Na+-dependent, potential-sensitive l-ascorbate transport across brush border membrane vesicles from kidney cortex

Toggenburger, Gerhard; Häsermann, Max; Mütsch, B; Genoni, Giulio; Kessler, Markus; Weber, F.; Hornig, D.; O'Neill, Brigitte; Semenza, Giorgio

doi:10.1016/0005-2736(81)90312-6

Cited by 51 publications

(8 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In bovine adrenal chromaffin cells (Diliberto, et al, 1983) and pars intermedia cells , AA uptake was inhibited by phloridzin but not by glucose. On the other hand, in small intestine brush border (Siliprandi et al, 1979) and kidney cortex brush border (Toggenburger et al, 1981), AA uptake was not depressed by phloridzin, but was inhibited by glucose. In bovine pituitary neurosecretosomes, AA uptake was inhibited by both phloridzin and glucose.…”

Section: Discussionmentioning

confidence: 82%

Transport of ascorbic acid and dehydroascorbic acid by pancreatic islet cells from neonatal rats

Zhou

Nielsen

Farver

et al. 1991

Biochemical Journal

View full text Add to dashboard Cite

Several amidated biologically active peptides such as pancreastatin, thyrotropin-releasing hormone, pancreatic polypeptide and amylin are produced in endocrine pancreatic tissue which contains the enzyme necessary for their final processing, i.e. peptidylglycine alpha-amidating mono-oxygenase (EC 1.14.17.3). The enzyme needs ascorbic acid for activity as well as copper and molecular oxygen. The present work shows that pancreatic islet cells prepared from overnight cultures of isolated islets from 5-7-day-old rats accumulate 14C-labelled ascorbic acid by a Na(+)-dependent active transport mechanism which involves a saturable process (estimated Km 17.6 microM). Transport was inhibited by ouabain, phloridzin, cytochalasin B, amiloride and probenecid. Glucose inhibited or stimulated uptake, depending on the length of incubation time of the cells. The uptake of dehydroascorbic acid was linearly dependent on concentration. Dehydroascorbic acid was converted to ascorbic acid by an unknown mechanism after uptake. The uptake of both ascorbic acid and dehydroascorbic acid was inhibited by tri-iodothyronine, and uptake of ascorbic acid, but not of dehydroascorbic acid, was inhibited by glucocorticoids. Isolated secretory granules contained a fairly low concentration of iron but a high concentration of copper.

show abstract

Section: Discussionmentioning

confidence: 82%

Transport of ascorbic acid and dehydroascorbic acid by pancreatic islet cells from neonatal rats

Zhou

Nielsen

Farver

et al. 1991

Biochemical Journal

View full text Add to dashboard Cite

show abstract

“…The strong transinhibition of influx rates by Na + is a most prominent and reproducible feature in other Na+-coupled transport systems also (for L-ascorbate; Toggenburger et al, 1981;for L-leucine;F6rster, 1979) and may well be present in all Na+-coupled transport systems. Johnstone (1978) has likewise observed an intrinsic kinetic asymmetry of the Na +, glycine cotransporter in Ehrlich cells.…”

Section: The Asymmetry : a "Channel" (Or "Pore")mentioning

confidence: 97%

The small-intestinal Na+,d-glucose cotransporter: An asymmetric gated channel (or pore) responsive to ΔΨ

1983

Self Cite

View full text Add to dashboard Cite

At delta psi approximately equal to 0, D-glucose influx into, and efflux out of, membrane vesicles from small-intestinal brush borders are affected by trans Na+ and trans D-glucose to different extents. D-glucose influx and efflux respond to delta psi (negative at the trans side) to different extents. The small-intestinal Na+, D-glucose cotransporter is thus functionally asymmetric. This is not unexpected, in view of the structural asymmetry previously found. The characteristics of the delta psi-dependence of transinhibition by D-glucose are compatible with the mobile part of the cotransporter bearing a negative charge of at least 1 (in the substrate-free form). They are not compatible with its mobile part being electrically neutral. Pertinent equations are given in the Appendix. Partial Cleland's kinetic analysis and other criteria rule out (Iso) Ping Pong mechanisms and makes likely a Preferred Ordered mechanism, with Na+out binding to the cotransporter prior to the sugarout. A likely model is proposed aimed at providing a mechanism of flux coupling and active accumulation.

show abstract

“…Vitamin C is an antioxidant molecule that plays a pivotal role in the defense against reactive oxygen species (ROS)-induced cell damage by reducing DNA oxidation, protein damage, and lipid peroxidation (Levine et al, 1999;Saitoh et al, 2013). Vitamin C is mainly absorbed in the duodenum and proximal jejunum (Mellors et al, 1977;Siliprandi et al, 1979), and its homeostasis is maintained by active reabsorption in the renal tubules (Toggenburger et al, 1981;Martin et al, 1983). In aqueous solution, vitamin C is found both as a reduced (ascorbic acid, AA) and an oxidized (dehydroascorbic acid, DHA) form.…”

mentioning

confidence: 99%

“…Several studies (Toggenburger et al, 1981;Bianchi and Rose, 1985;Tsukaguchi et al, 1999;Lee et al, 2006) have shown that SVCT1 is specifically located in the apical membrane along segments S1-S3 of the proximal tubules in adult human and murine renal tissue (Castro et al, 2008). In contrast, SVCT2 is mainly expressed during pre-natal stages (Nualart et al, 2013).…”

mentioning

confidence: 99%

Aging Selectively Modulates Vitamin C Transporter Expression Patterns in the Kidney

Forman

Martínez

Cifuentes

et al. 2017

Journal Cellular Physiology

View full text Add to dashboard Cite

In the kidney, vitamin C is reabsorbed from the glomerular ultrafiltrate by sodium-vitamin C cotransporter isoform 1 (SVCT1) located in the brush border membrane of the proximal tubules. Although we know that vitamin C levels decrease with age, the adaptive physiological mechanisms used by the kidney for vitamin C reabsorption during aging remain unknown. In this study, we used an animal model of accelerated senescence (SAMP8 mice) to define the morphological alterations and aging-induced changes in the expression of vitamin C transporters in renal tissue. Aging induced significant morphological changes, such as periglomerular lymphocytic infiltrate and glomerular congestion, in the kidneys of SAMP8 mice, although no increase in collagen deposits was observed using 2-photon microscopy analysis and second harmonic generation. The most characteristic histological alteration was the dilation of intracellular spaces in the basolateral region of proximal tubule epithelial cells. Furthermore, a combination of laser microdissection, qRT-PCR, and immunohistochemical analyses allowed us to determine that SVCT1 expression specifically increased in the proximal tubules from the outer strip of the outer medulla (segment S3) and cortex (segment S2) during aging and that these tubules also express GLUT1. We conclude that aging modulates vitamin C transporter expression and that renal over-expression of SVCT1 enhances vitamin C reabsorption in aged animals that may synthesize less vitamin C. J. Cell. Physiol. 232: 2418-2426, 2017. © 2016 Wiley Periodicals, Inc.

show abstract

Na+-dependent, potential-sensitive l-ascorbate transport across brush border membrane vesicles from kidney cortex

Cited by 51 publications

References 26 publications

Transport of ascorbic acid and dehydroascorbic acid by pancreatic islet cells from neonatal rats

Transport of ascorbic acid and dehydroascorbic acid by pancreatic islet cells from neonatal rats

The small-intestinal Na+,d-glucose cotransporter: An asymmetric gated channel (or pore) responsive to ΔΨ

Aging Selectively Modulates Vitamin C Transporter Expression Patterns in the Kidney

Contact Info

Product

Resources

About