Dehydroascorbic acid

Other Names

(5R)-5-(1,2-Dihydroxyethyl)tetrahydrofuran-2,3,4-trione(5R)-5-[(1S)-1,2-Dihydroxyethyl]-2,3,4(5H)-furantrione(5R)-5-[(1S)-1,2-Dihydroxyethyl]furan-2,3,4(5H)-trione(5R)-5-[(1S)-1,2-dihydroxyethyl]oxolane-2,3,4-trione1-Dehydroascorbate1-Dehydroascorbic acid5-(1,2-Dihydroxyethyl)-2,3,4(5H)-furantrione5-(1,2-dihydroxyethyl)-5-hydrofuran-2,3,4-trione5-(1,2-dihydroxyethyl)furan-2,3,4(5H)-trione5-(1,2-Dihydroxyethyl)oxolane-2,3,4-trioneAcid, DehydroascorbicBis(dehydro-L-ascorbic acid)Bis-DHAC05422D-Dehydroascorbic acidD-Dehydroisoascorbic acidDehydro-L-(+)-ascorbic acid dimerDehydro-L-ascorbateDehydro-L-ascorbic acidDehydroascorbateDHADHAAL-Ascorbic acid oxidizedL-Dehydro Ascorbic AcidL-DehydroascorbateL-Dehydroascorbic acidL-threo-2,3-Hexodiulosonic acid gamma-lactoneL-threo-2,3-Hexodiulosonic acid γ-lactoneL-threo-Dehydroascorbic acidOxidized ascorbic acidOxidized vitamin Cthreo-2,3-hexodiulosono-1,4-lactone

Synopsis

Dehydroascorbic Acid

1. Identity, Chemistry, and Common Forms

Chemical Identity

Dehydroascorbic acid (DHA) is the major oxidized form of ascorbic acid (vitamin C). Chemically, it is known as threo-2,3-hexodiulosonic acid-γ-lactone (CAS 490-83-5), with the molecular formula C₆H₆O₆ and a molecular weight of 174.1 g/mol. It is also catalogued under synonyms including L-dehydroascorbic acid, oxidized ascorbate, and oxidized vitamin C.

DHA forms reversibly from ascorbic acid through the loss of two hydrogen atoms via two-electron oxidation, and in aqueous solutions at physiological pH, it predominantly exists as a colorless bicyclic hemiketal rather than the tricarbonyl structure often depicted in older literature. The actual structures of the various forms of dehydroascorbic acid have been known for at least a quarter of a century, so that the continued use of the oversimplified tricarbonyl structure is hard to excuse.

As a reducing agent and electron donor antioxidant, ascorbic acid can undergo two consecutive one-electron oxidation reactions and deprotonation of both hydroxyl groups at positions 2 and 3, resulting in the formation of dehydroascorbic acid. Ascorbate can donate an electron to another molecule, becoming oxidized to the ascorbyl radical — a comparatively stable and nonharmful radical form — and two ascorbyl radicals can subsequently dismutate into one molecule of ascorbate and one molecule of dehydroascorbic acid.

Occurrence in Human Blood and Tissues

Vitamin C is present in human blood at an average concentration of 50–100 μM, and at least 95% of that is typically in the reduced ascorbic acid form, while the remaining 5% is in the oxidized dehydroascorbic acid form. While the reduced form of ascorbate is dominant in the plasma of healthy humans, DHA is present at a very low level, indicating that ascorbate is taken up and accumulated in cells primarily by sodium-dependent vitamin C transporters (SVCTs). At neutral pH, DHA is unstable and if it is not reduced to regenerate reduced ascorbate by thioredoxin or glutathione, DHA is broken down into threonic acids, oxalic and diketogulonic acids by the kidney; consequently, ascorbate is present in the form of DHA in very small fractions in vivo, at concentrations not likely to be above 1–2 μM.

Natural Sources

Dehydroascorbic acid is naturally present in dietary sources, particularly fruits and vegetables, where it typically accounts for 5–20% of the total vitamin C content. Examples include citrus fruits such as oranges, grapefruits, and lemons, as well as broccoli, in which initial ratios of dehydroascorbic acid to total vitamin C often exceed 10% and can rise further during post-harvest storage. Vitamin C — including ascorbic acid and dehydroascorbic acid — is one of the most important nutritional quality factors in many horticultural crops; its content can be influenced by various factors such as genotypic differences, preharvest climatic conditions and cultural practices, maturity, and postharvest handling procedures.

