6‐Deoxy‐D‐glucose and D‐xylose: Analogs for the study of D‐glucose transport by mouse 3T3 cells

Romano, Antonio H.; Connell, Nancy

doi:10.1002/jcp.1041110112

Cited by 15 publications

(9 citation statements)

References 27 publications

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“…Indeed, as shown in Figure 6, the addition of 2-deoxyglucose to galactose-fed, NOtreated, cells led to a dose-dependent protection of the cultured cells without altering the glycolytic utilization of galactose ( Table 1). Preincubation of the cells with 6-deoxyglucose, a compound that enters the cells but is not phosphorylated [42], never exerted protective effects against RNOS, a finding showing that the protective effect depends on the conversion of 2-deoxyglucose into 2-deoxyglucose 6-phosphate. To further examine the mechanisms accounting for the protection by 2-deoxyglucose, we measured (i) "%CO # production from 2-deoxy[1-"%C]glucose and (ii) intracellular GSH levels, which are linked directly to NADPH recycling.…”

Section: % Inhibition Of Cytotoxicitymentioning

confidence: 90%

The in vitro manipulation of carbohydrate metabolism: a new strategy for deciphering the cellular defence mechanisms against nitric oxide attack

et al. 1999

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This study was aimed at examining the effects of manipulating the carbohydrate source of the culture medium on the cellular sensitivity of epithelial cells to an oxidative attack. Our rationale was that substituting galactose for glucose in culture media would remove the protection afforded by glucose utilization in two major metabolic pathways, i.e. anaerobic glycolysis and\or the pentose phosphate pathway (PPP), which builds up cellular reducing power. Indeed, we show that the polarized human colonic epithelial cell line HT29-Cl.16E was sensitive to the deleterious effects of the NO donor PAPANONOate [3-(2-hydroxy-2-nitroso-1-propylhydrazino)-1-propanamine] only in galactose-containing medium. In such medium NO attack led to cytotoxic and apoptotic cell death, associated with formation of derivatives of NO auto-oxidation (collectively termed NOx) and peroxynitrite, leading to intracellular GSH depletion and nitrotyrosine formation. The addition of 2-deoxyglucose, a non-

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Section: % Inhibition Of Cytotoxicitymentioning

confidence: 90%

The in vitro manipulation of carbohydrate metabolism: a new strategy for deciphering the cellular defence mechanisms against nitric oxide attack

et al. 1999

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“…Thus, the results suggest that 2-DOG and 3-OMG may be taken up into the cell by different carrier systems. Differences in uptake observed using 2-DOG and 3-OMG have led to the suggestion that there may be different carriers for these sugars in chick embryo fibroblasts (Christopher et al, 1976a;Kletzein and Perdue, 1974), rat adipocytes (Olefsky, 1978;Foley et al, 1980), and mouse 3T3 cells (Colby and Romano, 1975;Romano and Connell, 1982).…”

Section: Discussionmentioning

confidence: 99%

Hexose transport in L6 rat myoblasts. I. Rate‐limiting step, kinetic properties, and evidence for two systems

D’Amore

1986

Journal Cellular Physiology

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The hexose transport system of undifferentiated L6 rat myoblasts was investigated. 2-Deoxy-D-glucose (2-DOG) and 2-deoxy-2-fluoro-D-glucose (2FG) were used as analogues to investigate the rate-limiting step of hexose uptake into the cell. Virtually all of the 2-DOG or 2FG taken up into the cell was found to be in the phosphorylated form. No significant pool of intracellular free sugar could be detected. This demonstrates that hexose transport, not phosphorylation, is the rate-limiting step. The inhibitory effect of various glucose analogues on 2-DOG and 3-O-methyl-D-glucose (3-OMG) uptake revealed that these two sugars may be taken up into the cell by different carriers. In addition, kinetics analysis of the transport of both sugars also indicates that two hexose transport systems may be present in L6 cells. 2-DOG is transported by high and low affinity transport systems (Km 0.6 mM and 2.9 mM, respectively), whereas 3-OMG is transported by a low affinity system (Km 3.5 mM). Treatment of cells with ionophores or energy uncouplers results in inactivation of the high affinity system, but not the low affinity system.

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“…2C). The initial uptake rate of D-glucose was somewhat higher, probably because of the higher affinity of glucose for the carrier (Romano and Connell, 1982b); again, 6-deoxy-Dglucose reached a steady state level after 5 min, whereas D-glucose uptake continued as a result of intracellular phosphorylation. When the concentration of D-glucose was reduced to one eighth its normal level (0.7 mM), and 6-deoxy-D-glucose was present in sevenfold excess, glucose uptake was reduced to approximately 2070 of the total sugar uptake (Fig.…”

Section: Resultsmentioning

confidence: 96%

Effect of glucose uptake on growth rate of mouse 3T3 cells

Romano

Connell

1982

Journal Cellular Physiology

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The objective of this investigation was to determine whether the rate of glucose uptake by mouse 3T3 cells was a primary determinant of growth rate. The experimental approach was to control the rate of glucose uptake into intracellular pools by supplying this sugar at varying concentration in minimal Eagle's medium with dialyzed serum in the absence and presence of 6-deoxy-D-glucose, a metabolically inert homomorphic analog of D-glucose that competitively inhibits the uptake of D-glucose. Total hexose (D-glucose and 6-deoxy-D-glucose) concentration was maintained at the physiological concentration of 5.5 mM, in order to maintain saturation and maximum activity of the D-glucose transport system; thus the flux of D-glucose into the cell was controlled by adjusting its concentration relative to its competing nonmetabolizable analog. It was found that even when the concentration of D-glucose was reduced to 0.7 mM, one eighth of the "normal" level of 5.5 mM, and 6-deoxy-D-glucose was present in sevenfold excess (4.8 mM), conditions under which glucose uptake was reduced to 20% of that shown by cells in the presence of 5.5 mM D-glucose, and intracellular pools of glucose and phosphorylated sugars derived from glucose were reduced to approximately 14% of normal, there was not a significant decrease in growth rate. These data support the view that the rate of glucose uptake is not a primary determinant of growth rate under the usual conditions of cell culture.

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6‐Deoxy‐D‐glucose and D‐xylose: Analogs for the study of D‐glucose transport by mouse 3T3 cells

Cited by 15 publications

References 27 publications

The in vitro manipulation of carbohydrate metabolism: a new strategy for deciphering the cellular defence mechanisms against nitric oxide attack

The in vitro manipulation of carbohydrate metabolism: a new strategy for deciphering the cellular defence mechanisms against nitric oxide attack

Hexose transport in L6 rat myoblasts. I. Rate‐limiting step, kinetic properties, and evidence for two systems

Effect of glucose uptake on growth rate of mouse 3T3 cells

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