Vitamin C: Functions and Food Sources
Vitamin C: Functions and Food Sources
Vitamins are essential nutrients that are required for various biochemical and physiological
processes in the body. It is well known that most of the vitamins cannot be synthesized in the
body and hence their supplementation in diet is essential. Vitamins are classified on the basis of
their solubility as water soluble (C and B complexes) and fat soluble vitamins (A, D, E, K).
Vitamin C or ascorbic acid (AA) was first isolated in 1923 by Hungarian biochemist and Nobel
laureate Szent-Gyorgyi and synthesized by Haworth and Hirst (Haworth WN, 1933). It is a
simple low-molecular-weight carbohydrate with an ene-diol structure that has made it a
ubiquitous and essential water-soluble electron donor in nature. It exists in reduced (ascorbate)
and oxidized forms as dehydroascorbic acid which are easily inter-convertible and biologically
active thus it acts as important antioxidant. Vitamin C is easily oxidized acid and destroyed by
oxygen, alkali and high temperature. Most of the plant and animal species have the ability to
synthesize vitamin C from glucose and galactose through uronic acid pathway but man and other
primates cannot do so because of deficiency of enzyme gulonolactone oxidase required for it’s
biosynthesis. Deficiency of this enzyme is a result of a mutation which occurred approximately
40 million years ago (Nishikimi M, Fukuyama R, Minoshima S, Shimizu N, Yagi K, 1994).
Vitamin C acts as a reductant, i.e., it donates an electron to a substrate while itself being oxidized
to an ascorbyl radical, a relatively stable free radical. Two molecules of ascorbyl free radical can
dismutate into 1 molecule of ascorbate and 1 molecule of dehydroascorbic acid, the fully reduced
and oxidized forms of vitamin C, respectively.
The body requires vitamin C for normal physiological functions. It helps in the synthesis and
metabolism of tyrosine, folic acid and tryptophan, hydroxylation of glycine, proline, lysine
carnitine and catecholamine. It facilitates the conversion of cholesterol into bile acids and hence
lowers blood cholesterol levels. It also increases the absorption of iron in the gut by reducing
ferric to ferrous state. As an antioxidant, it protects the body from various deleterious effects of
free radicals, pollutants and toxins. The therapeutic effect of vitamin C was explored by Linus
Pauling however his work on therapeutic role of vitamin C in his later years generated much
controversy yet he was the first to introduce the concept of high doses of vitamin C for the
treatment of various conditions from common cold to cancer (Dunitz JD. Linus Carl Pauling,
Page | 1
1996). Since then mega doses of vitamin C have been widely used in the treatment and
prevention of a large number of disorders like diabetes, atherosclerosis, common cold, cataracts,
glaucoma, macular degeneration, stroke, heart diseases, cancer and so on.
Deficiency of this vitamin is often associated with anemia, infections, bleeding gums, scurvy,
poor wound healing, capillary haemorrhage, muscle degeneration, atherosclerotic plaques and
neurotic disturbances. For the correction of deficiency, vitamin C is often supplemented in large
doses and unlike fat soluble vitamins, toxicity is rare. Recently the role of vitamin C in infection
and immunity has also been investigated. In view of the vast biological, physiological functions
and therapeutic role of vitamin C, this review is an attempt to summarise various evidences in
this context.
FOOD SOURCES
Fruit and vegetables are good sources of vitamin C, and ~90% of the daily intake in the general
population comes from these sources. The content varies between species. Vitamin C is found in
citrus fruits, green peppers, red peppers, strawberries, tomatoes, broccoli, brussels sprouts,
turnip, Indian gooseberry and other leafy vegetables. The animal sources are poor in vitamin C
content and the level is usually <30–40 mg/100 g. Therefore plant sources become important
because of high content of vitamin C up to 5,000 mg/100 g. It’s absorption in the buccal cavity is
by passive diffusion however in gastrointestinal tract absorption is by active sodium dependent
vitamin C transporters Because vitamin C degrades when heated and during storage, the
processing and preparation procedures should be considered when estimating dietary intake of
vitamin C. A total of 5–9 servings of fresh, minimally processed, or frozen fruit and vegetables
per day is estimated to equal ~200 mg of vitamin C. The presence of vitamin C in dietary
products other than fruit and vegetables is typically due to its addition as a preservative to
processed foods to protect against oxidation. In areas where vegetation is sparse, such as the
arctic regions, people have traditionally relied on alternative sources of vitamin C, such as
medicinal herbs (herbal teas and tinctures from rose hips, pine needles, and tree barks) and
animal organs, such as raw liver and whale skin. (Stevenson NR, Brush MK, 1969; Malo C,
Wilson JX, 2003)
Page | 2
BIOAVAILABILITY OF VITAMIN C
Together, intestinal absorption and renal excretion controls the serum level of vitamin C and thus
its bioavailability. At low concentrations, most vitamin C is absorbed in the small intestine and
reabsorbed from the renal tubule (Nelson EW, Lane H, Fabri PJ, Scott B, 1978). However, at
high concentrations, SVCT1 is down regulated (MacDonald L, Thumser AE, Sharp P, 2002)
which limits the amount of AA absorbed from the intestine and kidney (Wilson JX, 2005)
Vitamin C levels in circulating blood cells, such as platelets, are much higher than the plasma
(Levine M, Conry-Cantilena C, Wang Y, Welch RW, Washko PW, Dhariwal KR, et al, 1996), as
these cells express the SVCT2 transporter (Dixon SJ, Wilson JX, 1992), which mediates
intracellular ascorbate accumulation (Li Y, Schellhorn Herb E, 2007).