This oxidized form arises from the spontaneous or enzymatic conversion of ascorbic acid and contributes to the overall bioavailability of vitamin C in the human diet. In plant tissues, dehydroascorbic acid forms under stress conditions such as mechanical wounding or pathogen attacks, where ascorbate oxidase in the apoplastic space catalyzes the oxidation of ascorbic acid.

Commercial and Preparation Forms

Dehydroascorbic acid dimer (DDHA) is the commercially available form of oxidized vitamin C. Ever since the elucidation of the chemical structure of vitamin C in the mid-1930s, it has been known that vitamin C occurs naturally as two different compounds — ascorbic acid and dehydroascorbic acid — and that both AA and DHA are unstable compounds. In aqueous solutions, factors affecting the rate of their destruction include the pH of the solution and exposure to various metal ions, heat, light, and air, with DHA being considerably less stable than AA under comparable conditions.

To prepare aqueous solutions of DHAA from the solid form requires prolonged mixing at temperatures well above 37°C, making solutions of DHAA much more difficult to manufacture than solutions of AA. Since the conditions needed to solubilize it efficiently do not exist in the gut of humans or other animals, substantial doubt exists about whether the dry, solid form of DHAA can be absorbed when ingested — reasons why DHAA has not been widely utilized as the source of vitamin C for dietary supplements or topical products.

Certain commercial supplement formulations such as Ester-C® contain mainly calcium ascorbate but also small amounts of vitamin C metabolites including dehydroascorbic acid (oxidized ascorbic acid), calcium threonate, and trace levels of xylonate and lyxonate.

2. Historical and Traditional Context

DHA as a discrete chemical entity was not recognized in traditional medicine systems — its existence as the oxidized counterpart of ascorbic acid was established only in the 20th century. The broader historical narrative is that of vitamin C and scurvy prevention.

Scurvy was endemic wherever fruit and vegetables were in short supply; military campaigns from the Crusades to the Napoleonic Wars, the American Civil War, and even World War I were stymied by widespread and often fatal scurvy among troops. The antiscorbutic principle was identified and named ascorbic acid (vitamin C) in 1932. In 1932, Charles Glen King isolated an antiscorbutic compound from lemon juice recognized as the hexuronic acid found by Albert Szent-Györgyi, who had shown that 1 mg/day of hexuronic acid provided ample protection against scurvy.

Ever since the elucidation of the chemical structure of vitamin C in the mid-1930s, it has been known that vitamin C occurs naturally as two different compounds: ascorbic acid and its oxidized form, dehydroascorbic acid. Early researchers investigating DHA focused on whether it retained antiscorbutic properties. Early studies demonstrated that DHA is antiscorbutic when given orally, suggesting a metabolic conversion to ascorbic acid in vivo. Indeed, dehydroascorbic acid prevents scurvy in human subjects.

Vitamin C has been postulated to be connected to diabetes for more than 70 years, with at least one proposed mechanism related to dehydroascorbic acid. The first connection noted was that dehydroascorbic acid at pharmacologic doses was toxic to pancreatic islets, whose beta cells produce insulin, based on its structural similarity to the beta cell toxin alloxan. These early investigations from the 1940s and 1950s were conducted largely in animal models and informed the modern understanding of DHA's relationship to glucose transport and insulin-producing tissues.

3. Key Constituents, Biochemistry, and Active Mechanisms

Oxidation–Reduction Cycle and Ascorbate Recycling

Vitamin C exists in two forms — the reduced form ascorbic acid and its two-electron oxidation product dehydroascorbic acid. All known biological functions of vitamin C are related to its reduced form. DHA itself is regarded principally as a vehicle through which the body recovers and recycles ascorbic acid, rather than as an independent bioactive agent.

Dehydroascorbic acid is taken up by most cell types and efficiently reduced to ascorbate either chemically by glutathione or enzymatically by glutathione-dependent dehydroascorbic acid reductases or NADPH-dependent dehydroascorbic acid reductases such as thioredoxin reductase, thereby preventing metabolic loss of vitamin C. This process is referred to as ascorbate recycling.

Activated neutrophils secrete reactive oxygen species that oxidize extracellular ascorbic acid to DHA. DHA is rapidly transported into the neutrophil by the glucose transporters GLUT1 and GLUT3 and immediately reduced to ascorbic acid by glutaredoxin (GRX), producing a 10-fold increase in neutrophil internal ascorbic acid concentration. Glutathione (GSH), used during DHA reduction, is regenerated from glutathione disulfide (GSSG) by glutathione reductase (GRD) and NADPH.

