Or pick up a Vitamin C supplement that claims to boost your immune system. At most, taking 1, mg of Vitamin C regularly could reduce your cold by a meager 8 percent. So where did the belief in Vitamin C as a cold-buster come from? A Nobel Prize-winning scientist from the s. Our mission has never been more vital than it is in this moment: to empower through understanding. Financial contributions from our readers are a critical part of supporting our resource-intensive work and help us keep our journalism free for all.
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Powered by Deploy Dental. Sansome Dental Your local San Francisco dentist. By Dr. Sean Moran on February 27, in Patient Education. Neurons possess very high intracellular concentrations of vitamin C, which can reach 10 mM, while the concentration in glial cells is similar to other body cells.
Vitamin C is apparently crucial for the correct functions of the brain and its levels in central nervous system are less affected by vitamin C starving than other tissues [ 73 ].
The absence of SVCT2 is incompatible with life [ 69 , 70 ]. It was shown that the expression of SVCT2 is increased after experimental vascular brain injury [ 53 ]. According to animal studies, SVCT2 is also important for the transport of vitamin C from the mother to the fetus, but SVCT1 likely participates in this process [ 69 , 70 , 78 ].
The plasma levels of vitamin C in the fetus are higher than in the mother in early pregnancy, which apparently suggests that the fetal uptake of vitamin C is preferred at the expense of the mother [ 78 ].
Radioactive labelled vitamin C administered to three humans showed that most of the amount is eliminated by the kidney. This means that the excess of vitamin C is efficiently eliminated in the urine to maintain the homeostatic vitamin C plasma levels. The player responsible for the saturable reabsorption is, like in the intestine, the SVCT1 transporter, which is expressed on the brush border of the proximal tubules Figure 2 B.
Since the pH of urine is also lower, passive diffusion was suggested but apparently plays a minor, if any, role at all [ 52 , 53 ]. The saturable mechanism of reabsorption is responsible for the maintenance of vitamin C plasma concentration together with the saturability of absorption. The elimination half-life of vitamin C is generally about 2 h [ 52 ].
However, an elevation of vitamin C levels was also seldomly described [ 80 , 82 , 83 ]. An effect of individual SNPs on the vitamin C system level has an additive character, which depends on genotype and an allele dosage additive effect that was also described. Furthermore, there have also been hundreds of less common or rare SNPs of both genes.
Their frequency in populations is unknown, and, therefore, the global significance of SNPs on circulating vitamin C levels as well as their association with diseases needs further investigation [ 2 , 83 , 85 ]. In addition, no associations were reported between one common variation of SLC23A1 and arterial blood pressure or different metabolic parameters [ 89 ]. Common variations of SLC23A2 were linked to increased or decreased risk of gastric cancer depending on a discrete genotype [ 85 , 90 ], decreased risk of colorectal adenocarcinoma [ 91 ], HPVpositive head and neck cancer [ 92 ], increased risk of bladder cancer [ 93 ], non-Hodgkin lymphoma [ 87 ], chronic lymphocytic leukemia [ 94 ], preterm delivery [ 84 ], open-angle glaucoma [ 95 ], and acute coronary syndrome in women [ 96 ].
Vitamin C has been undergoing extensive research and we know many processes in which it is involved. Its function appears to be linked dominantly with its electron-donating property [ 6 ]. The enzymatic roles of vitamin C are linked with either dioxygenases synthesis of collagen and carnitine, involvement in gene transcription, and regulation of translation via different mechanisms and elimination of tyrosine or monooxygenases synthesis of hormones. All these vitamin C-dependent oxygenases have a metal, iron, or copper in their active site.
The involvement of vitamin C in these enzymatic reactions is well documented. The precise mechanism is, however, not fully elucidated, but appears to be related to reduction or maintenance of these metals in the reduced state.
In some cases, vitamin C is reduced stoichiometrically within the reaction, suggesting direct involvement. However, in others, the stoichiometry is more complicated, implicating rather that vitamin C can recover the enzymatic function if the central metal atom is oxidized.
It should be mentioned that vitamin C seems to be an ideal cofactor for these enzymes. It can be potentially, but not always, replaced by other reductants, which are, however, apparently less active. Individual enzymes and their groups will now be briefly discussed.
