In vitro sugar uptake by grapefruit (Citrus paradisi) juice-sac cells

2005 ◽  
Vol 32 (4) ◽  
pp. 357 ◽  
Author(s):  
Moshe Huberman ◽  
Uri Zehavi ◽  
Wilfred D. Stein ◽  
Ed Etxeberria ◽  
Raphael Goren

To further our understanding of the mechanisms of sugar uptake and accumulation into grapefruit (Citrus paradisi Macf. cv. Marsh seedless), the patterns of uptake and utilisation of sucrose, glucose and fructose by Citrus juice cells was investigated. Analyses were conducted on sliced juice sacs that were incubated in radioactive [14C]-sugar solutions with unlabelled sugars, in the presence or absence of metabolic inhibitors. Both hexoses demonstrated an initial uptake peak in December and a second uptake peak in February–March. From March through April the rates of sucrose uptake increased to levels comparable to those of glucose and fructose. Sucrose and its moieties fructose and glucose entered the juice cells of Citrus juice fruit by an insaturable, and mostly by an independent, process. However, NaN3 and carbonylcyanide m-chlorophenylhydrazone (CCCP) produced slight inhibition of these processes. Cells took up hexoses at a greater rate than sucrose, with accumulation reaching a plateau by 4–8 h, and then continuing unabated, in the case of glucose, for 42 h. Uptake of all three sugars increased linearly in the range of sugar concentrations tested, which extended from 0.01 to 320 mm, denoting an insaturable system for sugar uptake. 14CO2 evolution was relatively low in all the experiments, the lowest evolution being recorded when the uptake of [14C]-sucrose was studied, while the highest 14CO2 evolution was recorded when the uptake of [14C]-glucose was studied. The data demonstrate a preferential utilisation of glucose over fructose and sucrose. In all the experiments, the two metabolic inhibitors significantly inhibited the decarboxylation of the three sugars.

1978 ◽  
Vol 235 (3) ◽  
pp. E272
Author(s):  
H M Middleton

The phosphorylation and dephosphorylation of absorbed vitamin was studied in rat jejunal everted sacs during in vitro uptake of [3H]pyridoxine.HCl. Kinetic studies during 4-min incubations demonstrated that phosphorylation was saturable (Km, 13.3 micron; Vmax, 0.906 nmol/4 min/g wet tissue) and was significantly inhibited by both structural and metabolic inhibitors. Longer incubations (30-min) demonstrated similar saturation and inhibition of net phosphorylation. Dephosphorylation of the phosphate esters formed by the phosphorylation step also occurred, as demonstrated by pulse-chase experiments. Disappearance of these phosphates was initially rapid, approximated first order kinetics, and apparently was mediated by a phosphatase. Whereas phosphorylation did not appear to affect initial uptake rates for [3H]pyridoxine.HCl by the jejunum, net phosphorylation after more prolonged incubations qualitatively paralleled accumulation of total absorbed vitamin in tissue over the same time. The primary effect of phosphorylation during jejunal uptake of pyridoxine by rat jejunum was to increase the accumulation of absorbed pyridoxine in tissue during prolonged incubations. Dephosphorylation had the net effect of limiting the magnitude of that accumulation.


2018 ◽  
Vol 238 ◽  
pp. 384-390 ◽  
Author(s):  
Witchulada Yungyuen ◽  
Gang Ma ◽  
Lancui Zhang ◽  
Misato Futamura ◽  
Makoto Tabuchi ◽  
...  

2015 ◽  
Vol 63 (32) ◽  
pp. 7230-7235 ◽  
Author(s):  
Gang Ma ◽  
Lancui Zhang ◽  
Kazuki Yamawaki ◽  
Masaki Yahata ◽  
Jae-Hoon Choi ◽  
...  

2011 ◽  
Vol 63 (2) ◽  
pp. 871-886 ◽  
Author(s):  
Lancui Zhang ◽  
Gang Ma ◽  
Masaya Kato ◽  
Kazuki Yamawaki ◽  
Toshihiko Takagi ◽  
...  

2017 ◽  
Vol 217 ◽  
pp. 1-7 ◽  
Author(s):  
Witchulada Yungyuen ◽  
Gang Ma ◽  
Lancui Zhang ◽  
Kazuki Yamawaki ◽  
Masaki Yahata ◽  
...  

1970 ◽  
Vol 65 (3) ◽  
pp. 517-524 ◽  
Author(s):  
Olav Unhjem

ABSTRACT The ability of various steroids and metabolic inhibitors to influence the binding of androgen to soluble macromolecules in the rat ventral prostate was evaluated in vitro. The results obtained revealed some structural requirements of steroids for binding to the macromolecules. An androstane skeleton with the α-configuration of the hydrogen atom at position 5 seemed to be essential for binding as well as a keto group at position 3. N-ethylmaleimide, Na-iodoacetate and p-hydroxymercuribenzoate inhibited the binding of androgen to macromolecules. The androgen-macromolecular complexes appeared to be rather stable at temperatures below 5°C.


