scholarly journals Corticosteroids and ascorbic acid transport in adrenal cortex in vitro

1964 ◽  
Vol 92 (3) ◽  
pp. 564-573 ◽  
Author(s):  
SK Sharma ◽  
RM Johnstone ◽  
JH Quastel
Keyword(s):  
Ascorbic Acid ◽  
Adrenal Cortex ◽  
Acid Transport ◽  
Ascorbic Acid Transport

Ascorbic acid transport in mammalian kidney

1986 ◽  
Vol 250 (4) ◽  
pp. F627-F632 ◽  
Author(s):  
R. C. Rose
Keyword(s):  
Ascorbic Acid ◽  
Brush Border Membrane ◽  
Renal Tissue ◽  
Metabolic Inhibitors ◽  
Bathing Solution ◽  
Acid Transport ◽  
Low Concentrations ◽  
Sodium Dependent ◽  
Ascorbic Acid Transport

Ascorbic acid is known to circulate free in the plasma of several species and is therefore filtered in the kidney; reabsorption subsequently takes place and prevents urinary loss. However, no specific mechanism of renal ascorbic acid transport has previously been presented. In the present study, rat and guinea pig kidney were incubated as slices or as isolated tubules in vitro in the presence of low concentrations of [14C]ascorbic acid. The kidneys of both species handle ascorbic acid similarly. Ascorbic acid accumulates in the renal tissue to a concentration three to four times that present in the bathing media. Recently absorbed ascorbic acid diffuses freely from the kidney and is predominantly nonmetabolized during absorption. Uptake is reduced following replacement of bathing solution sodium by lithium or cesium, or when incubation is performed in the presence of metabolic inhibitors or at low temperatures. The results indicate that ascorbic acid is reabsorbed in the kidney by a sodium-dependent active transport mechanism that operates by concentrating ascorbic acid in the cellular fluid. Renal slices and tubules both appear to transport ascorbic acid and galactose across the brush-border membrane; this indicates that the tubular lumens in these preparations are not collapsed or sealed off.

Requirement for Na(+)-dependent ascorbic acid transport in osteoblast function

1995 ◽  
Vol 268 (6) ◽  
pp. C1430-C1439 ◽  
Author(s):  
R. T. Franceschi ◽  
J. X. Wilson ◽  
S. J. Dixon
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Disulfonic Acid ◽  
Acid Transport ◽  
Transport Activity ◽  
Intracellular Accumulation ◽  
Extracellular Medium ◽  
Isoascorbic Acid ◽  
Transport Inhibitors ◽  
Ascorbic Acid Transport

Ascorbic acid is necessary for expression of the osteoblast phenotype. We examined whether Na(+)-dependent transport is required for MC3T3-E1 preosteoblast cells to respond to vitamin C and investigated the role of membrane transport in the intracellular accumulation and function of ascorbate. MC3T3-E1 cells were found to possess a saturable, stereoselective, Na(+)-dependent ascorbic acid transport activity that is sensitive to the transport inhibitors sulfinpyrazone, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, and phloretin. Transport activity showed no competition with glucose or 2-deoxyglucose and was not inhibited by cytochalasin B, indicating that it is distinct from known hexose transporters. On addition of 100 microM ascorbic acid to the extracellular medium, intracellular concentrations of 10 mM were reached within 5-10 h and remained constant for up to 24 h. A good correlation was observed between intracellular ascorbic acid concentration and rate of hydroxyproline synthesis. Although ascorbic acid was transported preferentially compared with D-isoascorbic acid, both isomers had equivalent activity in stimulating hydroxyproline formation once they entered cells. Marked stereoselectivity for extracellular L-ascorbic acid relative to D-isoascorbic acid was also seen when alkaline phosphatase and total hydroxyproline were measured after 6 days in culture. Moreover, ascorbic acid transport inhibitors that prevented intracellular accumulation of vitamin blocked the synthesis of hydroxyproline. Thus Na(+)-dependent ascorbic acid transport is required for MC3T3-E1 cells to achieve the millimolar intracellular vitamin C concentrations necessary for maximal prolyl hydroxylase activity and expression of the osteoblast phenotype.

