Ascorbic acid efflux and re-uptake in endothelial cells: maintenance of intracellular ascorbate

@article{May2008AscorbicAE,
  title={Ascorbic acid efflux and re-uptake in endothelial cells: maintenance of intracellular ascorbate},
  author={J. M. May and Z. Qu},
  journal={Molecular and Cellular Biochemistry},
  year={2008},
  volume={325},
  pages={79-88}
}
  • J. M. May, Z. Qu
  • Published 2008
  • Chemistry, Medicine
  • Molecular and Cellular Biochemistry
Entry of vitamin C or ascorbate into most tissues requires its movement across the endothelial cell barrier of vessels. If trans-cellular ascorbate movement occurs, then it should be evident as ascorbate efflux from endothelial cells. Cultured EA.926 endothelial cells that had been loaded to about 3.5 mM intracellular ascorbate lost 70–80% of ascorbate to the medium over several hours at 37°C via a non-saturable process that was insensitive to anion transport inhibitors and thiol reagents… Expand
Ascorbic acid efflux from human brain microvascular pericytes: role of re-uptake.
TLDR
Results suggest that ascorbate efflux from vascular pericytes occurs on a DIDS-inhibitable transporter or channel different from VRACs, providing a potential regulatory mechanism. Expand
Transfer of ascorbic acid across the vascular endothelium: mechanism and self-regulation.
TLDR
Results show that ascorbate traverses the endothelial barrier by a paracellular route that is regulated by cell metabolism, ion channels, and ascorin itself, and could reflect a role for the vitamin in control of endothelial Barrier function in vivo. Expand
Oxidized LDL up-regulates the ascorbic acid transporter SVCT2 in endothelial cells
TLDR
It is suggested that up-regulation of endothelial cell SVCT2 expression and function may help to maintain intracellular ascorbate during oxLDL-induced oxidative stress, and that asCorbate in turn can prevent this effect. Expand
On the physiological and cellular homeostasis of ascorbate
TLDR
The proposed approach provides, for the first time, a mechanistic account of processes leading to ascorbate physiological and cellular distribution, which helps to explain numerous experimental and clinical observations. Expand
Ascorbate and plasma membrane electron transport--enzymes vs efflux.
TLDR
mounting evidence suggests that cellular export of ascorbate (and concomitant import of its two-electron oxidation product, dehydroascorbate) may constitute a novel and physiologically relevant form of asCorbate-dependent tPMET. Expand
Cellular pathways for transport and efflux of ascorbate and dehydroascorbate.
The mechanisms allowing the cellular transport of ascorbic acid represent a primary aspect for the understanding of the roles played by this vitamin in pathophysiology. Considerable research effortExpand
Ascorbic acid prevents increased endothelial permeability caused by oxidized low density lipoprotein
TLDR
A role for endothelial cell ascorbate is suggested in ameliorating an important facet of endothelial dysfunction caused by mLDL, an effect mimicked by other cell-penetrant antioxidants. Expand
The active role of vitamin C in mammalian iron metabolism: much more than just enhanced iron absorption!
TLDR
Evidence strongly suggests that in addition to the known ability of dietary ascorbate to enhance nonheme iron absorption in the gut, asCorbate within mammalian systems can regulate cellular iron uptake and metabolism, and is a novel modulator of the classical transferrin-iron uptake pathway. Expand
The Glutamate Aspartate Transporter (GLAST) Mediates l-Glutamate-Stimulated Ascorbate-Release Via Swelling-Activated Anion Channels in Cultured Neonatal Rodent Astrocytes
TLDR
It is suggested that an impairment of astrocytic ascorbate-release may exacerbate neuronal dysfunction in neurodegenerative disorders and acute brain injury in which excitotoxicity and/or GLAST deregulation have been implicated. Expand
Ascorbic acid prevents VEGF-induced increases in endothelial barrier permeability
TLDR
Ascorbate prevention of VEGF-induced increases in endothelial permeability opens the possibility that its repletion could benefit diabetic macular edema, and suggest that VEGf-induced barrier leakage uncouples eNOS. Expand
...
1
2
3
...

References

SHOWING 1-10 OF 43 REFERENCES
Transport and intracellular accumulation of vitamin C in endothelial cells: relevance to collagen synthesis.
  • J. M. May, Z. Qu
  • Chemistry, Medicine
  • Archives of biochemistry and biophysics
  • 2005
TLDR
Results show the necessity of transport for this crucial function of the vitamin in endothelium, which was markedly stimulated by ascorbate in a time-dependent manner, and was saturable with increasing medium concentrations of theitamin. Expand
Ascorbic acid recycling enhances the antioxidant reserve of human erythrocytes.
TLDR
On the basis of the ascorbate-dependent rate of ferricyanide reduction, erythrocytes at a 45% hematocrit can regenerate theAscorbic acid present in whole blood every 3 min, and may contribute more to the antioxidant reserve of blood than is evident from plasma asCorbate concentrations alone. Expand
Erythrocyte ascorbate recycling: antioxidant effects in blood.
TLDR
Rec recycling of ascorbate in erythrocytes helps to maintain the antioxidant reserve of whole blood and protected endogenous alpha-tocopherol in human LDL from oxidation by a water soluble free radical initiator. Expand
Development of ascorbate transporters in brain cortical capillary endothelial cells in culture
TLDR
Although the SVCT2 is induced by culture of cortical capillary endothelial cells, its absence in vivo remains perplexing, given the need for intracellular ascorbate to facilitate type IV collagen maturation and release by endothelial Cells. Expand
Efflux of hepatic ascorbate: a potential contributor to the maintenance of plasma vitamin C.
TLDR
Results show that hepatocytes take up and reduce DHA and subsequently release part of the AH formed, probably via a membrane transporter, suggesting that the liver might contribute to the maintenance of plasma AH, a process that could be important under conditions of oxidative stress. Expand
Ascorbate uptake in pig coronary artery endothelial cells
TLDR
Surprisingly, endothelial cells had similar kinetic parameters as smooth muscle cells, except for a slightly lower uptake velocity in endothelialocytes, and both tissue types expressed mRNA for SVCT2. Expand
Ascorbic acid blunts oxidant stress due to menadione in endothelial cells.
TLDR
The ability of ascorbic acid to protect cultured human-derived endothelial cells (EA.hy926) from oxidant stress generated by the redox cycling agent menadione is studied, which may help to preserve nitric oxide synthase activity under conditions of excessive oxidant Stress. Expand
Protection and Recycling of α-Tocopherol in Human Erythrocytes by Intracellular Ascorbic Acid
Abstract Ascorbic acid can recycle α-tocopherol from the tocopheroxyl free radical in lipid bilayers and in micelles, but such recycling has not been demonstrated to occur across cell membranes. InExpand
The physiologically induced release of ascorbate in rat brain is dependent on impulse traffic, calcium influx and glutamate uptake
TLDR
A novel dialysis electrode is used which allows continuous monitoring of physiologically induced ascorbate release from the striatum in freely moving rats and a neuroprotective function for this coupling of asCorbate and glutamate release is discussed. Expand
Accumulation of intracellular ascorbate from dehydroascorbic acid by astrocytes is decreased after oxidative stress and restored by propofol
TLDR
Oxidative stress, induced in astrocytes by the lipophilic radical generator tert‐butyl hydroperoxide, decreased intracellular glutathione concentration and inhibited accumulation of intrACEllular ascorbate from dehydroascorbic acid, consistent with a novel mechanism ofAstrocytic ascorBate accumulation that is inhibited bylipophilic radicals and protected by lipophile antioxidants such as propofol. Expand
...
1
2
3
4
5
...