Reduced bioavailability of vitamin C is often seen in stress, alcohol intake, smoking, fever, viral
illnesses, usage of antibiotics, pain killers, exposure to petroleum products or carbon monoxide,
heavy metals toxicity and so on. However, the precise mechanism behind low vitamin C level in
the body is not well defined. Presumably, an increased utilization of this vitamin in these
conditions and/or a decreased absorption from the gut could be a cause of decreased vitamin C
level (Kallner AB, Hartmann D, Horning DH, 1979). In the event of high consumption, AA and
its metabolites such as dehydroascorbic acid, 2,3-diketogulonic acid and oxalic acid are excreted
via kidney in humans. AA is generally non-toxic but at high doses (2–6 g/day) it can cause
gastrointestinal disturbances or diarrhoea (Anderson D, Phillips BJ, Yu T, Edwards AJ, Ayesh R,
Butterworth KR, 1997; Johnson CS, 1999). The side effects are generally not serious and can be
easily reversed by reducing the intake of AA(Naidu AK, 2003).
Page | 3
BIOCHEMICAL FUNCTIONS OF VITAMIN C
The biochemical functions of AA are largely dependent on the oxido-reduction properties of L-
AA which is a co-factor for hydroxylation and activity of mono-oxygenase enzymes in the
synthesis of collagen, carnitine and neurotransmitters (Levin M, 1986). AA accelerates
hydroxylation reactions by maintaining the active centre of metal ions in a reduced state for
optimal activity of enzymes hydroxylase and oxygenase. Thus, it is crucial in the maintenance of
collagen which represents about one-third of the total body protein.
Collagen constitutes the principal protein of skin, bones, teeth, cartilage, tendons, blood vessels,
heart valves, inter vertebral discs, cornea, eye lens. AA is essential to maintain the enzyme prolyl
and lysyl hydroxylase in an active form. AA deficiency results in reduced hydroxylation of
proline and lysine, thus affecting collagen synthesis. AA is also an essential co-factor for
hydroxylations involved in the synthesis of muscle carnitine “β-hydroxybutyric acid” (Hulse JD,
Ellis SR, Henderson LM, 1978; Rebouche CJ, 1991). Carnitine is required for the transport and
transfer of long chain fatty acids into mitochondria for energy production. Further, AA is also a
co-factor for the enzyme dopamine-β-hydroxylase, which catalyzes the conversion of
neurotransmitter dopamine to norepinephrine (Naidu AK, 2003). It is also involved in the
transformation of cholesterol to bile acids as it modulates the microsomal 7α-hydroxylation, the
rate limiting reaction of cholesterol catabolism in liver(Anon, 1973).
USES OF VITAMIN C
Apart from the well accepted role of vitamin C in the prevention of scurvy, the most widely
known health beneficial effect of AA is in the prevention and relief of common cold. Pauling
was the first to introduce the concept of high dose of vitamin C and suggested that ingestion of
1–3 g of AA effectively prevents/ameliorates common cold (Pauling L, 1970)
Wound healing requires synthesis and accumulation of collagen and subsequent cross-linking of
the fibre to give new tensile strength to the damaged tissue. An early study demonstrated that
maximum tensile strength of scar tissue in guinea pig was achieved after supplementation of
vitamin C (Bourne GH, 1946).
Page | 4
AA is known to enhance the availability and absorption of iron from non-heme iron sources
(Hallberg L, 1981). It’s supplementation is found to facilitate the dietary absorption of iron. The
reduction of iron by AA has been suggested to increase dietary absorption of non-heme iron
(Bendich A, Cohen M, 1990; Zhang Y, Zhao D, Xu J, Xu C, Dong C, Liu Q, et al, 2013).