Glucose Transporter–Mediated Cellular Entry

Dehydroascorbic acid forms a hydrate that cyclizes to a bicyclic hemiacetal, which is structurally similar to glucose and is therefore transported to cells by glucose transporters (GLUTs). GLUT1 is a facilitative glucose transporter that can transport oxidized vitamin C (i.e., dehydroascorbic acid) and complements the action of reduced vitamin C transporters.

Ascorbic acid is taken up by most cell types via a high-affinity/low-capacity mechanism through sodium-dependent vitamin C transporters (SVCT-1 and SVCT-2), whereas dehydroascorbic acid is accumulated via sodium-independent facilitative GLUTs, followed by intracellular reduction.

Sodium Vitamin C Transporters (SVCTs) are mainly responsible for vitamin C transport into cells in humans and other mammals. SVCT1 is primarily expressed in absorptive tissues, including the intestinal epithelium and the kidney. SVCT2 is expressed in most body tissues, as are glucose transporters (GLUTs). SVCT1 and SVCT2 transport ascorbic acid but not dehydroascorbic acid into cells.

Structural Basis of GLUT Transport

To identify the residues involved in human GLUT1's transport of dehydroascorbic acid, docking studies were performed in the glucose-binding cavity of GLUT1. The interactions of the bicyclic hemiacetal form of dehydroascorbic acid with GLUT1 through hydrogen bonds were found to be less favorable than the interactions with sugars normally transported by GLUT1. Both DHA and glucose share the same eight key residues in GLUT1, albeit with a differential contribution of residue N317, marking the first work to identify structural determinants of oxidized vitamin C's transport via GLUT1.

Intracellular Fate and Catabolism

DHA suffers irreversible hydrolysis to 2,3-diketo-L-gulonic acid, with subsequent decarboxylation resulting in carbon dioxide and components of the pentose phosphate cycle, or oxalic acid and threonic acid. DHA is kinetically unstable and is hydrolyzed to 2,3-diketogulonic acid (DKG), which has no vitamin C activity.

DHA in water gradually hydrolyses to DKG, more rapidly at higher pH values. At pH 4.7, hydrolysis is slow with a half-life of approximately 8 hours. At pH 6.5, the half-life of DHA is approximately 20 minutes, as evidenced by partial hydrolysis during electrophoretic analysis. These kinetics are critically important to its practical formulation and its bioavailability in vivo.

Dehydroascorbic acid is first hydrolyzed to 2,3-diketo-L-gulonate and then further metabolized to a range of compounds. In some animals, products of vitamin C catabolism may enter the pentose phosphate pathway or other pathways of carbohydrate metabolism.

4. Scientific Evidence by Area of Use

4.1 Vitamin C Bioavailability and Antiscorbutic Activity

The claim that DHA is not equivalent to ascorbic acid runs counter to the widely held understanding that ascorbic acid and dehydroascorbic acid possess roughly equivalent bioavailability in humans. As both molecules are commonly thought to be bioavailable, the vitamin C content of foods is usually reported as total vitamin C — the sum of ascorbic acid and dehydroascorbic acid contents.

Both dehydroascorbic acid and ascorbic acid are absorbed from the lumen of the human intestine, as demonstrated by measuring transport rates in luminal membrane vesicles. The absorption sites are found along the entire length of the small intestine. Most dehydroascorbic acid may be reduced enzymatically to ascorbic acid in the wall of the intestine before passing into the blood, since dehydroascorbic acid reductases are present within human enterocytes. These enzymes keep the intracellular concentration of DHA low and thereby maintain a gradient favoring continued uptake of oxidized vitamin C across the enterocytes' luminal membrane.

Dehydroascorbic acid given orally has been shown to be absorbed in humans; however, these studies only examined relative bioavailability. In vitro studies have found that oxidized vitamin C (dehydroascorbic acid) enters cells via some facilitated glucose transporters and is then reduced internally to ascorbic acid. The physiologic importance of dehydroascorbic acid uptake and its contribution to overall vitamin C economy remain uncertain.

