scholarly journals Iron regulates the uptake of ascorbic acid and the expression of sodium-dependent vitamin C transporter 1 (SVCT1) in human intestinal Caco-2 cells

2011 ◽  
Vol 105 (12) ◽  
pp. 1734-1740 ◽  
Author(s):  
Nathalie M. Scheers ◽  
Ann-Sofie Sandberg
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Cellular Uptake ◽  
Sodium Ascorbate ◽  
Acid Uptake ◽  
Compartment System ◽  
Treatment And Prevention ◽  
Acid Deficiency ◽  
The Impact ◽  
O 10

Ascorbic acid (vitamin C) has major effects on the intestinal uptake and utilisation of Fe in humans. The objective of the present study was to investigate the impact of Fe on the acquisition of ascorbic acid. The strategy was to study the cellular uptake and transport of ascorbic acid in the presence of Fe and also to observe the expression of the Na-dependent vitamin C transporter 1 (SVCT1) protein in human intestinal Caco-2 cells. SVCT1 is involved in the cellular uptake of ascorbic acid and is therefore a candidate for playing a role in the regulation of Fe utilisation. Caco-2 cells were cultured on transmembrane inserts in a three-compartment system followed by treatment with various combinations of FeCl2·4H2O (10–20 μmol/l) and sodium ascorbate (150 μmol/l). ELISA and Western blot analyses revealed that both SVCT1 and ferritin expressions were up-regulated in the presence of ascorbic acid in the basal compartment underneath the cells (10 and 22 %, respectively). Furthermore, when cells deficient in ascorbic acid were exposed to Fe, SVCT1 expression increased significantly (23·7 %). The increase in SVCT1 expression correlated with an increase in ascorbic acid uptake (285 %) in Fe-treated cells, as indicated by the SVCT1 inhibitor quercetin. We conclude that Fe plays an important role in regulating the uptake of ascorbic acid in human intestinal Caco-2 cells. This new angle could change the conceptual thinking of Fe and ascorbic acid utilisation and assist in the treatment and prevention of ascorbic acid-deficiency syndromes such as scurvy.

scholarly journals Ascorbic Acid Changes Growth of Food-Borne Pathogens in the Early Stage of Biofilm Formation

2020 ◽  
Vol 8 (4) ◽  
pp. 553
Author(s):  
Jana Przekwas ◽  
Natalia Wiktorczyk ◽  
Anna Budzyńska ◽  
Ewa Wałecka-Zacharska ◽  
Eugenia Gospodarek-Komkowska
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Food Industry ◽  
Early Stage ◽  
Food Additives ◽  
Bacterial Biofilm ◽  
Biofilm Inhibition ◽  
E Coli ◽  
Food Borne ◽  
The Impact

Since bacterial biofilm may contribute to the secondary contamination of food during the manufacturing/processing stage there is a need for new methods allowing its effective eradication. Application of food additives such as vitamin C already used in food industry as antioxidant food industry antioxidants may be a promising solution. The aim of this research was evaluation of the impact of vitamin C (ascorbic acid), in a range of concentrations 2.50 µg mL−1–25.0 mg mL−1, on biofilms of Staphylococcus aureus, Escherichia coli, and Listeria monocytogenes strains isolated from food. The efficacy of ascorbic acid was assessed based on the reduction of optical density (λ = 595 nm). The greatest elimination of the biofilm was achieved at the concentration of vitamin C of 25.0 mg mL−1. The effect of the vitamin C on biofilm, however, was strain dependent. The concentration of 25.0 mg mL−1 reduced 93.4%, 74.9%, and 40.5% of E. coli, L. monocytogenes, and S. aureus number, respectively. For E. coli and S. aureus lower concentrations were ineffective. In turn, for L. monocytogenes the biofilm inhibition was observed even at the concentration of 0.25 mg mL−1. The addition of vitamin C may be helpful in the elimination of bacterial biofilms. Nonetheless, some concentrations can induce growth of the pathogens, posing risk for the consumers’ health.

scholarly journals Dehydroascorbic acid uptake in a human keratinocyte cell line (HaCaT) is glutathione-independent

2000 ◽  
Vol 345 (3) ◽  
pp. 665-672 ◽  
Author(s):  
Isabella SAVINI ◽  
Sylvie DUFLOT ◽  
Luciana AVIGLIANO
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Reductase Activity ◽  
Thioredoxin Reductase ◽  
Dehydroascorbic Acid ◽  
Reduction Process ◽  
Enzymic Activity ◽  
Glutathione Depletion ◽  
Acid Uptake ◽  
Hacat Cells

Vitamin C plays an important role in neutralizing toxic free radicals formed during oxidative metabolism or UV exposure of human skin. This study was performed to investigate the mechanisms that regulate the homoeostasis of vitamin C in HaCaT cells by identifying the events involved in the transport and in the reduction of dehydroascorbic acid. Dehydroascorbic acid accumulated to a greater extent and faster compared with ascorbic acid; its transport appeared to be mediated by hexose transporters and was entirely distinct from ascorbic acid transport. Dehydroascorbate reductase activity was unaffected by glutathione depletion, although it was sensitive to thiol protein reagents. These observations, as well as the subcellular distribution of this enzymic activity and the cofactor specificity, indicate that thioredoxin reductase and lipoamide dehydrogenase play an important role in this reduction process. HaCaT cells were able to enhance their dehydroascorbic acid reductase activity in response to oxidative stress.