In humans, it represents about 80 enzymes responsible for the modification of important biological substances and processes Table 2 [ 97 , 98 , 99 ].
Overview of the most important groups of iron-dependent and 2-oxoglutarate-dependent dioxygenases. PLODs, pro-collagen lysine 2-oxoglutarate 5-dioxygenases. HIF, hypoxia-inducible factor. PHDs, prolyl hydroxylase domain-containing proteins. KDMs, lysine demethylases.
FTO, fat-mass and obesity-associated protein. MINA53, Myc-induced nuclear antigen NO66, nucleolar protein TET, ten-eleven translocases. TMLHE, trimethyllysine hydroxylase epsilon.
BBOX, gamma-butyrobetaine dioxygenase. The 2OGO were initially identified in the s when studying collagen biosynthesis—a formation of hydroxyproline by collagen prolylhydroxylase enabling collagen cross-linking and, hence, correct formation of connective tissue. It does not need to be emphasized that vitamin C is essential to avoid the symptoms of scurvy related to impaired formation of connective tissue. The role s of vitamin C in this reaction cycle is are not fully elucidated, but likely the most important role is to maintain the iron atom in the reduced form [ , ].
In any case, vitamin C seems to be irreplaceable for the physiological function of these enzymes. It seems to be oxidized during the process, but the oxidation is not stoichiometric in relation to the reaction. A simple, non-selective reduction is rather improbable since glutathione, L-cysteine, or dithiothreitol are inactive. There are also some reports claiming that vitamin C is not needed, but they were questioned since ferrous ions could, at least, briefly substitute the lack of vitamin C [ ].
It is possible that there are differences between individual 2OGO as carnitine synthesis, which does not require vitamin C, according to a complex animal study, and the authors suggested that glutathione can replace it in this case [ ]. A relatively new discovery is the finding that vitamin C is the specific cofactor of 2OGO involved in cellular stress-signalling and epigenetics reviewed in References [ 98 , , , , , ].
One of the most known enzyme groups are Jumonji-C JmjC domain-containing proteins responsible for hydroxylation of specific histone lysines leading to histone demethylation JmjC demethylases, e. Ribosomal oxygenases, other members of JmjC domain-containing enzymes with a specific structure containing C-terminal winged-helix WH -domains, catalyze histidine-hydroxylation in ribosomal proteins rpL27a MYC-induced nuclear antigen 53, Mina53 , and rpL8 Nucleolar protein 66, NO66 [ , ].
Currently, we distinguish nine AlkB homologues. Generally, 2OGO catalyze specific hydroxylation of substrates, which, in turn, leads to demethylations via other catalytic cycles or downstream pathway involving thymine-DNA-glycosylase, which catalyzed base excision with DNA base excision repair [ , ]. The last known vitamin C-dependent dioxygenase is 4 -hydroxyphenylpyruvate dioxygenase. It has a ferrous ion again in the active site and needs oxygen.
It catalyzes an uncommon reaction in humans, which involves decarboxylation, substituent migration, and aromatic oxygenation in a single catalytic cycle.
The 4-hydroxyphenylpyruvate is converted to homogentisate 2,5-dihydroxyphenylacetate, Figure 6 as a part of the tyrosine elimination pathway. Furthermore, here, the superiority of vitamin C over other reducing agents was shown [ 4 , ]. The reaction catalyzed by human 4-hydroxyphenylpyruvate dioxygenase. The products of this reaction are homogentisate 2,5-dihydroxyphenylacetate and carbon dioxide. The origin of oxygen is highlighted in a blue and red color.
Both are, hence, associated with the synthesis of hormones. There is a significant homology both in the amino acid sequence and the final structure between them [ 72 ]. It is a dimer or tetramer containing identical subunits with each possessing two catalytical copper ions. Ascorbic acid seems to be involved in the reduction of copper.