Evidence strength: The equivalence of DHA and ascorbic acid as antiscorbutic agents is supported by human evidence going back to the mid-20th century, and is the scientific basis for counting total vitamin C (reduced plus oxidized forms) in food composition. However, the NIH notes that the precise physiological importance of DHA's separate transport route remains an open question. No modern randomized controlled trials have specifically compared DHA supplementation versus ascorbic acid in controlled scurvy-repletion or bioavailability designs using current plasma measurement standards.

4.2 Blood–Brain Barrier Transport and Central Nervous System Vitamin C Delivery

Vitamin C concentrations in the brain exceed those in blood by 10-fold, and in both tissues the vitamin is present primarily in the reduced form, ascorbic acid. Research identified the chemical form of vitamin C that readily crosses the blood–brain barrier and the mechanism of this process: ascorbic acid was not able to cross the blood–brain barrier, whereas the oxidized form, dehydroascorbic acid, readily entered the brain and was retained there in the form of ascorbic acid.

Transport of dehydroascorbic acid into the brain was inhibited by D-glucose but not by L-glucose. The facilitative glucose transporter GLUT1 is expressed on endothelial cells at the blood–brain barrier and is responsible for glucose entry into the brain; this transporter also transports dehydroascorbic acid into the brain. These findings define the transport of dehydroascorbic acid by GLUT1 as a mechanism by which the brain acquires vitamin C, and point to the oxidation of ascorbic acid as a potentially important regulatory step in the accumulation of the vitamin by the brain.

Dehydroascorbic acid was reduced to ascorbic acid after passing the blood–brain barrier and was retained in the brain as ascorbic acid. This trapping mechanism allows for the accumulation of higher concentrations of vitamin C in the brain than in the blood, and points to the oxidation of ascorbic acid as the critical step in the regulation of the accumulation of vitamin C in the brain.

The glucose transporter protein syndrome (GTPS) is caused by defective transport of glucose across the blood–brain barrier via GLUT1, resulting in hypoglycorrhachia, infantile seizures, and developmental delay. Investigation of the transport of vitamin C in its oxidized form (dehydroascorbic acid) via GLUT1 into erythrocytes of two patients with GTPS found that uptake of oxidized vitamin C was 61% of the mothers' values, consistent with the observation that vitamin C is transported in its oxidized form via GLUT1.

Evidence strength: The blood–brain barrier transport mechanism of DHA via GLUT1 is established at the mechanistic and animal level, with confirmatory human clinical evidence from the GTPS model. The JCI study of Agus et al. (1997) was conducted in rodent models; the human GTPS data provide indirect clinical validation. The full implications for supplementation in healthy humans remain unexplored in dedicated clinical trials.

4.3 Neuroprotection and Ischemic Stroke

Neuronal injury in ischemic stroke is partly mediated by cytotoxic reactive oxygen species. Although the antioxidant ascorbic acid does not penetrate the blood–brain barrier, its oxidized form, dehydroascorbic acid, enters the brain by means of facilitative transport.

A landmark preclinical study published in Proceedings of the National Academy of Sciences (2001) investigated DHA as a neuroprotective agent: Reversible or permanent focal cerebral ischemia was created by intraluminal middle cerebral artery occlusion in mice treated with vehicle, ascorbic acid, or DHA (40, 250, or 500 mg/kg), either before or after ischemia. Given before ischemia, DHA caused dose-dependent increases in postreperfusion cerebral blood flow, with reductions in neurological deficit and mortality. In reperfused cerebral ischemia, mean infarct volume was reduced from 53% and 59% in vehicle- and AA-treated animals, respectively, to 15% in 250 mg/kg DHA-treated animals (P < 0.05).

This promising murine result prompted investigation in a large-animal model: DHA, a blood–brain barrier transportable form of ascorbic acid, confers robust neuroprotection following murine stroke. In an effort to translate this strategy into human clinical trial, postischemic DHA administration was evaluated in a large-animal model; thirty-six adult male baboons were randomized to undergo transient cerebral artery occlusion and to receive postischemic dosing of either 500 mg/kg of DHA or vehicle, with primary outcomes of infarct volume and neurological function. The midpoint interim analysis revealed that DHA administration did not significantly improve either infarct volume or neurological function, and the study was terminated after a determination of statistical futility. The investigators were unable to confirm a neuroprotective effect for postischemic DHA administration in their large-animal model using a dosing scheme that was previously successful in rodents, and concluded that further analysis of the efficacy of DHA administration must be undertaken prior to clinical translation.