Chemical Methods for the Determination of Clinical Vitamin C (Ascorbic Acid) Deficiency

1940 ◽  
Vol 10 (12) ◽  
pp. 882-893 ◽  
Author(s):  
George J. Kastlin ◽  
C. G. King ◽  
Clara R. Schlesinger ◽  
J. West Mitchell
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Chemical Methods ◽  
Ascorbic Acid Deficiency ◽  
Acid Deficiency

scholarly journals Unintended Consequence of High-Dose Vitamin C Therapy for an Oncology Patient: Evaluation of Ascorbic Acid Interference With Three Hospital-Use Glucose Meters

2020 ◽  
pp. 193229682093218
Author(s):  
Brooke M. Katzman ◽  
Brandon R. Kelley ◽  
Gayle R. Deobald ◽  
Nikki K. Myhre ◽  
Sean A. Agger ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
High Dose ◽  
Oncology Patient ◽  
Glucose Meter ◽  
High Doses ◽  
The Impact ◽  
Very High ◽  
High Dose Vitamin ◽  
Hospital Use

The use of high-dose vitamin C in cancer care has offered promising results for some patients. However, the intravenous (IV) doses used for these patients can reach concentrations that interfere with some strip-based glucose meters. We characterized the impact of vitamin C interference, from standard to the very high doses used for some cancer protocols, using three different hospital-use glucose meters. For two of the three devices tested, increasing concentrations of ascorbic acid caused false elevations in the glucose measurements. The third glucose meter did not provide inaccurate results, regardless of the vitamin C concentration present. Rather, above a certain threshold, the device generated error messages and no results could be obtained.

scholarly journals Decreased expression of the vitamin C transporter SVCT1 by ascorbic acid in a human intestinal epithelial cell line

2002 ◽  
Vol 87 (2) ◽  
pp. 97-100 ◽  
Author(s):  
Lauren MacDonald ◽  
Alfred E. Thumser ◽  
Paul Sharp
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Cell Model ◽  
Human Kidney ◽  
The Body ◽  
Epithelial Cell Line ◽  
High Dose ◽  
Acid Uptake ◽  
Cellular Processes ◽  
High Doses

Vitamin C (ascorbic acid) is an essential nutrient that is involved in a number of cellular processes. However, unlike most mammals, man is unable to synthesize vitamin C and it must therefore be acquired from the diet. Absorption of vitamin C is achieved by two transporters, SVCT1 and SVCT2, recently cloned from rat and human kidney. SVCT1 is thought to be the predominant transporter in the intestine. Vitamin C supplements are increasingly common, thus contributing to an increased dietary load, and therefore the aim of the present study was to investigate the effect of high doses of ascorbic acid on SVCT1 expression. Using the Caco-2 TC7 cell model of small intestinal enterocytes, we measured the effects of ascorbic acid (4·5 mg/ml culture medium) on L-[14C]ascorbic acid uptake and SVCT1 expression (determined by reverse transcription-polymerase chain reaction). Ascorbic acid uptake was decreased significantly in Caco-2 TC7 cells exposed to ascorbate for 24 h (-50 %, P<0·0005). Expression of SVCT1 was also significantly reduced by exposure to elevated levels of ascorbate for 24 h (-77 %, P<0·005). Taken together these results suggest that high-dose supplements might not be the most efficient way of increasing the body pool of vitamin C.

scholarly journals Effect of Lipopolysaccharide and TNFα on Neuronal Ascorbic Acid Uptake

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Veedamali S. Subramanian ◽  
Trevor Teafatiller ◽  
Anshu Agrawal ◽  
Masashi Kitazawa ◽  
Jonathan S. Marchant
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Inhibitory Effect ◽  
Acid Uptake ◽  
Mrna Levels ◽  
The Central Nervous System ◽  
Factor Α ◽  
And Function

Vitamin C (ascorbic acid: AA) uptake in neurons occurs via the sodium-dependent vitamin C transporter-2 (SVCT2), which is highly expressed in the central nervous system (CNS). During chronic neuroinflammation or infection, CNS levels of lipopolysaccharide (LPS) and LPS-induced tumor necrosis factor-α (TNFα) are increased. Elevated levels of LPS and TNFα have been associated with neurodegenerative diseases together with reduced levels of AA. However, little is known about the impacts of LPS and TNFα on neuronal AA uptake. The objective of this study was to examine the effect of LPS and TNFα on SVCT2 expression and function using in vitro and in vivo approaches. Treatment of SH-SY5Y cells with either LPS or TNFα inhibited AA uptake. This reduced uptake was associated with a significant decrease in SVCT2 protein and mRNA levels. In vivo exposure to LPS or TNFα also decreased SVCT2 protein and mRNA levels in mouse brains. Both LPS and TNFα decreased SLC23A2 promoter activity. Further, the inhibitory effect of LPS on a minimal SLC23A2 promoter was attenuated when either the binding site for the transcription factor Sp1 was mutated or cells were treated with the NF-κB inhibitor, celastrol. We conclude that inflammatory signals suppress AA uptake by impairing SLC23A2 transcription through opposing regulation of Sp1 and NF-κB factors.