The process appears to be very similar to PAM [ 4 , 72 , , ]. PAM is a bifunctional enzyme catalyzing two-step carboxyterminal amidation of peptides. It is expressed in at least seven protein forms, which are the results of different RNA splicing ranging from trans-Golgi membrane-bound to free forms. The enzyme can also amidate non-proteins such as fatty acid glycines [ 72 ]. The former active site is composed of two copper ions and the corresponding reaction is ascorbate-dependent.
Ascorbate likely enables conversion between a cupric and cuprous state and is reduced stoichiometrically to an ascorbyl radical. Other reductants can replace ascorbic acid but are less potent [ 4 , 72 , , , ]. The involvement of vitamin C as an endogenous antioxidant, e.
Its role has been clearly and repeatedly demonstrated in vitro, but in vivo, the situation is less clear [ 5 , 6 , , , ]. A good example is a fetus without an SVCT2 transporter. These fetuses have no vitamin C in the cortex and lungs together with lower levels of vitamin C in the placenta. The markers of lipid peroxidation are clearly elevated in the cortex and placenta but not in the lungs [ 69 ]. Interconnection between antioxidant effects of vitamin C and E.
A : Unsaturated fatty acid within the LDL low-density lipoproteins particle is oxidized e. Ascorbate can be recovered either via dehydroascorbic acid 6 or directly 7. The are several ways how these reactions can be accomplished either non-enzymatically or enzymatically.
A : normal conditions, B : lack of vitamin C and oxidative stress, C : physiological levels of vitamin C and oxidative stress in the vascular system, D : i. Trihydrobiopterin radical BH 3. Ascorbate is recovered from the ascorbyl radical 3 by several pathways discussed in this article. This decreases the availability of this cofactor and may lead to the formation of dihydrobiopterin BH 2 , 4. BH 2 can be reduced back to BH 4 by dihydrofolate reductase 5.
Similarly, if BH 3. BH 2 binds to eNOS, but causes uncoupling. Such an enzyme can no longer produce NO, but produces superoxide instead 7. Oxidative stress is demonstrated since elevated levels of superoxide in circulation cannot be normalized by physiological concentrations of vitamin C, which has a lower affinity to superoxide 8 than superoxide has to NO.
As a result, the protective NO is reacting with superoxide into highly reactive peroxynitrite 9. However, when vitamin C is given in high doses intravenously, it reaches mM levels and is considered to compete with NO for the superoxide The superoxide is neutralized by such a high concentration of vitamin C and NO can exert its endothelial protective function. Oxidative modification of protein moiety of low-density lipoproteins LDL can happen in vivo due to oxidative stress via the ROS formed, e.
The formed ascorbate ascorbyl free radical, also known as monodehydroascorbate or semidehydroascorbate, is quite stable and can be detected in biological fluids in a concentration of 10 nM [ 73 , ]. This radical is not very reactive and its preferred reaction is the formation of dehydroascorbic acid from two molecules of this radical. Again here, redundant pathways apparently exist.
The mechanism of how vitamin C maintains BH 4 levels is not fully clear. Vitamin C recovers BH 4 from the trihydrobiopterin radical. Although this reaction is relatively specific and thiols like glutathione are not active, the same reduction to BH 4 can also be performed by the enzyme endothelial NO-synthase eNOS itself.
Hence, the protection of BH 4 due to scavenging of other radicals that can oxidize BH 4, is a more likely mechanism. For example, the affinity of BH 4 and ascorbate for superoxide are about the same magnitude. One of the oxidation products is also dihydrobiopterin BH 2 , which binds to eNOS, but causes the mentioned uncoupling [ 68 , , , , , ]. However, ascorbate cannot recover BH 4 from BH 2 [ ]. The role of vitamin C in the prevention of endothelial dysfunction is further supported by other findings: 1 it prevents leucocytes adhesion to endothelial cells caused by both oxidized LDL and cigarette smoke [ ], 2 it decreases ROS levels in endothelial cells in vitro [ ], 3 it recovers flow-dependent vasodilation impaired by smoking and normalizes TBARS thiobarbituric acid reactive substances, a non-selective marker of lipid peroxidation in smokers [ 63 ], and, 4 similarly, flow-dependent vasodilation was also improved in patients with coronary artery disease after administration of vitamin C [ ].
