Ascorbate uptake is decreased in the hippocampus of ageing rats

2011 ◽  
Vol 58 (4) ◽  
pp. 527-532 ◽  
Author(s):  
Ionara Rodrigues Siqueira ◽  
Viviane Rostirolla Elsner ◽  
Marina Concli Leite ◽  
Cláudia Vanzella ◽  
Felipe dos Santos Moysés ◽  
...  
Keyword(s):  
Ascorbate Uptake

Ascorbate uptake enables tubular mitophagy to prevent septic AKI by PINK1-PARK2 axis

2021 ◽  
Vol 554 ◽  
pp. 158-165
Author(s):  
Zhi-Dong Chen ◽  
Bang-Chuan Hu ◽  
Xue-Ping Shao ◽  
Jun Hong ◽  
Yang Zheng ◽  
...  
Keyword(s):  
Ascorbate Uptake

Ascorbate uptake by isolated rat alveolar macrophages and type II cells

1983 ◽  
Vol 54 (1) ◽  
pp. 208-214 ◽  
Author(s):  
V. Castranova ◽  
J. R. Wright ◽  
H. D. Colby ◽  
P. R. Miles
Keyword(s):  
Alveolar Macrophages ◽  
Membrane Surface ◽  
Lung Cells ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Sodium Influx ◽  
Saturation Kinetics ◽  
Ascorbate Uptake ◽  
Isolated Rat

Studies were conducted to measure intracellular ascorbate content and to characterize ascorbate uptake in three fractions of isolated rat pneumocytes (i.e., alveolar macrophages, alveolar type II epithelial cells, and another fraction of small pneumocytes that contains neither macrophages nor type II cells). When cells are incubated in medium containing 0.1 mM ascorbate (i.e., the concentration normally found in plasma), intracellular ascorbate concentrations are 3.2 mM in alveolar macrophages and type II cells and 0.9 mM in other lung cells; ascorbate influx is 1.5 nmol . 10(7) cells-1 . h-1 for alveolar macrophages, 0.24 nmol . 10(7) cells-1 . h-1 for type II cells, and very slow in other pneumocytes. Ascorbate influx displays saturation kinetics in both alveolar macrophages (K1/2 = 2 mM; Vmax = 32.2 nmol . 10(7) cells-1 . h-1) and type II cells (K1/2 = 5 mM; Vmax = 14.2 nmol . 10(7) cells-1 . h-1). After correction for differences in the membrane surface areas of these two types of lung cells, the rates for maximum ascorbate influx (Vmax) are similar in alveolar macrophages and type II cells. In addition, ascorbate uptake by alveolar macrophages and type II cells is dependent on metabolic activity and extracellular sodium. In contrast, ascorbate uptake in other lung cells does not exhibit saturation kinetics and is not dependent on metabolism or sodium. Thus alveolar macrophages and type II cells possess an energy-dependent cotransport system for ascorbate and sodium influx. The high ascorbate content and the existence of a specialized transport mechanism for ascorbate uptake may explain the relative resistance of alveolar macrophages and type II cells to oxidant injury.

Dietary regulation of intestinal ascorbate uptake in guinea pigs

1991 ◽  
Vol 260 (1) ◽  
pp. G108-G118 ◽  
Author(s):  
W. H. Karasov ◽  
B. W. Darken ◽  
M. C. Bottum
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Brush Border ◽  
Guinea Pigs ◽  
Dietary Regulation ◽  
Intestinal Brush Border ◽  
Pregnancy And Lactation ◽  
Human Adults ◽  
Ascorbate Uptake

We measured ascorbic acid (AA) uptake across the intestinal brush border in vitro in intact tissue from guinea pigs fed maintenance AA (200 mg/kg diet) or made hypervitaminotic (5,000 mg/kg diet) or hypovitaminotic (chronically and acutely). Total uptake per centimeter ileum was 25-50% lower in hypervitaminotic juvenile, adult male, and lactating guinea pigs compared with their respective controls, whereas carrier-mediated D-glucose uptake and Na(+)-independent AA uptake were similar. High dietary ascorbate specifically reduced the Vmax for carrier-mediated AA uptake. Hypovitaminosis had no significant effect on uptake of AA or other solutes. We performed diet-switching experiments (high-AA diet to maintenance diet) with young and adult guinea pigs to determine the reversibility of the downregulation. In adult guinea pigs, the downregulation of AA uptake was reversible within 7 days. In the young of mothers fed high AA during pregnancy and lactation, and which fed on high AA for 14 days after weaning, the downregulation was reversible within 14 days. Thus regulation of AA uptake is reversible and therefore probably does not play a significant role in the development of vitamin C dependency in human adults, or their young, after ingestion of megadoses of ascorbic acid.

scholarly journals The Role of Physiological Vitamin C Concentrations on Key Functions of Neutrophils Isolated from Healthy Individuals

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1363 ◽  
Author(s):  
Stephanie M. Bozonet ◽  
Anitra C. Carr
Keyword(s):  
Vitamin C ◽  
Immune Cell ◽  
Dehydroascorbic Acid ◽  
Optimal Level ◽  
Neutrophil Function ◽  
Neutrophil Extracellular Trap ◽  
Healthy Individuals ◽  
Healthy Humans ◽  
Ascorbate Uptake