Because of available data, dehydroascorbic acid given intravenously has been proposed as an excellent candidate for human clinical trials in stroke; the broader context is that over several decades, multiple drugs effective in animal stroke models have uniformly failed when studied in humans.

Evidence strength: Compelling in murine models; not reproduced in a non-human primate (baboon) model at an equivalent dose scheme. No completed human clinical trials for stroke treatment have been published. The transition from rodent to large-animal models revealed a failure to replicate, significantly tempering enthusiasm for clinical translation.

4.4 Antiviral Activity

The literature contains many reports on the antiviral effects of vitamin C, and one study suggests dehydroascorbic acid has stronger antiviral effects and a different mechanism of action than ascorbic acid. Both AA and DHA have been shown to have antiviral effects in vitro against viruses including HSV-1 (herpes simplex virus type 1), influenza virus, and poliovirus, and DHA reportedly has much stronger antiviral effects than AA.

Evidence strength: In vitro only. No controlled human clinical trials have been conducted to assess DHA's antiviral effects as a discrete compound. All findings in this domain are preclinical and cannot be extrapolated to clinical efficacy.

4.5 Oncology — Cancer Research

Research into DHA as an anti-cancer agent is early-stage and largely theoretical or preclinical. In 1993, researchers found that cancer cells (but not normal cells) contain measurable quantities of homocysteine thiolactone. More recently, it was found that dehydroascorbic acid reacts with homocysteine thiolactone, converting it to the toxic compound 3-mercaptopropionaldehyde. These findings suggest that rapidly dividing tumor cells make unusually large amounts of homocysteine thiolactone and that administered dehydroascorbic acid entering cells could convert the thiolactone to mercaptopropionaldehyde, which could kill the cancer cells.

Evidence strength: Theoretical and in vitro only. This mechanism has not been validated in human clinical trials. The hypothesis is highly preliminary.

4.6 Skin and Cosmetic Applications

As a cosmetic ingredient, dehydroascorbic acid is used to enhance the appearance of the skin. It may be used in a process for permanent waving of hair and in a process for sunless tanning of skin. In human skin cells, DHA is reported to be absorbed up to five times faster and to levels two times higher than ascorbic acid; it is almost instantly converted to ascorbic acid once absorbed into a cell.

Evidence strength: The cosmetic use is empirically established and commercially practiced. The claim of faster skin absorption over ascorbic acid is referenced in patent literature; confirmatory peer-reviewed clinical data are limited.

5. Body Systems and Health Areas Associated with DHA

Central nervous system: The highest tissue concentrations of vitamin C are found in the brain, eyes, and adrenal glands. DHA's ability to cross the blood–brain barrier positions it as the primary vehicle by which brain tissue acquires and maintains ascorbate.
Immune system / neutrophils: Activated neutrophils secrete reactive oxygen species that oxidize extracellular ascorbic acid to DHA, which is then rapidly transported into the neutrophil and reduced to ascorbic acid, producing a 10-fold increase in internal ascorbic acid concentration.
Cardiovascular / red blood cells: Because red blood cells are less deformable in diabetes, research has explored an original concept linking decreased RBC deformability to RBC ascorbate and hyperglycemia, finding an inverse relationship between RBC ascorbate concentrations and osmotic deformability.
Endocrine / pancreas: It has been proposed that DHA might damage beta cells, though studies have given diverging results. Elevated DHA has been shown to inhibit insulin secretion in mice, and exposure of isolated mouse islets to DHA can reduce responsiveness of islets or lead to decreased insulin secretion.
Gastrointestinal: Both DHA and ascorbic acid are absorbed from the lumen of the human intestine, with absorption sites found along the entire length of the small intestine.
Antioxidant defense: Oxidative stress — an imbalance between oxidant and antioxidant agents — is associated with inflammation, aging, and diseases such as cancer, obesity, diabetes, and atherosclerosis. DHA participates in cellular antioxidant defense through the ascorbate recycling cycle.