In addition, the phenomenon of nitrate tolerance, which can also be associated with ROS, can be abolished by vitamin C [ ]. However, there are also reports opposing the antioxidant theory.
Multiple studies showed no effect of vitamin C on markers of lipid peroxidation in healthy humans or animals [ 63 , 66 , ]. Furthermore, very high-mortality of mice injected by Klebsiella pneumoniae was markedly abolished by vitamin C, but the effect was not associated with antioxidant activity since vitamin C did not impact neither lipid nor protein oxidation [ ].
Notwithstanding the positive effect on flow-mediated dilation, markers of lipid and protein oxidation were not positively modified after the administration of vitamin C in patients with coronary artery disease [ ]. The scavenging effects of ascorbic acid on a superoxide are also debatable. In simple experiments, vitamin C is a very active superoxide scavenger. However, in competition with NO, a concentration of vitamin C about 10 mM is needed to block the interaction of NO with the superoxide by effective scavenging of the latter [ ].
The reaction of the superoxide with NO is preferred and leads to the production of reactive peroxynitrite [ ]. A high concentration of vitamin C can be, however, present intracellularly, as mentioned, in neurons or in plasma after i.
On the other hand, glutathione has about x lower affinity to superoxide than vitamin C. In general, it appears that ascorbate is the first line hydrophilic antioxidant. Contrarily, glutathione is about twice more active in scavenging peroxynitrite than ascorbate [ 68 ]. Higher doses of vitamin C can behave as a prooxidant [ , , ] and this property is potentially useful for cancer treatment and will be discussed in the chapter entitled Cancer. The last known function of vitamin C is associated again with its potential to reduce ferric ions into ferrous ones.
In this way, vitamin C increases iron absorption even with a low amount of vitamin C corresponding to its content in a normal diet [ 5 , ]. Vitamin C deficiency is known as scurvy. Typical symptoms of scurvy are muscle weakness, swollen and bleeding gums, loss of teeth, petechial hemorrhaging, spontaneous ecchymoses, anemia, impaired would healing, hyperkeratosis, weakness, myalgia, arthralgia, and weight loss there can also be a paradoxical weight increase due to swelling while the early manifestations encompass lethargy, lassitude, and irritability.
Dyspnea can be observed as well. Similarly, symptoms are not seen unless the total vitamin C content in the body falls below — mg [ 2 , 3 , 6 , , ]. The direct links of vitamin C with symptoms of scurvy are not easily ascertained due to the complexity of vitamin C functions and its partial replaceability with different reductants [ 4 ]. It can also be related to decreased synthesis of hormones, e.
Peripheral neuropathy after vitamin C encompassing numbness of calves and pain might be related to the epigenetic effect of vitamin C. It is known that vitamin C is needed for myelin formation by Schwann cells and it is thought that these symptoms of peripheral neuropathy can be due to the lack of demethylating effects of vitamin C, which can affect the epigenomic way of activation, proliferation, and differentiation of Schwann cells [ ].
In the absence of vitamin C, prolylhydroxylase and lysyl hydroxylases cannot catalyze the hydroxylation. Collagen synthesis is defective and this leads to symptoms of scurvy. Hydroxylation of prolyl residues is needed for the formation of a stable triple-helical procollagen, while lysyl hydroxylation seems to participate in collagen crosslinking as well as in enabling other posttranslational modifications, such as glycosylation and phosphorylation [ , , ].
Some mild decreases in the hydroxylation of amino acids in collagen were observed in models of vitamin C deficiency. The effect of the absence of vitamin C might be more complex and, in addition to low hydroxylation, there are also reports of decreased synthesis of collagen and other extracellular matrix proteins. Additionally, other connective tissue proteins are physiologically hydroxylated in proline residues, e.
Fetuses without vitamin C in the brain have severe hemorrhages and there is apparently less collagen type IV in the basement membrane of brain vessels [ 69 , 70 ]. Hence, the overt symptoms of vitamin C deficiency such as bleeding or poor healing are associated with abnormalities in connective tissue synthesis. Although the time when scurvy was a relatively frequent phenomenon has gone, in the relatively close past and even in the current time, the vitamin C deficiency is not fully overcome [ 3 ].