“IN VIVO” AND “IN VITRO” EFFECT OF ASCORBIC ACID AND ACTH ON THE RAT ADRENAL CORTEX

1952 ◽  
Vol 30 (3) ◽  
pp. 157-162
Author(s):  
A. DesMarais ◽  
J. Leblanc
Keyword(s):  
Ascorbic Acid ◽  
Adrenal Cortex ◽  
Adrenal Glands ◽  
Secretory Activity ◽  
In Vitro Experiments ◽  
Hypophysectomized Rats ◽  
Vitro Effect ◽  
Histochemical Examination

Histochemical examination of adrenal glands of hypophysectomized rats given both ascorbic acid and ACTH showed an enlargement of the cortex and a decrease of sudanophilic substances, as compared to adrenals of hypophysectomized rats receiving ACTH alone. “In vitro” experiments on incubated slices of adrenal glands have shown that ascorbic acid and ACTH have a synergistic effect on the secretory activity of the cells of the adrenal cortex.

STUDIES ON THE TIME COURSE OF THE RESPONSE OF THE ADRENAL CORTEX TO HISTAMINE AND COLD

1959 ◽  
Vol 37 (3) ◽  
pp. 399-404 ◽  
Author(s):  
E. Schönbaum ◽  
W. G. Bruce Casselman ◽  
Rosemary E. Large
Keyword(s):  
Ascorbic Acid ◽  
Adrenal Cortex ◽  
Time Course ◽  
Adrenal Glands ◽  
Transient Elevation

Rats were injected with histamine or exposed to cold. In either case there was a transient elevation in the output of corticosteroids by the excised adrenal glands in vitro but a prolonged fall in adrenal ascorbic acid. The return of steroid formation to pre-exposure or even lower rates within three hours was not accompanied by any further change of the concentration of adrenal ascorbic acid.

ACTIVE TRANSPORT OF ASCORBIC ACID IN ADRENAL CORTEX AND BRAIN CORTEX IN VITRO AND THE EFFECTS OF ACTH AND STEROIDS

1963 ◽  
Vol 41 (1) ◽  
pp. 597-604 ◽  
Author(s):  
Shail K. Sharma ◽  
R. M. Johnstone ◽  
J. H. Quastel
Keyword(s):  
Ascorbic Acid ◽  
Adrenal Cortex ◽  
Active Transport ◽  
Brain Cortex ◽  
Acid Uptake ◽  
Dependent Process ◽  
Brain Cortex Slices ◽  
Cortex Slices ◽  
Energy Dependent

Uptake of ascorbic acid-1-C14in brain cortex and adrenal cortex slices is an energy-dependent process. Concentration ratios (i.e. ratios of tissue ascorbic acid-1-C14to medium ascorbic acid-1-C14) greater than 4 have been obtained with both tissues in vitro. Ouabain as well as 2, 4-dinitrophenol suppresses ascorbic acid uptake into brain cortex slices.ACTH inhibits the uptake of ascorbic acid-1-C14in adrenal cortex, but not in brain cortex slices. The presence of glucose is necessary for the inhibition. Several cortical steroids, as well as adenosine-3′,5′-monophosphate, at small concentrations inhibit the uptake. The results are consistent with the interpretation that ACTH inhibits the uptake of ascorbic acid in the adrenal cortex through the steroids produced in its presence.

scholarly journals Endocrine Regulation of Ascorbic Acid Transport and Secretion in Luteal Cells1

1996 ◽  
Vol 54 (2) ◽  
pp. 399-406 ◽  
Author(s):  
Biljana Musicki ◽  
Pinar H. Kodaman ◽  
Raymond F. Aten ◽  
Harold R. Behrman
Keyword(s):  
Ascorbic Acid ◽  
Endocrine Regulation ◽  
Acid Transport ◽  
Ascorbic Acid Transport

Ascorbic Acid Transport by Isolated Bovine Adrenal Cortical Cells*

Endocrinology ◽  
1980 ◽  
Vol 106 (3) ◽  
pp. 811-817 ◽  
Author(s):  
FRANCES M. FINN ◽  
PHILLIP A. JOHNS
Keyword(s):  
Ascorbic Acid ◽  
Acid Transport ◽  
Cortical Cells ◽  
Adrenal Cortical Cells ◽  
Ascorbic Acid Transport
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