Function of vitamin c:
1) It is used to prevent and treat scurvy.[9]
2) Vitamin C is an essential nutrient involved in the repair of tissue
3) enzymatic production of certain neurotransmitters.
4) It is required for the functioning of several enzymes and is important for immune
system function.
5) It also functions as an antioxidant.
6) Another biochemical role of vitamin C is to act as an antioxidant (a reducing agent) by
donating electrons to various enzymatic and non-enzymatic reactions.[10] Doing so converts
vitamin C to an oxidized state - either as semidehydroascorbic acid or dehydroascorbic acid.
These compounds can be restored to a reduced state by glutathione and NADPH-
dependent enzymatic mechanisms.[23][24][25]
protect cells and keeping them healthy
. maintaining healthy skin, blood vessels, bones and cartilage.
For many years, vitamin C has been a popular household remedy for the common cold
Heal wounds and form scar tissue
Aid in the absorption of iron
Sources
Foods containing vitamin C include citrus fruits, kiwifruit, guava, broccoli, Brussels sprouts, bell
peppers and strawberries
The richest natural sources of vitamin C are fruits and vegetables.[11] The vitamin is the most widely
taken nutritional supplement and is available in a variety of forms,[11] including tablets, drink mixes,
and in capsules.
Amount
Plant source[86]
(mg / 100g)
Kakadu plum 1000–5300[87]
Camu camu 2800[85][88]
Acerola 1677[89]
Seabuckthorn 695
Indian gooseberry 445[90][91]
Rose hip 426
Guava 228
Blackcurrant 200
Yellow bell pepper/capsicum 183
Red bell pepper/capsicum 128
Kale 120
Amount
Plant source[86]
(mg / 100g)
Kiwifruit, broccoli 90
Green bell pepper/capsicum 80
Loganberry, redcurrant, Brussels
80
sprouts
Cloudberry, elderberry 60
Papaya, strawberry 60
Orange, lemon 53
Pineapple, cauliflower 48
Cantaloupe 40
Grapefruit, raspberry 30
Passion fruit, spinach 30
Cabbage, lime 30
Amount
Plant source[86]
(mg / 100g)
Mango 28
Blackberry 21
Potato, honeydew melon 20
Tomato 14
Cranberry 13
Blueberry, grape 10
Apricot, plum, watermelo
10
n
Avocado 8.8
Onion 7.4
Cherry, peach 7
Carrot, apple, asparagus 6
Animal-sourced foods do not provide much vitamin C, and what there is, is largely destroyed by the
heat of cooking. For example, raw chicken liver contains 17.9 mg/100 g, but fried, the content is
reduced to 2.7 mg/100 g. Chicken eggs contain no vitamin C, raw or cooked.[86] Vitamin C is present
in human breast milk at 5.0 mg/100 g and 6.1 mg/100 g in one tested sample of infant formula, but
cow's milk contains only 1.0 mg/ 100 g
Toxicity
Large doses may cause gastrointestinal discomfort, headache, trouble sleeping, and flushing of the
skin.[9][13] Normal doses are safe during pregnancy.
or adults, the recommended daily amount for vitamin C is 65 to 90 milligrams (mg) a
day, and the upper limit is 2,000 mg a day. Although too much dietary vitamin C is
unlikely to be harmful, megadoses of vitamin C supplements might cause:
Diarrhea
Nausea
Vomiting
Heartburn
Abdominal cramps
Headache
Insomnia
Remember, f
Deficiency
Vitamin C cannot be made by the human body and so is an
essential component of the diet. It is needed for the health and
repair of various tissues in your body, including skin, bone, teeth
and cartilage. Persistent lack of vitamin C in your diet can lead to
a condition called scurvy. Symptoms of scurvy include easy
bruising, easy bleeding and joint and muscle pains. Vitamin C
deficiency can be treated with supplements of vitamin C and a
diet rich in vitamin C.
Tiredness and weakness.
Muscle and joint pains.
Easy bruising.
Spots that look like tiny, red-blue bruises on your skin.
Other symptoms can include:
Dry skin.
Splitting hair.
Swelling and discoloration of your gums.
Sudden and unexpected bleeding from your gums.
Nosebleeds.
Poor healing of wounds.
Problems fighting infections.
Bleeding into joints, causing severe joint pains.
Changes in your bones.
Tooth loss.
Weight loss.
Chemistry[edit]
ascorbic acid
(reduced form)
dehydroascorbic acid
(oxidized form)
Main article: Chemistry of ascorbic acid
The name "vitamin C" always refers to the L-enantiomer of ascorbic acid and its oxidized forms, such
as dehydroascorbate (DHA). Therefore, unless written otherwise, "ascorbate" and "ascorbic acid"
refer in the nutritional literature to L-ascorbate and L-ascorbic acid respectively. Ascorbic acid is
a weak sugar acid structurally related to glucose. In biological systems, ascorbic acid can be found
only at low pH, but in solutions above pH 5 is predominantly found in the ionized form, ascorbate. All
of these molecules have vitamin C activity and thus are used synonymously with vitamin C, unless
otherwise specified.
Numerous analytical methods have been developed for ascorbic acid detection. For example,
vitamin C content of a food sample such as fruit juice can be calculated by measuring the volume of
the sample required to decolorize a solution of dichlorophenolindophenol (DCPIP) and then
calibrating the results by comparison with a known concentration of vitamin C.