The situation seems to be gradually improving since, apparently, vitamin C supplements and socioeconomic status are important factors [ 61 ]. As already discussed, smokers are at much higher risk [ 2 ]. Additionally, there are several pathologies and other situations in which the level of vitamin C drops in plasma [ ].
These are likely associated with an enhanced need for vitamin C. Not surprisingly, surgery, trauma, sepsis, and burns are causing a decrease in blood vitamin C and, in very serious injuries, the drop can be very pronounced [ , ]. Furthermore, acute myocardial infarction is associated with rapid loss of vitamin C both in plasma and tissues [ 60 , ]. Lower levels are also observed in cancer patients. The low intake of vitamin C is markedly contributing to those patients [ ]. In patients suffering from atopic dermatitis, the plasma vitamin C levels are normal, but their dermis contains approximately four times less vitamin C [ ].
As mentioned, patients with cancer often have lower plasma levels of vitamin C than healthy adults. Moreover, vitamin C deficiency is associated with higher C-reactive protein levels and with higher mortality [ 2 , , ].
Some clinical trials with high doses of vitamin C failed to show a benefit in cancer patients because vitamin C was administered orally in these studies [ , , ]. This seems to be largely based on the limits of oral vitamin C to elevate plasma levels. For vitamin C to have a therapeutic impact on cancer, it should be given intravenously to achieve plasma levels in mM. Low concentrations of vitamin C achieved by oral administration are antioxidant while higher procurable by intravenous administration of grams doses are prooxidant and also increase the effect of some cytostatics e.
It was shown that vitamin C given intravenously increases the production of hydrogen peroxide dose-dependently in extracellular fluid but not in blood. This was considered a consequence of increased levels of ascorbyl radical, which achieved nM in extracellular fluid [ 67 , ]. The levels of ascorbyl radical and hydrogen peroxide in the tumour or s.
The elevated levels of hydrogen peroxide seem to be one of the possible reasons for the anticancer effect of high doses of vitamin C. The viability of healthy cells is not affected by vitamin C even at 20 mM concentration, i. Tumor cells are much more, although variably, sensitive to vitamin C, with EC 50 of vitamin C below 20 mM in all tested cases of human and mouse cancer cells lines [ , ]. However, most of these studies were not designed as large-scale randomized clinical trials and clear verifications of the clinical efficacy of vitamin C are currently rather limited [ , , , ].
On the other hand, the therapy with a high dose of vitamin C can also have some relevant risks for the patients with some type of cancer treatment. There is some evidence that vitamin C administered orally may be effective to prevent the development of certain types of malignities e. On the other hand, there is a reasonable discussion of how much these studies were confounded by other factors such as healthier diet, etc.
Summing up, through low toxicity and low financial cost, high-dose intravenous vitamin C may be possibly a beneficial adjuvant for conventional cancer therapy in certain types of tumors.
Oral intake of vitamin C in high doses could be effective in cancer prevention. High-quality placebo-controlled clinical trials are, however, crucially needed to verify and specify the effect of vitamin C both in the treatment and prevention of cancer. Based on the reported positive antioxidant effect of vitamin C in relation to endothelial dysfunction, many studies investigated the possible protective effect of vitamin C on cardiovascular diseases.
Higher levels of plasma vitamin C are correlated with a lower risk of coronary artery disease and mortality in terms of cardiovascular diseases.
However, this relationship seems to be valid only for inadequate plasma levels. In adequate vitamin C plasma levels, supplementation with vitamin C has a little effect [ 2 , 5 , ]. Recent umbrella review brings only limited evidence for the effect of vitamin C supplementation on biomarkers of cardiovascular diseases or its risk factors, such as arterial stiffness, blood pressure, endothelial function, glycemic control, and lipid profile. Some recent systematic reviews and meta-analyses suggested that vitamin C significantly decreased the incidence of atrial fibrillation, ventilation time, length-of-stay in the intensive care unit, and hospital length-of-stay, but it had no significant effect on in-hospital mortality or incidence of stroke, acute kidney injury, or ventricular arrhythmia in cardiac surgery patients.
