blood cells (neutrophil) counts was observed after 7 days. After 4 weeks, WBC counts were increased to 20,700/microliters (neutrophil counts 6,400/microliters) Maturation tendency of leukemic cells was also proved in the bone marrow. In vitro studies showed that morphological differentiation was recognizable in cultured leukemic cells treated with 10(-6)M all-trans retinoic acid after 6 days, but not in controls. Responses in the NBT reduction test were slightly less than in the clinical study. The administration of Retinol Palmitate may be a new regimen to treat AML (M3) in aged patients in poor condition.
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PMID:[Differentiating effect of oral administration of retinol palmitate (Chocola-A) for an aged AML (M3) with severe complications]. 146 82

The experiment was carried out on 50 slaughter cocks, aged 5 weeks. The purpose of the experiment was to estimate the effect of beta-carotene and apo-beta-carotenoic acid (10% Carophyll yellow) on some indices of cellular immunity in chicks receiving the feed of high vitamin A content. Chl and NBT proved that carotenoids increased phagocytic activity of neutrophiles in peripheral blood. Similarly, in the case of beta-carotene it was found by blastic transformation test that on 30-40th day of the experiment, the value IS of peripheral blood lymphocytes was increased. On the other hand, chicks fed apo-beta-carotenoic acid showed such an effect on 40th day of observation only in the case when the lowest dose of preparation (24 mg/kg of feed) and Con A as mitogen were applied. In each experimental group, the chicks exhibited increased flavin content in liver and markedly increased retinol content due to apo-beta-carotenoic acid (24 mg/kg of feed). On the other hand, the contents of alpha tocopherol and ascorbic acid did not show significant differences between experimental and control groups. Similar were the results with iron, zinc and magnesium. Copper content of the liver was markedly increased in the birds receiving apo-beta-carotenoic acid in the dose of 24 mg/kg of feed. The increased content of manganese was observed in the liver of birds receiving beta carotene (6 mg/kg of feed).
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PMID:[Effect of carotenoids on selected indicators of cellular immunity in cockerels receiving food with high level of vitamin A]. 213 44

The terminal differentiation, keratinization, of a rat bladder tumor cell line, NBT II, occurred in multicellular aggregates. After aggregation, these cells did not undergo a round of mitosis before keratinization. 5-Bromodeoxyuridine added to the monolayer cell culture 2 days before aggregation completely prevented this differentiation; it was ineffective when added at the time of cell aggregation. Vitamin A prevented the keratinization of NBT II cells in aggregates but did not inhibit aggregate formation; it enhanced the number of cells engaged in DNA synthesis. This model appears to be very useful for analyzing the mechanisms of terminal differentiation and its modulation by vitamin A in tumor cells.
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PMID:Keratinization and the effect of vitamin A in aggregates of a squamous carcinoma cell line NBT II. 615 20

Several studies have suggested that vitamin A (retinol, ROH) presents pro-oxidant properties in biological systems. Recent studies point out that xantine oxidase, a ROS-generating enzyme, catalyses ROH oxidation to RA in vitro. These works stimulated the authors to investigate whether xanthine oxidase could be involved on the ROH pro-oxidative effects reported in cultured Sertoli cells. In vitro, it was demonstrate that xanthine oxidase generates superoxide in the presence of ROH as assessed by superoxide mediated-NBT reduction. Superoxide production is potentiated in the presence of NADH and inhibited by allopurinol. In Sertoli cells, ROH treatment increased xanthine oxidase activity and inhibition of the enzyme with allopurinol attenuated ROH-induced ROS production, protein damage and cytotoxicity. Moreover, inhibition of ROH oxidation to RA by retinaldehyde dehydrogenase inhibitor potentiated both xanthine oxidase-dependent ROS production and cell damage in ROH-treated cells. The data show that xanthine oxidase may play a role on vitamin A pro-oxidant effects.
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PMID:Xanthine oxidase-dependent ROS production mediates vitamin A pro-oxidant effects in cultured Sertoli cells. 1856 17