Pharmacokinetics[edit]
Absorption[edit]
From the U.S. National Institutes of Health: [In humans] "Approximately 70%–90% of vitamin C is
absorbed at moderate intakes of 30–180 mg/day. However, at doses above 1,000 mg/day,
absorption falls to less than 50%."[12] It is transported through the intestine via both glucose-sensitive
and glucose-insensitive mechanisms, so the presence of large quantities of sugar in the intestine
can slow absorption.[114]
Ascorbic acid is absorbed in the body by both active transport and simple diffusion. Sodium-
Dependent Active Transport—Sodium-Ascorbate Co-Transporters (SVCTs) and Hexose
transporters (GLUTs)—are the two transporter proteins required for active
absorption. SVCT1 and SVCT2 import the reduced form of ascorbate across plasma membranes.
[115]
GLUT1 and GLUT3 are glucose transporters, and transfer only the dehydroascorbic acid (DHA)
form of vitamin C.[116] Although dehydroascorbic acid is absorbed in higher rate than ascorbate, the
amount of dehydroascorbic acid found in plasma and tissues under normal conditions is low, as cells
rapidly reduce dehydroascorbic acid to ascorbate.[117]
Transport[edit]
SVCTs appear to be the predominant system for vitamin C transport in the body, [115] the notable
exception being red blood cells, which lose SVCT proteins during maturation.[118] In both vitamin C
synthesizers (example: rat) and non-synthesizers (example: human) cells with few exceptions
maintain ascorbic acid concentrations much higher than the approximately 50 micromoles/liter
(µmol/L) found in plasma. For example, the ascorbic acid content of pituitary and adrenal glands can
exceed 2,000 µmol/L, and muscle is at 200-300 µmol/L.[119] The known coenzymatic functions of
ascorbic acid do not require such high concentrations, so there may be other, as yet unknown
functions. Consequences of all this organ content is that plasma vitamin C is not a good indicator of
whole-body status, and people may vary in the amount of time needed to show symptoms of
deficiency when consuming a diet very low in vitamin C.[119]
Excretion[edit]
Excretion can be as ascorbic acid, via urine. In humans, during times of low dietary intake, vitamin C
is reabsorbed by the kidneys rather than excreted. Only when plasma concentrations are 1.4 mg/dL
or higher does re-absorption decline and the excess amounts pass freely into the urine. This salvage
process delays onset of deficiency.[120] Ascorbic acid also converts (reversibly) to dehydroascorbate
(DHA) and from that compound non-reversibly to 2,3-diketogluonate and then oxalate. These three
compounds are also excreted via urine. Humans are better than guinea pigs at converting DHA back
to ascorbate, and thus take much longer to become vitamin C deficient
Vitamin C was discovered in 1912, isolated in 1928 and synthesized in 1933, making it the first
vitamin to be synthesized.[17] Shortly thereafter Tadeus Reichstein succeeded in synthesizing the
vitamin in bulk by what is now called the Reichstein process.[177] This made possible the inexpensive
mass-production of vitamin C. In 1934 Hoffmann–La Roche trademarked synthetic vitamin C under
the brand name Redoxon[178] and began to market it as a dietary supplement.[b]
In 1907 a laboratory animal model which would help to identify the antiscorbutic factor was
discovered by the Norwegian physicians Axel Holst and Theodor Frølich, who when studying
shipboard beriberi, fed guinea pigs their test diet of grains and flour and were surprised when scurvy
resulted instead of beriberi. By luck, this species did not make its own vitamin C, whereas mice and
rats do.[180] In 1912, the Polish biochemist Casimir Funk developed the concept of vitamins. One of
these was thought to be the anti-scorbutic factor. In 1928, this was referred to as "water-soluble C,"
although its chemical structure had not been determined.[181]
Albert Szent-Györgyi, pictured here in 1948, was awarded the 1937 Nobel Prize in Medicine "for his discoveries
in connection with the biological combustion processes, with special reference to vitamin C and the catalysis of
fumaric acid".[21]
From 1928 to 1932, Albert Szent-Györgyi and Joseph L. Svirbely's Hungarian team, and Charles
Glen King's American team, identified the anti-scorbutic factor. Szent-Györgyi isolated hexuronic
acid from animal adrenal glands, and suspected it to be the antiscorbutic factor. [182] In late 1931,
Szent-Györgyi gave Svirbely the last of his adrenal-derived hexuronic acid with the suggestion that it
might be the anti-scorbutic factor. By the spring of 1932, King's laboratory had proven this, but
published the result without giving Szent-Györgyi credit for it. This led to a bitter dispute over priority.
[182]
In 1933, Walter Norman Haworth chemically identified the vitamin as L-hexuronic acid, proving
this by synthesis in 1933.[183][184][185][186] Haworth and Szent-Györgyi proposed that L-hexuronic acid be
named a-scorbic acid, and chemically L-ascorbic acid, in honor of its activity against scurvy.[186][17] The
term's etymology is from Latin, "a-" meaning away, or off from, while -scorbic is from Medieval
Latin scorbuticus (pertaining to scurvy), cognate with Old Norse skyrbjugr, French scorbut,
Dutch scheurbuik and Low German scharbock.[187] Partly for this discovery, Szent-Györgyi was
awarded the 1937 Nobel Prize in Medicine,[188] and Haworth shared that year's Nobel Prize in
Chemistry.[21]
In 1957, J.J. Burns showed that some mammals are susceptible to scurvy as their liver does not
produce the enzyme L-gulonolactone oxidase, the last of the chain of four enzymes that synthesize
vitamin C.[189][190] American biochemist Irwin Stone was the first to exploit vitamin C for its food
preservative properties. He later developed the theory that humans possess a mutated form of the L-
gulonolactone oxidase coding gene.[191]
In 2008, researchers at the University of Montpellier discovered that in humans and other primates
the red blood cells have evolved a mechanism to more efficiently utilize the vitamin C present in the
body by recycling oxidized L-dehydroascorbic acid (DHA) back into ascorbic acid for reuse by the
body. The mechanism was not found to be present in mammals that synthesize their own vitamin C.
[144]