The data on the effect of vitamin C on clinical outcomes in patients undergoing cardiac surgery is still insufficient to draw firm conclusions [ , , , ]. The role of vitamin C in the protection of infections was nicely summarized in a recent review [ ].
It can be shortly summarized that vitamin C is important for the differentiation and function of immune cells and epithelial barrier cells. Patients with infections have lower levels of vitamin C and animal models have largely shown a protective effect of vitamin C on different infections or intoxications with bacterial toxins [ , ]. The human studies are, however, much less clear.
The Cochrane library has not documented the preventive effect of vitamin C administration on the incidence of the common cold and found only a very mild effect on the duration of the common cold. The effect of vitamin C in the prevention and treatment of pneumonia is uncertain as well [ , ]. Notwithstanding that the effect is absent in the general population, vitamin C can be effective under specific conditions, such as low levels of vitamin C, e.
The recent clinical trial did not find the effect of intravenous vitamin C infusion on organ failure and biological markers of inflammation and vascular injury in patients with sepsis and acute respiratory distress syndrome, but vitamin C compared with the placebo was associated with a significant reduction in day all-cause mortality [ ]. There are also some other clinical limited reports showing that vitamin C can improve the consequences of sepsis [ ].
Due to the possible positive effects on respiratory diseases, acute respiratory distress syndrome and sepsis, low cost and excellent safety profile, administrations of vitamin C to patients with hypovitaminosis C, and severe respiratory infections, e. However, there is currently only one small clinical trial reporting the possible effect on mortality in more severely ill COVID patients who received vitamin C intervention. Currently, there are many randomized controlled trials registered globally assessing the effect of intravenous vitamin C in patients with COVID in which outcomes are awaited with interest [ , ].
Vitamin C was also claimed to decrease the pH of urine and, hence, to be useful in the prevention of recurrent urinary infections. However, it was shown that even high doses of vitamin C do not decrease the pH of urine [ ]. Vitamin C is frequently added to oral preparations containing iron in order to increase iron absorption [ 5 , ].
In a recent meta-analysis, patients who received intravenous vitamin C perioperatively had significant pain reduction and decreased morphine requirements [ ]. However, this is not recommended. Intake with food can decrease these adverse reactions [ 3 , 5 , , ]. High, in particular i. Interestingly, even very high doses of i. Vitamin C is metabolized partly into oxalate Figure 4 in the human organism.
Vitamin C increases oxalate levels in urine dose-dependently and there are concerns about possible urinary stone formation. The question is somehow controversial since early methods overestimated oxalate levels in urine due to experimental artifacts [ 5 , 55 , , , , ].
Interestingly, parenteral preparations of vitamin C might also contain oxalate, likely because oxalate is easily formed in vitro from vitamin C at a higher pH [ ]. In any case, although urinary oxalate is the crucial player in calcium stone formation, the risk of urinary stone formation seems to be very low after intake, even of high vitamin C doses.
The major reason is that, in general, long-term high concentrations of oxalate in urine are needed for developing the stones. It cannot be, however, ignored since some persons might be at higher risk. For this reason, higher doses of vitamin C than 1 g daily should not be routinely recommended [ 5 ].
Of note, high doses of vitamin C were also described to increase urate excretion transiently [ 5 , 55 ]. Intravenous vitamin C or very high oral vitamin C doses can precipitate hemolysis in glucosephosphate deficiency patients [ 5 ]. Oral ascorbic acid can worsen hemolysis in patients suffering from paroxysmal nocturnal hemoglobinuria [ ]. In vitro, the effect of vitamin C on the lysis of red blood cells from these patients is concentration-dependent with worsening in low concentrations while inhibition occurred in high concentrations [ , ].
It should also be mentioned that a high intake of vitamin C in mothers can result in rebound scurvy in new-borns [ 3 ]. In general, determining the presence of L-ascorbic acid in a biological sample is a difficult task due to the possible interference with several variables.
The stability of L-ascorbic acid is the major problem. Since vitamin C is a known antioxidant, its oxidation in the human body into dehydroascorbic acid has been proposed as an in vitro marker of oxidative stress. However, the oxidation occurs rather quickly and, hence, also artificially after collecting the sample. Although dehydroascorbic acid is far more stable than L-ascorbic acid, it may still undergo irreversible hydrolysis in 2,3-diketogluconate Figure 4.
