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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carbohydrate metabolism by four rat hepatoma cell lines in culture, namely, Reuber H35, MH1C1, RLC, and HTC, has been investigated. Glucose utilization by H35 and MH1C1 cells is lower than that by RLC and HTC cells. The four cell lines also differ with respect to the accumulation of lactic acid in the growth medium; in particular, H35 cells show uptake of lactic acid, rather than accumulation in the medium. Specific activities of a number of enzymes involved in glycolysis, gluconeogenesis, pentose phosphate pathway, and glycogen formation were determined in the four cell lines. A direct relationship between the differences was found for the activities of some enzymes belonging to carbohydrate metabolism, namely, hexokinase, pyruvate kinase, aldolases A and B, glucose-6-phosphate dehydrogenase, and phosphogluconate dehydrogenase and the differences found for glucose utilization by the different cell lines.
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PMID:Comparative studies of glucose metabolism in HTC, RLC, MH1C1, and Reuber H35 rat hepatoma cells. 42 45

The effect of methyl mercury and two selenium compounds have been studied in cell cultures. Methyl mercury in concentrations above 1 microM had a pronounced inhibiting effect on the growth of rat Morris hepatoma cells. Glucose and lactate uptake in relation to cell protein was appreciably stimulated by the organic mercury compound. Selenite in low concentration (0.5 microM) and seleno-di-N-acetyl glycine in thousandfold higher concentrations offered considerable protection against these effects of methyl mercury. The same selenite concentration (0.5 microM), which did not affect cell growth, caused an appreciable protection against methyl mercury (6 microM), even if it was added 3 days after methyl mercury. The methyl mercury inhibited the growth of human embryonic fibroblasts and the DNA-synthesis in the human lymphocytes. However, no protective effect of selenite were observed in these cell types. These results suggest that selenium compounds exert their protective effect through cell specific processes rather than by a direct chemical reaction between selenite and methyl mercury.
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PMID:The influence of selinium on methyl mercury toxicity in rat hepatoma cells, human embryonic fibroblasts and human lymphocytes in culture. 53 35

Two independent dedifferentiated variants, H5 and FaoflC2, derived from the Reuber H35 hepatoma, produce trans-acting diffusible substances(s) that extinguish the expression of liver-specific proteins when hybridized with a well-differentiated cell line of the same origin (Fao and Fu5-5, respectively). H5 x Fao hybrids show total and stable extinction of four liver functions and clonal variability in the expression of three others. FaoflC2 x Fu5-5 hybrids are initially flat (like FaoflC2 cells), and die in glucose-free medium where survival requires expression of hepatic gluconeogenic enzymes, but then evolve to hepatoma-like and finally round morphology; these latter cells express all liver functions analyzed including the gluconeogenic enzymes. Two exceptional clones that remained flat long enough for complete analysis showed extinction of all hepatic functions not expressed by FaoflC2 cells. We conclude that this transitory extinction reflects the action and then loss of extinguishing factor(s) contributed by FaoflC2. When crossed with BW1-J mouse hepatoma cells. FaoflC2 causes stable extinction of mouse aldolase B. We propose that production of extinguishing factor(s) is the rule for dedifferentiated variants.
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PMID:Dedifferentiated variants of a rat hepatoma: analysis by cell hybridization. 54 20

The metabolic fate of [U-14C]glucose has been examined in detail in adult rat hepatocytes in primary monolayer culture, as well as in two permanent cell lines--Buffalo rat liver (BRL) and transplantable rat hepatoma (HTC) cells-derived from normal rat liver and from rat hepatoma, respectively. Under defined conditions of incubation, at a glucose concentration of 5.5 mM, the three types of cultured liver cells exhibited pronounced differences in glucose metabolism. Primary cultures, like the intact liver, differed from the cell lines in consuming relatively small amounts of glucose and converting approximately 50% of the total metabolized glucose to lactate. By contrast, the permantent cell lines consumed glucose at a 40-fold greater rate than did primary cultures, converting 80--90% of the carbohydrate to lactate. Oxidative metabolism of glucose carbon also differed among the three types of liver culture. Of the total [U-14C]glucose consumed, primary cultures converted approximately 30% to labeled CO2 per hour, whereas the liver cell lines converted 5--10%. Finally, glucose metabolism in primary culture exhibited adaptation as hepatocytes aged in culture, shifting progressively toward the pattern exhibited by the permanent cell lines. This change occurred over a time course similar to that for other kinds of functional change in hepatocytes in primary culture and thus may be relevant to the general problem of phenotypic alteration in liver cell culture.
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PMID:Glucose metabolism by adult hepatocytes in primary culture and by cell lines from rat liver. 62 33

