Characteristics of folic acid transport in the L1210 leukemia cell

1969 ◽  
Vol 193 (2) ◽  
pp. 456-467 ◽  
Author(s):  
Norman S. Lichtenstein ◽  
Vincent T. Oliverio ◽  
I.David Goldman
Keyword(s):  
Folic Acid ◽  
Leukemia Cell ◽  
L1210 Leukemia ◽  
Acid Transport

Folic acid transport by mammalian small intestine.

1978 ◽  
Vol 235 (6) ◽  
pp. E678 ◽  
Author(s):  
R C Rose ◽  
M J Koch ◽  
D L Nahrwold
Keyword(s):  
Folic Acid ◽  
Acid Concentration ◽  
Bathing Solution ◽  
Acid Transport ◽  
Additional Information ◽  
Carrier Mechanism ◽  
Sodium Gradient ◽  
Saturation Kinetics ◽  
Sodium Dependent ◽  
Free Media

The unidirectional influx of folic acid across the mucosal border of hamster duodenum and rat jejunum was determined. Influx follows saturation kinetics, is sodium-dependent, and is inhibited by methotrexate and is sodium-dependent, and is inhbited by methotrexate and folinic acid in the mucosal bathing solution. In hamster duodenum, the maximal influx is 1.2 nmol/(cm2.h), and the folic acid concentration required to give a half maximal influx (Km) is 7.2 micron.. At mucosal folic acid concentration of 1.5 micron, influx is reduced at least 65% by removal of sodium from the bathing solution. The influx process is significantly inhibited by cyanide and 2,4-dinitrophenol. The possibility was evaluated that the acidic microclimate at the brush border regulates the rate of folic acid transport and that inhibition of transmural transport by sodium-free media, ouabain, and methotrexate is brought about indirectly by an increase in pH of the microclimate. The data favor the alternative concept of a sodium-dependent carrier mechanism for entry of folic acid into the cells. The information presented is consistent with active transport of folic acid by a sodium-gradient mechanism, but additional information will be necessary to substantiate such a model.

scholarly journals Folate transport in intestinal brush border membrane: involvement of essential histidine residue(s)

1993 ◽  
Vol 290 (1) ◽  
pp. 237-240 ◽  
Author(s):  
H M Said ◽  
R Mohammadkhani
Keyword(s):  
Folic Acid ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Inhibitory Effect ◽  
Histidine Residue ◽  
Acid Transport ◽  
Intestinal Brush Border Membrane ◽  
Intestinal Brush Border ◽  
Rabbit Intestine

We examined the possible existence of histidine residue(s) in the folate transporter of rabbit intestine. This was done with use of the histidine-specific reagent diethyl pyrocarbonate (DEPC) and purified intestinal brush-border-membrane vesicles. DEPC caused significant concentration- and time-dependent inhibition of folic acid transport. The inhibition was only seen when transport was examined in vesicles incubated in buffer at pH 5.2 and not in those incubated in buffer at pH 7.4. The addition of unlabelled folic acid to vesicle suspension before treatment with DEPC (2.5 mM) led to a significant (P < 0.01) protection (84%) against the inhibition of folic acid transport. Treating vesicles pretreated with DEPC (2.5 mM) with reducing reagents (dithiothreitol, 2-mercaptoethanol and 2,3-dimercaptopropanol, all at a final concentration of 10 mM) did not reverse the inhibitory effect of DEPC on folic acid transport. On the other hand, treating the DEPC-pretreated vesicles with hydroxylamine (140 mM) led to a significant reversal (P < 0.01) (54%) of the inhibition of folic acid transport. The inhibitory effect of DEPC on carrier-mediated folic acid transport was found to be mediated through a decrease in the Vmax. (i.e. a decrease in the number and/or activity) of the carriers and an increase in the apparent Km (i.e. a decrease in their affinity), classifying the effect as a mixed-type inhibition. These results demonstrate the existence of critical histidine residue(s) in the intestinal brush-border-membrane folate transporter which is essential for its interaction with, and transport of, the vitamin. These findings also suggest that the histidine residue(s) is located at (or near) the substrate-binding site.

Synthesis of Trimethylamine-[14C]carboxyborane and Trimethylamine-[14C]carboxymethoxyborane and L1210 Leukemia Cell Uptake

1996 ◽  
Vol 10 (3-4) ◽  
pp. 279-282 ◽  
Author(s):  
S. Y. Chen ◽  
Bruce S. Burnham ◽  
Bernard F. Spielvogel ◽  
A. Sood ◽  
Steven D. Wyrick ◽  
...  
Keyword(s):  
Leukemia Cell ◽  
Cell Uptake ◽  
L1210 Leukemia

Effect of insulin on folic-acid transport in cultured fibroblasts

1982 ◽  
Vol 111 (2) ◽  
pp. 218-222 ◽  
Author(s):  
Y. Eilam ◽  
M. Ariel ◽  
N. Grossowicz
Keyword(s):  
Folic Acid ◽  
Acid Transport ◽  
Cultured Fibroblasts

scholarly journals Effect of Folate-deficient Diet and 5-Fluorouracil Treatment In the zn VlVO Model of Mice L1210 Leukemia

Pteridines ◽  
1994 ◽  
Vol 5 (3) ◽  
pp. 107-110
Author(s):  
Julita Graczyk
Keyword(s):  
Folic Acid ◽  
Thymidylate Synthase ◽  
Cytotoxic Effect ◽  
Leukocyte Count ◽  
L1210 Leukemia ◽  
Deficient Diet ◽  
Synthetic Diet ◽  
Antineoplastic Effect ◽  
Lower Blood ◽  
Serum Folic Acid

Summary The present study investigated the effect of reduced folic acid content in the organism, due to deficient diet, on the survival time of mice with L1210 leukemia, treated with fluorouracil. One of the mechanisms of the cytotoxic effect of fluorouracil is the inhibition of thymidylate synthase by binding fluorodeoxyuridylate, a 5-fluorouracil metabolite. Tetrahydrofoliane factor, for which folic acid is the substrate, takes part in this process. From the presented study it follows that the synthetic diet prepared without the addition of folic acid caused significantly lower blood serum folic acid levels, reduction of vitamin Bl2 level, anemia, as well as lowered leukocyte count. The antineoplastic effect of fluorouracil on L1210 leukemia was in that group of mice weaker than the effect of fluorouracil in mice receiving synthetic diet which met their folic acid requirement.

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