Abstract
Parenteral administration of ascorbate raises plasma and tissue concentrations of the vitamin and may decrease morbidity. Ascorbate quickly accumulates in microvascular endothelial cells, scavenges reactive oxygen species, and acts through tetrahydrobiopterin to stimulate nitric oxide production by endothelial nitric oxide synthase. A major reason for the long duration of the improvement in microvascular function is that cells retain high levels of ascorbate, which alter redox-sensitive signaling pathways to diminish septic induction of NADPH oxidase and inducible nitric oxide synthase.
These observations are consistent with the hypothesis that microvascular function in sepsis may be improved by parenteral administration of ascorbate as an adjuvant therapy.
Identification
It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone.
Vitamin C is considered an antioxidant. Administration of ascorbic acid completely reverses the symptoms of ascorbic acid deficiency. The two forms found in body fluids are physiologically active.
Some ascorbic acid is metabolized to inactive compounds including ascorbic acid-2-sulfate and oxalic acid. Hover over products below to view reaction partners Ascorbic acid ascorbic acid-2-sulfate Dehydroascorbate 2,3-dikeogulonic acid Erythrulose Threosone Oxalic acid
Route of elimination
Not Available
Half-life
16 days (3.4 hours in people who have excess levels of vitamin C)
Clearance
Not Available
Adverse Effects
Toxicity
Not Available
Pathways
Pharmacogenomic Effects/AD.
Related Terms:
Ascorbic acid is mainly found in fresh fruits (e.g., blackcurrant, strawberry, lemon, orange, lime) and vegetables (e.g., broccoli, Brussels sprouts, cauliflower, cabbage).
Intestinal absorption of ascorbic acid is an active, energy-requiring and saturable process. In plasma, vitamin C is nonprotein-bound and is present in a reduced form. The body ascorbic acid pools are regulated by intestinal absorption, renal tubule reabsorption, and the catabolism of ascorbic acid [33].
Excess ascorbic acid is filtered at the glomerulus and excreted intact in the urine. Ascorbic acid can be oxidized to DHAA and then to a variety of compounds including L-xylose, threonic acid and oxalic acid which are excreted in urine. The methods for assessment of ascorbic acid have evolved from colorimetric methods, based on the reductive properties of ascorbic acid, to HPLC technology which is sensitive and specific [33].
The oxidized form of ascorbic acid, the ascorbyl free radical (AFR), can be detected by electron paramagnetic resonance spectroscopy. Ascorbic acid is measured in plasma, which reflects recent dietary intake, and in leukocytes, which gives a more accurate estimate of the body pool of ascorbic acid. The function of ascorbic acid is largely due to its reversible reducing power.
For instance, ascorbic acid plays an important role in metal catalysed hydroxylations by reducing the metal catalyst and by allowing the metal–enzyme complex to reconstitute after it is oxidized.
Vitamin C
Ascorbic acid is mainly found in fresh fruits (e.g., blackcurrant, strawberry, lemon, orange, lime) and vegetables (e.g., broccoli, Brussels sprouts, cauliflower, cabbage). About 70 to 90% of the usual dietary vitamin C intake is absorbed, but this fraction decreases substantially when large loads of ascorbic acid are ingested.
Ascorbic acid enters the cell by active transport. The body ascorbic acid pools are regulated by intestinal absorption, renal tubule reabsorption, and the catabolism of ascorbic acid [33]. The methods for assessment of ascorbic acid have evolved from colorimetric methods, based on the reductive properties of ascorbic acid, to HPLC technology which is sensitive and specific [33].
Ascorbic acid is measured in plasma, which reflects recent dietary intake, and in leukocytes, which gives a more accurate estimate of the body pool of ascorbic acid. For instance, ascorbic acid plays an important role in metal catalysed hydroxylations by reducing the metal catalyst and by allowing the metal–enzyme complex to reconstitute after it is oxidized.