Cytochalasin B inhibits glucose transport in human erythrocytes by competing with glucose for the carrier on the inner surface of the cell membrane, but there is no cytochalasin site associated with the outware-facing form of the carrier. Such asymmetry may be demonstrated by zero trans exit and entry experiments, whereas Sen-Widdas exit experiments are not easily interpretable. The orientation of the transport system appears to be reversed in certain other cell types: chich embryo fibroblasts, Novikoff hepatoma cells and HeLa cells. Here the cytochalasin site is present in the external but not internal carrier form.
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PMID:Cytochalasin B and the kinetics of inhibition of biological transport: a case of asymmetric binding to the glucose carrier. 66 49

Detailed time courses of uptake of labeled 3-O-methyl-D-glucose and 2-deoxy-D-glycose by untreated and ATP-depleted Novikoff rat hepatoma cells were determined as function of concentration (0.2-10 mM) by a rapid mixing/sampling technique which allows uptake measurements in time intervals as short as 1.5 seconds. Intracellular accumulation of 3-O-methylglucose in untreated and ATP-depleted cells and of deoxyglucose in ATP-depleted cells to equilibrium followed pseudo-first order kinetics and initial velocities were computed from overall time courses of substrate accumulation. Initial velocity was a Michaelis-Menten function of exogenous substrate concentration. The estimated kinetic constants for zero-trans transport of 3-O-methylglucose were about the same for untreated and ATP-depleted cells (Kztm = 1.73 +/- 0.24 mM; Vztmax = 28.8 +/- 3.6 pmoles/microliter cell H2O. sec) and were similar to those for deoxyglucose transport in ATP-depleted cells (Kztm = 0.65 +/- 0.1 mM; Vztmax = 19.6 +/- 1.6 pmoles/microliter cell H2O. sec). Similar kinetic parameters were obtained for the transport of D-glucose and D-galactose in ATP-depleted cells. The transport of 3-O-methylglucose and deoxyglucose were inhibited by each other in a simple competitive manner with apparent Ki's similar to their transport Km's. In untreated cells, in which deoxyglucose was phosphorylated, intracellular steady-state levels of free deoxyglucose accumulated within 10 to 20 seconds of incubation regardless of its concentration in the medium. Thereafter, the rate of deoxyglucose incorporation into total cell material reflected the rate of phosphorylation rather than the transport rate. The rate of deoxyglucose transport exceeded the initial rate of its phosphorylation by 20-40 %. The intracellular steady-state-levels observed during the first 2 minutes of incubation decreased from about 40% of equilibrium level at 0.2 mM deoxyglucose to about 8% at 10 mM. Computer fits of a kinetic equation describing transport and phosphorylation as independent processes operating in tandem to these data are consistent with the observed kinetic constants for hexose transport and hexokinase activity with deoxyglucose as substrate. Upon longer incubation (2-10 minutes) the rate of deoxyglucose uptake by the phosphorylating cells decreased progressively, concomitant with a decrease in intracellular ATP and an increase in intracellular deoxyglucose to equilibrium levels. It is demonstrated that the rate of deoxyglucose uptake, measured at two or more minutes, seriously underestimates the hexose transport rate and yields misleading conclusions regarding the extent and type of inhibition by transport inhibitors, such as persantin or cytochalasin B. Persantin inhibited hexose transport in a simple non-competitive manner (Ki = 20 muM) indicating that the drug affects the function of the hexose carrier.
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PMID:Deoxyglucose and 3-O-methylglucose transport in untreated and ATP-depleted Novikoff rat hepatoma cells. Analysis by a rapid kinetic technique, relationship to phosphorylation and effects of inhibitors. 67 Mar 3