Vitamin C (ascorbate) is important for neutrophil function and immune health. Studies showing improved immune function have primarily used cells from scorbutic animals or from individuals with infectious conditions or immune cell disorders. Few studies have focused on the requirements of neutrophils from healthy adults. Therefore, we have investigated the role of vitamin C, at concentrations equivalent to those obtained in plasma from oral intakes (i.e., 50–200 µmol/L), on key functions of neutrophils isolated from healthy individuals. Cells were either pre-loaded with dehydroascorbic acid, which is rapidly reduced intracellularly to ascorbate, or the cells were activated in the presence of extracellular ascorbate. We measured the effects of enhanced ascorbate uptake on the essential functions of chemotaxis, oxidant production, programmed cell death and neutrophil extracellular trap (NET) formation. We found that neutrophils isolated from healthy individuals already had replete ascorbate status (0.35 nmol/106 cells), therefore they did not uptake additional ascorbate. However, they readily took up dehydroascorbic acid, thus significantly increasing their intracellular ascorbate concentrations, although this was found to have no additional effect on superoxide production or chemotaxis. Interestingly, extracellular ascorbate appeared to enhance directional mobilityin the presence of the chemoattractant formyl-methionyl-leucyl-phenylalanine (fMLP). Stimulation of the cells in the presence of ascorbate significantly increased intracellular ascorbate concentrations and, although this exhibited a non-significant increase in phosphatidylserine exposure, NET formation was significantly attenuated. Our findings demonstrate the ability of neutrophils to regulate their uptake of ascorbate from the plasma of healthy humans to maintain an optimal level within the cell for proper functioning. Higher oral intakes, however, may help reduce tissue damage and inflammatory pathologies associated with NET formation.

Ascorbate uptake by isolated rat lung cells

1981 ◽  
Vol 51 (6) ◽  
pp. 1477-1483 ◽  
Author(s):  
J. R. Wright ◽  
V. Castranova ◽  
H. D. Colby ◽  
P. R. Miles
Keyword(s):  
Plasma Level ◽  
Metabolic Inhibitors ◽  
Lung Cells ◽  
Rat Lung ◽  
Ascorbate Concentration ◽  
Ascorbate Uptake ◽  
Extracellular Sodium ◽  
Energy Dependent ◽  
Isolated Rat Lung ◽  
Isolated Rat

Experiments were done to determine the intracellular concentration of ascorbate in isolated rat lung cells and the concentration in plasma and to study ascorbate influx in these cells. The intracellular ascorbate concentration was 2.25 mM and the plasma level was about 0.14 mM; i.e., the lung cell ascorbate concentration was about 16 times greater than the plasma level. When the cells were incubated in medium containing physiological levels of ascorbate (0.1 mM), influx increased linearly up to 60 min of incubation and was 0.54 +/- 0.04 nmol.10(7) cells-1.h-1. Influx was dependent on the extracellular ascorbate concentration. At concentrations ranging from 0.025 to 1 mM, uptake appeared to exhibit saturation kinetics with an apparent Km of 0.16 mM. At physiological levels of extracellular ascorbate (0.1 mM) at least 90% of the uptake appeared to be carrier mediated, and this influx was inhibited by various metabolic inhibitors. In addition, ascorbate influx was inhibited by ouabain and removal of extracellular sodium. These results suggest that lung cells contain a transport mechanism for ascorbate that is energy-dependent and that may be coupled to Na+ influx.

Ascorbate uptake and antioxidant function in peritoneal macrophages

2005 ◽  
Vol 440 (2) ◽  
pp. 165-172 ◽  
Author(s):  
James M. May ◽  
Liying Li ◽  
Zhi-chao Qu ◽  
Junjun Huang
Keyword(s):  
Peritoneal Macrophages ◽  
Antioxidant Function ◽  
Ascorbate Uptake

scholarly journals Erythrocyte Ascorbate Is a Potential Indicator of Steady-State Plasma Ascorbate Concentrations in Healthy Non-Fasting Individuals

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 418 ◽  
Author(s):  
Juliet M. Pullar ◽  
Susannah Dunham ◽  
Gabi U. Dachs ◽  
Margreet C. M. Vissers ◽  
Anitra C. Carr
Keyword(s):  
Steady State ◽  
Vitamin C ◽  
Plasma Levels ◽  
Normal Diet ◽  
Plasma Vitamin ◽  
Stable Measure ◽  
Fasting Plasma ◽  
Plasma Ascorbate ◽  
Ascorbate Uptake ◽  
State Plasma

Plasma vitamin C concentrations fluctuate in response to recent dietary intake; therefore levels are typically determined in the fasting state. Erythrocyte ascorbate concentrations have been shown to be similar to plasma levels, but little is known about the kinetics of ascorbate accumulation in these cells. In this study, we investigated ascorbate uptake into erythrocytes after dietary supplementation with vitamin C and compared it to changes in plasma ascorbate concentrations. Seven individuals with baseline fasting plasma vitamin C concentrations ≥ 50 µmol/L were depleted of vitamin C-containing foods and drinks for one week, and then supplemented with 250 mg vitamin C/day in addition to resuming their normal diet. Fasting or steady-state plasma ascorbate concentrations declined to almost half of their baseline concentration over the week of vitamin C depletion, and then returned to saturation within two days of beginning supplementation. Erythrocyte ascorbate concentrations exhibited a very similar profile to plasma levels, with values ~76% of plasma, and a strong linear correlation (r = 0.89, p < 0.0001). Using a pharmacokinetic study design in six individuals with baseline fasting plasma vitamin C concentrations ≥50 µmol/L, we also showed that, unlike plasma, which peaked between 2 and 4 h following ingestion of 200 mg of vitamin C, erythrocyte ascorbate concentrations did not change in the six hours after supplementation. The data from these two intervention studies indicate that erythrocyte ascorbate concentration provides a stable measure of steady-state plasma ascorbate status and could be used to monitor ascorbate status in healthy non-fasting individuals.

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