Turnover rates of <scp>D</scp>-isoascorbic acid and <scp>L</scp>-ascorbic acid in guinea pig organs

Pelletier, Omer

doi:10.1139/y69-162

Cited by 29 publications

(9 citation statements)

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“…Regulation of ascorbate transport rates is a plausible mechanism for controlling intracellular ascorbate concentrations in the face of a constantly changing extracellular supply. The results of previous in vivo studies are consistent with regulation of vitamin C transport by external ascorbate levels, i) In guinea pigs, which cannot synthesize ascorbate, ascorbate-deficient diets lead to a prolonged half-life of vitamin C in brain (13). ii) Ingestion of excess vitamin C by guinea pigs slowly changes intestinal ascorbate transport with the result that initial uptake rates are decreased (30,31).…”

Section: Discussionsupporting

confidence: 69%

“…Ascorbate is essential for nervous system function because it is a cofactor in biosynthesis of myelin (1,2) and catecholamines (3), facilitates release of transmitters (4)(5)(6), modulates binding of ligands to neural receptors (7)(8)(9), and slows rates of transmitter clearance (10)(11)(12). Vitamin C homeostasis in the central nervous system is maintained even when plasma ascorbate levels are drastically lowered (13) or elevated (14,15).…”

Section: Introductionmentioning

confidence: 99%

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Substrate regulation of ascorbate transport activity in astrocytes

et al. 1990

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Astrocytes possess a concentrative L-ascorbate (vitamin C) uptake mechanism involving a Na(+)-dependent L-ascorbate transporter located in the plasma membrane. The present experiments examined the effects of deprivation and supplementation of extracellular L-ascorbate on the activity of this transport system. Initial rates of L-ascorbate uptake were measured by incubating primary cultures of rat astrocytes with L-[14C]ascorbate for 1 min at 37 degrees C. We observed that the apparent maximal rate of uptake (Vmax) increased rapidly (less than 1 h) when cultured cells were deprived of L-ascorbate. In contrast, there was no change in the apparent affinity of the transport system for L-[14C]ascorbate. The increase in Vmax was reversed by addition of L-ascorbate, but not D-isoascorbate, to the medium. The effects of external ascorbate on ascorbate transport activity were specific in that preincubation of cultures with L-ascorbate did not affect uptake of 2-deoxy-D-[3H(G)]glucose. We conclude that the astroglial ascorbate transport system is modulated by changes in substrate availability. Regulation of transport activity may play a role in intracellular ascorbate homeostasis by compensating for regional differences and temporal fluctuations in external ascorbate levels.

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Section: Discussionsupporting

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Substrate regulation of ascorbate transport activity in astrocytes

et al. 1990

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“…On the contrary, Pelletier (7) reported that the disappearance rate of [1-14C] AsA from the tissues of ErA-supplemented animals was faster than that in AsA-deficient animals . The results of this study indicated that ErA may neither reduce the AsA body pools nor accelerate the catabolism of AsA, since the administration of ErA did not stimulate the loss of AsA from the tissues.…”

Section: Discussionmentioning

confidence: 93%

Effect of erythorbic acid administration on ascorbic acid content in guinea pig tissues.

Arakawa

Suzuki

Kurata

et al. 1986

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryThe effect of erythorbic acid (ErA) on ascorbic acid (AsA) content in the tissues of normal and AsA-deficient guinea pigs was studied . The animals were sacrificed at varying intervals during the experimental period, and the liver, adrenal glands, spleen and kidneys were removed. The amounts of AsA and ErA in the tissues were measured by HPLC. The content of AsA in the tissues of the animals administered both AsA and ErA was lower than that of the animals administered only AsA. But the disappearance rate of AsA from the tissues of the AsA-deficient animals was similar to that of the animals administered only ErA. The amount of AsA in the tissues of the animals administered both AsA and ErA during the repletion period was lower than that of the animals administered only AsA. These results suggest that ErA administration may affect the amount of AsA in the tissues by inhibiting its tissue uptake or its storage in the tissues, and not by accerelating the catabolism of AsA in the tissues.

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“…2) (Siushansian et al 1996(Siushansian et al 1997. Recycling of vitamin C by astrocytes may account for the half-life of ascorbate being longer in brain than in other organs (Hammarstrom 1966;Pelletier 1969).…”

Section: Injuries In Vitromentioning

confidence: 99%

Antioxidant defense of the brain: a role for astrocytes

Wilson¹

1997

Can. J. Physiol. Pharmacol.

359

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Partially reduced forms of oxygen are produced in the brain during cellular respiration and, at accelerated rates, during brain insults. The most reactive forms, such as the hydroxyl radical, are capable of oxidizing proteins, lipids, and nucleic acids. Oxidative injury has been implicated in degenerative diseases, epilepsy, trauma, and stroke. It is a threshold phenomenon that occurs after antioxidant mechanisms are overwhelmed. Oxidative stress is a disparity between the rates of free radical production and elimination. This imbalance is initiated by numerous factors: acidosis; transition metals; amyloid beta-peptide; the neurotransmitters dopamine, glutamate, and nitric oxide; and uncouplers of mitochondrial electron transport. Antioxidant defenses include the enzymes superoxide dismutase, glutathione peroxidase, and catalase, as well as the low molecular weight reductants alpha-tocopherol (vitamin E), glutathione, and ascorbate (reduced vitamin C). Astrocytes maintain high intracellular concentrations of certain antioxidants, making these cells resistant to oxidative stress relative to oligodendrocytes and neurons. Following reactive gliosis, the neuroprotective role of astrocytes may be accentuated because of increases in a number of activities: expression of antioxidant enzymes; transport and metabolism of glucose that yields reducing equivalents for antioxidant regeneration and lactate for neuronal metabolism; synthesis of glutathione; and recycling of vitamin C. In the latter process, astrocytes take up oxidized vitamin C (dehydroascorbic acid, DHAA) through plasma membrane transporters, reduce it to ascorbate, and then release ascorbate to the extracellular fluid, where it may contribute to antioxidant defense of neurons.

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Turnover rates of D-isoascorbic acid and L-ascorbic acid in guinea pig organs

Cited by 29 publications

References 0 publications

Substrate regulation of ascorbate transport activity in astrocytes

Substrate regulation of ascorbate transport activity in astrocytes

Effect of erythorbic acid administration on ascorbic acid content in guinea pig tissues.

Antioxidant defense of the brain: a role for astrocytes

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