6. Dosage Forms and Dosages Reported in Studies

DHA is not currently approved or widely marketed as a standalone dietary supplement in standard tablet or capsule form, due largely to its instability in aqueous media. The following dosages appear in the scientific and patent literature and are reported exactly as stated in those sources:

Ischemic stroke — murine model (PNAS, 2001): Reversible or permanent focal cerebral ischemia in mice was treated with DHA at doses of 40, 250, or 500 mg/kg, administered either before or after ischemia.
Ischemic stroke — non-human primate model (PubMed, 2014): Thirty-six adult male baboons were randomized to receive postischemic dosing of either 500 mg/kg of DHA or vehicle.
Bioavailability (oral, human — older studies): Dehydroascorbic acid given orally has been shown to be absorbed in humans, though these studies only examined relative bioavailability and have measurement limitations. Specific doses from these historical publications were not detailed in the indexed abstracts.
Parenteral nutrition context: The degradation of ascorbic acid stored in parenteral nutrition regimens is initially by oxidation, catalyzed by trace elements (particularly copper), with the initial degradation product being dehydroascorbic acid.
Intravenous proposals for stroke: Because of available data, dehydroascorbic acid given intravenously has been put forward as a candidate for human trials. No specific intravenous human dose has yet been established in a completed clinical trial.

For total vitamin C intake at low to moderate oral doses (30–180 mg/day), absorption is efficient, with up to 90% bioavailability; however, beyond 1000 mg/day, fractional absorption declines sharply to less than 50%, primarily due to the saturation of intestinal SVCT1. These pharmacokinetic figures apply to ascorbic acid and, by extension, to vitamin C delivered as DHA that is converted intracellularly.

7. Safety Considerations and Interactions

Glucose Transporter Competition

Dehydroascorbate competitively inhibits the uptake of 2-deoxy-D-glucose and of 3-O-methyl-D-glucose by human blood neutrophils; conversely, 2-deoxyglucose and 3-O-methylglucose competitively inhibit dehydroascorbate uptake. This competitive interaction between DHA and glucose at GLUT transporters has direct implications in hyperglycemic states.

The balance between the concentration of ascorbic acid and DHA is influenced by glucose concentration. In healthy individuals, mainly ascorbic acid is found with minimal DHA; however, diabetic patients and their non-diabetic close relatives have been found to have remarkably high DHA concentrations.

Pancreatic Beta-Cell Toxicity at Pharmacologic Doses

Dehydroascorbic acid at pharmacologic doses was found to be toxic to pancreatic islets, whose beta cells produce insulin. The explanation was based on chemical structure, in that dehydroascorbic acid has a similar chemical structure to the beta cell toxin alloxan. It has been shown that elevated DHA inhibits insulin secretion in mice, and exposure of isolated mouse islets to DHA can reduce the responsiveness of the islets or lead to decreased insulin secretion. Impaired recycling of ascorbic acid as a result of increased glucose metabolism may have implications for the role of ascorbic acid/DHA in insulin secretion in diabetes.

These findings are largely from animal and in vitro models. The clinical relevance to humans consuming dietary DHA at physiological concentrations from food is not established.

Irreversible Degradation to an Inactive Compound

DHA is an unstable molecule. Vitamin efficacy is, according to most literature reports, lost upon hydrolysis of the lactone ring of DHA, resulting in the formation of 2,3-diketogulonic acid (DKG). DHA is hydrolyzed to 2,3-diketogulonic acid (DKG), which has no vitamin C activity. This means that DHA that is not rapidly reduced to ascorbic acid inside cells is irreversibly lost as a functional vitamin C compound.

Interaction with Glutathione

Dehydroascorbic acid is reduced to ascorbic acid at neutral pH in the presence of thiol-containing reducing agents such as cysteine, homocysteine, 2-mercaptoethanol, and DTT. Because DHA reduction consumes glutathione, high loads of DHA could theoretically deplete cellular glutathione. Glutathione (GSH), used during DHA reduction, is regenerated from glutathione disulfide (GSSG) by glutathione reductase and NADPH, which is a product of glucose metabolism through the pentose phosphate pathway.

Stability and Metal Ion Interactions

Both AA and DHA are unstable compounds. In aqueous solutions, factors affecting the rate of their destruction include the pH of the solution and exposure to various metal ions, heat, light, and air, with DHA being considerably less stable than AA when subjected to comparable conditions. Trace elements such as copper catalyze the initial degradation of ascorbic acid to DHA in parenteral nutrition preparations, and temperature accelerates this process.

Intravenous Administration Safety (Animal Data)

Based on all available animal information, DHAA is considered safe in the proposed dosing regimes proposed for stroke research. However, no completed phase I/II human safety studies for intravenous DHA administration have been published.

References

Health Conditions

Health conditions that Dehydroascorbic acid may help support.

No conditions available.

Body Systems

Body systems that Dehydroascorbic acid may help support.

No body systems available.