1992 ◽  
Vol 3 (5) ◽  
pp. 535-544 ◽  
Author(s):  
B C Gliniak ◽  
L S Park ◽  
L R Rohrschneider

The murine myeloid precursor cell line FDC-P1/MAC simultaneously expresses receptors for multi-colony-stimulating factor (CSF), granulocyte-macrophage (GM)-CSF, and macrophage (M)-CSF. Growth of FDC-P1/MAC cells in either multi-CSF or GM-CSF results in the posttranscriptional suppression of M-CSF receptor (c-fms proto-oncogene) expression. We use the term transregulation to describe this control of receptor expression and have further characterized this regulatory process. The removal of FDC-P1/MAC cells from GM-CSF stimulation resulted in the re-expression of c-fms mRNA independent of M-CSF stimulation and new protein synthesis. Switching FDC-P1/MAC cells from growth in M-CSF to GM-CSF caused the selective degradation of c-fms mRNA within 6 h after factor switching. Blocking protein synthesis or gene transcription with metabolic inhibitors effectively prevented GM-CSF stimulated degradation of c-fms mRNA. These results suggest that the transregulation of c-fms transcripts by GM-CSF requires the transcriptional activation of a selective mRNA degradation factor. In vitro analysis, the use of cytoplasmic cell extracts, provided evidence that a ribonuclease is preferentially active in GM-CSF stimulated cells, although the specificity for mRNA degradation in vitro is broader than seen in vivo. Together, these data suggest that GM-CSF can dominantly transregulate the level of c-fms transcript through the transcriptional activation of a ribonuclease degradation system.


1976 ◽  
Vol 54 (6) ◽  
pp. 822-833 ◽  
Author(s):  
R. E. Garfield ◽  
E. E. Daniel

Smooth muscle cells of different densities to transmission of electrons (termed light and dark cells) were found in rat myometrium examined in the electron microscope following fixation by immersion in glutaraldehyde. Light cells accounted for about 4% of the total population of cells. No light cells were found in tissues fixed in situ by intraarterial perfusion with glutaraldehyde. In addition to staining differences, light cells were distinguished from most dark cells by differences in nuclear, mitochondrial, endoplasmic reticular, and surface structures. The relative number of light and dark cells after in vitro fixation was not changed in tissues relaxed with adrenaline or contracted with oxytocin. Mechanical injury resulted in increased numbers of light cells. Similarly, chemical injury with metabolic inhibitors resulted in ATP depletion, followed by increased numbers of light cells and gain in water content. We concluded that light cells were produced by mechanical or metabolic damage, leading to loss of volume control mechanisms, swelling, and leakage of protein. Light cells found after fixation in vitro in numerous prior studies represent cells damaged during isolation, and not a physiological variant among smooth muscle cells.


1986 ◽  
Vol 123 (1) ◽  
pp. 325-344 ◽  
Author(s):  
KA HOU CHU

1. The midgut of Callinectes sapidus is capable of net transmural glucose absorption. 2. The mucosal glucose influx by the midgut has a sodium-dependent, saturable component and a sodium-independent, non-saturable counterpart. 3. The unidirectional mucosal to serosal flux and the mucosal influx of glucose are depressed by metabolic inhibitors, the presence of mucosal phlorizin or serosal ouabain. 4. The low rate of net transmural glucose flux and the kinetic characteristics of mucosal influx suggest that the midgut does not play an important role in total nutrient absorption. 5. Thin layer chromatographic analysis shows that most of the glucose appears as phosphorylated forms upon entering the midgut, suggesting that the efflux of free glucose across the serosal border requires an active mechanism.


2003 ◽  
Vol 285 (5) ◽  
pp. H2218-H2224 ◽  
Author(s):  
R. Nijmeijer ◽  
M. Willemsen ◽  
C. J. L. M. Meijer ◽  
C. A. Visser ◽  
R. H. Verheijen ◽  
...  

Type II secretory phospholipase A2 (sPLA2) is a cardiovascular risk factor. We recently found depositions of sPLA2 in the necrotic center of infarcted human myocardium and normally appearing cardiomyocytes adjacent to the border zone. The consequences of binding of sPLA2 to ischemic cardiomyocytes are not known. To explore a potential effect of sPLA2 on ischemic cardiomyocytes at a cellular level we used an in vitro model. The cardiomyocyte cell line H9c2 or adult cardiomyocytes were isolated from rabbits that were incubated with sPLA2 in the presence of metabolic inhibitors to mimic ischemia-reperfusion conditions. Cell viability was established with the use of annexin V and propidium iodide or 7-aminoactinomycin D. Metabolic inhibition induced an increase of the number of flip-flopped cells, including a population that did not stain with propidium iodide and that was caspase-3 negative. sPLA2 bound to the flip-flopped cells, including those negative for caspase-3. sPLA2 binding induced cell death in these latter cells. In addition, sPLA2 potentiated the binding of C-reactive protein (CRP) to these cells. We conclude that by binding to flip-flopped cardiomyocytes, including those that are caspase-3 negative and presumably reversibly injured, sPLA2 may induce cell death and tag these cells with CRP.


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