Transport model of the human Na+-coupled l-ascorbic acid (vitamin C) transporter SVCT1

2008 ◽  
Vol 294 (2) ◽  
pp. C451-C459 ◽  
Author(s):  
Bryan Mackenzie ◽  
Anthony C. Illing ◽  
Matthias A. Hediger
Keyword(s):  
Ascorbic Acid ◽  
Steady State ◽  
Vitamin C ◽  
Transport Model ◽  
Enzymatic Reactions ◽  
Acid Transport ◽  
Steady State Current ◽  
Charge Translocation ◽  
The Impact ◽  
Ascorbic Acid Transport

Vitamin C (l-ascorbic acid) is an essential micronutrient that serves as an antioxidant and as a cofactor in many enzymatic reactions. Intestinal absorption and renal reabsorption of the vitamin is mediated by the epithelial apical l-ascorbic acid cotransporter SVCT1 (SLC23A1). We explored the molecular mechanisms of SVCT1-mediated l-ascorbic acid transport using radiotracer and voltage-clamp techniques in RNA-injected Xenopus oocytes. l-Ascorbic acid transport was saturable ( K0.5 ≈ 70 μM), temperature dependent ( Q10 ≈ 5), and energized by the Na+ electrochemical potential gradient. We obtained a Na+-l-ascorbic acid coupling ratio of 2:1 from simultaneous measurement of currents and fluxes. l-Ascorbic acid and Na+ saturation kinetics as a function of cosubstrate concentrations revealed a simultaneous transport mechanism in which binding is ordered Na+, l-ascorbic acid, Na+. In the absence of l-ascorbic acid, SVCT1 mediated pre-steady-state currents that decayed with time constants 3–15 ms. Transients were described by single Boltzmann distributions. At 100 mM Na+, maximal charge translocation ( Qmax) was ≈25 nC, around a midpoint ( V0.5) at −9 mV, and with apparent valence ≈−1. Qmax was conserved upon progressive removal of Na+, whereas V0.5 shifted to more hyperpolarized potentials. Model simulation predicted that the pre-steady-state current predominantly results from an ion-well effect on binding of the first Na+ partway within the membrane electric field. We present a transport model for SVCT1 that will provide a framework for investigating the impact of specific mutations and polymorphisms in SLC23A1 and help us better understand the contribution of SVCT1 to vitamin C metabolism in health and disease.

scholarly journals Mechanisms and regulation of vitamin C uptake: studies of the hSVCT systems in human liver epithelial cells

2008 ◽  
Vol 295 (6) ◽  
pp. G1217-G1227 ◽  
Author(s):  
Jack C. Reidling ◽  
Veedamali S. Subramanian ◽  
Tamara Dahhan ◽  
Mohammed Sadat ◽  
Hamid M. Said
Keyword(s):  
Ascorbic Acid ◽  
Epithelial Cells ◽  
Vitamin C ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Active Form ◽  
Acid Uptake ◽  
Regulatory Pathways ◽  
Liver Epithelial Cells ◽  
Uptake Process

Humans use two sodium-ascorbate cotransporters (hSVCT1 and hSVCT2) for transporting the dietary essential micronutrient ascorbic acid, the reduced and active form of vitamin C. Although the human liver plays a pivotal role in regulating and maintaining vitamin C homeostasis, vitamin C transport physiology and regulation of the hSVCT systems in this organ have not been well defined. Thus, this research used a human hepatic cell line (HepG2), confirming certain results with primary human hepatocytes and determined the initial rate of ascorbic acid uptake to be Na+ gradient, pH dependent, and saturable as a function of concentration over low and high micromolar ranges. Additionally, hSVCT2 protein and mRNA are expressed at higher levels in HepG2 cells and native human liver, and the cloned hSVCT2 promoter has more activity in HepG2 cells. Results using short interfering RNA suggest that in HepG2 cells, decreasing hSVCT2 message levels reduces the overall ascorbic acid uptake process more than decreasing hSVCT1 message levels. Activation of PKC intracellular regulatory pathways caused a downregulation in ascorbic acid uptake not mediated by a single predicted PKC-specific amino acid phosphorylation site in hSVCT1 or hSVCT2. However, PKC activation causes internalization of hSVCT1 but not hSVCT2. Examination of other intracellular regulatory pathways on ascorbic acid uptake determined that regulation also potentially occurs by PKA, PTK, and Ca2+/calmodulin, but not by nitric oxide-dependent pathways. These studies are the first to determine the overall ascorbic acid uptake process and relative expression, regulation, and contribution of the hSVCT systems in human liver epithelial cells.

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