Moreover, the simultaneous determination of both is difficult because of the different physicochemical properties of these analytes. However, this procedure often lacks specificity and is prone to the interference of other reducing agents. This problem can be solved by combining different detection techniques. It should be pointed out, though, that vitamin C in urine can interfere with urine stripe tests. For example, vitamin C can cause false positive or false negative results during the detection of glucose, leukocytes, nitrite, and bilirubin [ ].
The stability of L-ascorbic acid in aqueous solutions can be affected by a number of factors including light, temperature, pH, and presence of oxygen and metal ions, which must be considered during its determination. These samples can be stable only for 1 h at room temperature.
Most of the published protocols for the extraction of L-ascrorbic acid from biological material use acidic pH 2. On the other hand, both L-ascorbic and dehydroascorbic acid display better stability at higher concentrations. Their stability decreases significantly when their concentration is lower than 0. The usage of anticoagulants for blood collection also plays an important role.
Heparin and ethylenediaminetetraacetic acid EDTA on ice are the most suitable since L-ascorbic acid is unstable with gel or fluoride anticoagulants [ ].
Thus, a number of preventive steps should be followed to avoid the degradation of the analytes when processing biological material for determining L-ascorbic and dehydroascorbic acid. In general, the rapid transport of the sample to the laboratory in a dark container at low temperature should be procured. Some stabilizers, such as meta-phosphoric acid trichloroacetic acid, homocysteine, trifluoroacetic acid, oxalic acid, and EDTA for chelating undesirable metal ions , are often added prior to sample storage or preparation.
Sometimes these substances can also be combined with buffers or organic solvents such as methanol and acetonitrile [ , , ]. The stability of L-ascorbic acid and dehydroascorbic acid in biological samples was studied in detail by Pullar et al. These authors pointed out, for example, the necessity of immediate separation of stabilized plasma from blood cells, the influence of hemolysis on ascorbate oxidation due to the release of catalytic iron from haemoglobin, and necessity to keep EDTA anticoagulant samples cold during handling.
Numerous methods for the determination of L-ascorbic acid in foods and pharmaceuticals have been published [ , , , ]. However, the determination of vitamin C in biological samples has not garnered further attention, likely because of its complexity.
The most common biological materials used for its determination are serum, plasma, urine, red and white blood cells, breast milk, and sweat [ , ]. The recent methods include capillary electrophoresis, liquid chromatography, and electrochemical biosensors in addition to commercially available kits that can be used in routine applications.
Some selected methods used for vitamin C determination in human biofluids are presented in Table 3. AA, ascorbic acid. DHA, dehydroascorbic acid. FLD, fluorescence detection.
LC-ECD, liquid chromatography with electrochemical detection. LC-CL, liquid chromatography with chemiluminescence detection. LC-MS, liquid chromatography with mass spectrometry detection. CE-ECD, capillary electrophoresis with electrochemical detection. CE-CL, capillary electrophoresis with chemiluminescence detection. CE-UV, capillary electrophoresis with ultraviolet detection. MCE-CL, microchip capillary electrophoresis with chemiluminescence detection. CZE-CL, capillary zone electrophoresis with chemiluminescence detection.
ECD, electrochemical detection. LC-UV, liquid chromatography with ultraviolet detection. Due to its sensitivity and good selectivity, capillary electrophoresis CE coupled with electrochemical detection ECD has been one of the most widely used techniques in the determination of AA in biological samples.
However, the high separation voltage could interfere with the electrochemical detection and the analysis of biomatrix samples could contaminate the electrode surface. Can high dose of vitamin C boost recovery after balance organ injury? Falls and balance. Prof Stephen Lord, Dr Jasmine Menant Walking is not automatic and requires attention and brain processing to maintain balance and prevent falling over.
How is this further impacted by psychological, physiological and medical factors eg. How does the brain control these balance tasks? Approach The experiments involve experimental paradigms that challenge cognitive functions of interest eg. We use cookies on our website to give you the most relevant experience by remembering your preferences and repeat visits.
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