A series of variant lines that utilize multiple pentoses for growth in place of glucose have been isolated from an 8-azaguanine resistant line of Novikoff hepatoma cells (N1S167). These variants utilize for growth ribose, xylose, arabinose, and/or deoxyribose. The variants growing on pentose containing medium (a) exhibit a density dependent cessation of growth, (b) have a morphology change to a more flattened cell type, (c) become binucleated in the presence of cyto chalasin B, and (d) show an altered sensitivity to trypsin treatment.
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PMID:Pentose utilizing variants of Novikoff hepatoma cells: modification of growth and morphological properties. 85 67

The nonmediated permeation of L-glucose, cytosine, and prednisolone into Novikoff rat hepatoma cells followed first order kinetics with rate constants of 0.00404, 0.173, and 2.4 min-1, respectively. The constants were estimated from a nonlinear least squares fit of the integrated first order rate equation. The rate constants were independent of substrate concentration and correlated with the partition coefficients of the substances in octanol-balanced salt solution (0.00158, 0.0352, and 17.8, respectively) and olive oil-balanced salt solution mixtures which were between 10- and 100-fold lower. Arrhenius plots for the permeation of L-glucose, cytosine, and prednisolone were linear and indicated activation energies of 24.2, 28.0, and 19.6 kcal/mol, respectively. The permeation of L-glucose and cytosine, but not of prednisolone, was impeded in a concentration-dependent manner by the presence of cytochalasin B and Persantin, heretofore thought of as specific inhibitors of facilitated diffusion processes. The relative degree of decrease of the permeation rates of L-glucose and cytosine, however, differed for cytochalasin B and Persantin.
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PMID:Effect of temperature and of cytochalasin B and persantin on the nonmediated permeation of non-electrolytes into cultured Novikoff rat hepatoma cells. 86 21

In human brain tumors of neuro-ectodermal and meningo-vascular series, using the method of enzymoelectrophoresis and specific tetrazole blue staining, three isoforms of hexokinase were revealed, these differ from each other by their activity and electrophoretic mobility in agar gel. Three isoforms of hexokinase were also found in benign and malignant uterine tumors in females, in 22 A mice hepatoma and homologous intact tissues. Morever, in muscles and muscle tumors (MOP, CRM-1) of rats and of these animals embryos two isoforms of hexokinase were found. The increased rate of hexose phosphorylation in malignant uterine tumors of female patients and in blastomas of mice liver and rat muscles is associated with the increased activity of I and II isoforms of hexokinase. An analogous phenomenon is observed in muscles of rat embryos. On the other hand, the decreased activity of phosphotransferases in blastomas of human brain depends on a decrease in the activity of separate isoforms of hexokinase.
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PMID:[Isoforms of human and animal tumor hexokinase]. 93 28

Incubation of cultured Novikoff rat hepatoma and mouse L cells in a glucose-free basal medium containing 5 mM KCN and 5 mM iodoacetate for about 10 minutes resulted in a complete depletion of the cells of ATP. ATP-depleted wild type cells or thymidine kinase-deficient sublines of Novikoff or L cells took up thymidine rapidly from the medium without concentrating it intracellularly, and exhibited countertransport of thymidine. Thus uptake was by facilitated diffusion. This transport system differs from the substrate-specific, low-Km (0.5 muM] thymidine transport system previously described for various types of cultured cells in that it exhibits an at least 100-fold higher Km and transports equally well various ribo- and deoxyribonucleosides. The results suggest that the rate-limiting step in thymidine incorporation into the nucleotide pool by wild type cells is phosphorylation rather than transport, or that the cells possess two transport systems, a facilitated diffusion system with low substrate specificity and a second system which involves substrate phosphorylation by thymidine kinase.
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PMID:Transport and countertransport of thymidine in ATP depleted and thymidine kinase-deficient Novikoff rat hepatoma and mouse L cells: evidence of a high Km facilitated diffusion system with wide nucleoside specificity. 95 73


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