Vitamin C rich fruits such as goose berry has been reported to increase the bioavailability of iron
from staple cereals and pulses (Gowri S, Patel K, Prakash J, Srinivasan K, 2001).
Vitamin C has been used in the management of male infertility on empirical grounds,
particularly in the presence of non-specific seminal infections (Mathur V, Murdia A, Hakim AA,
Suhalka ML, Shaktawat GS, Kothari LK, 1979). Chinoy (Chinoy NJ, 1978) stated that AA was
essential for the structural and functional integrity of androgen-dependent reproductive organs.
It was also reported that the deficiency of vitamin C leads to enhanced accumulation of
cholesterol in thoracic aorta along with pathomorphological changes in blood vessels (Ginter E,
Babla J, Cerven J, 1969; Sharma P, Pramod J, Sharma PK, Chaturvedi SK, Kothari LK, 1988;
Kothari LK, Sharma P, 1988). Various human trials have also indicated vitamin C induced
reduction in blood lipid levels in normal and hypercholesterolemic subjects (Vaney N, Sharma P,
Pramod J, Varandami J, Kothari LK., 1988; Gaur GS, Dixit AK, 2012)
The notion that vitamin C may have a preventive role in cancer was first proposed in 1949. It
was demonstrated by Cameron et al. (Cameron E, Campbell A, 1974; Cameron E, Pauling
L,1976; Cameron E, Pauling L, 1978), that high-dose vitamin C improved the survival of
patients with terminal cancer. Several research panels and committees have independently
concluded that high fruit and vegetable intake reduces the risk of different types of cancer (Block
G, Patterson B, Subar A, 1992; Steinmetz KA, Potter JD, 1996) and mortality rate was also
found to be inversely related to vitamin C intake (Loria CM, Klag MJ, Caulfield LE, Whelton
PK, 2000; Khaw KT, Bingham S, Welch A, Luben R, Wareham N, Oakes S, Day N, 2001).
Vitamin C has been associated with decreased risk of developing diabetes mellitus (DM). In
Norfolk Prospective Study the association between fruit and vegetable intake and plasma levels
of vitamin C and risk of type 2 DM was observed (Harding AH, Wareham NJ, Bingham SA,
Khaw K, Luben R, Welch A, et al, 2008). In recent experimental studies it has been found that
Vitamin C and E supplementation relieves oxidative stress in the blood and tissues of diabetic
Page | 5
aged rats by modulating the antioxidant system and lipid profile (Özkaya D, Naziroğlu M,
Armağan A, Demirel A, Köroglu BK, Çolakoğlu N, et al, 2011; Naziroğlu M, Butterworth PJ,
Sonmez TT, 2011).
Vitamin C affects several components of the human immune system. Vitamin C appears to play
a role in a number of neutrophil functions including increased chemotaxis, increased particulate
ingestion, enhanced lysozyme-mediated non-oxidative killing, protection against the toxic effects
of superoxide anion radical, inhibition of the halide-peroxide-myeloperoxidase system without a
pronounced bactericidal effect, and stimulation of the hexose monophosphate shunt (Leibovitz
B, Siegel BV, 1978)
Various experimental studies report the beneficial effect of vitamin C against heavy metal
toxicity. Lead is considered as one of the common environmental poison in which protective role
of vitamin C is extensively studied(Shaban El-Neweshy M, 2011). Vitamin C was also observed
to be protective against concomitant exposure to heavy metal and radiation in many experimental
studies. (Gajawat S, Sancheti G, Goyal PK, 2005).
Simple water soluble vitamin C, adequately present in fruits and vegetables had drawn attention
of the psychiatrists for the treatment of schizophrenia patients (Lucksch F, 1940). Oral
supplementation of vitamin C with antipsychotic reverses AA levels, reduces oxidative stress,
and improves BPRS score, hence both the drugs in combination can be used in the treatment of
schizophrenia (Dakhale GN, Khanzode SD, Khanzode SS, Saoji A, 2005)
To determine the concentration of Vitamin C(AA) by titration from given sample solution by (50
times) redox titration using Iodine Solution.
OBJECTIVE
Lemon, Lime, Tomato, Orange, Grapes(Green and Purple), Pomegranate, Apple, Kiwi, Basil,
Carrot, Radish, Bittergourd, Garlic, Coriander Leaves, Potato, Green Chilli, Green Pea, Brinjal,
Pumpkin, Pappaya, Cucumber, Onion, Cabbage, Beans, Cauliflower and Tamarind.
Page | 6
MATERIALS AND METHODS
Materials Required:
Glass
Burette
Burette Stand
100ml volumetric flask
Measuring Cylinder
Micropipette
Weighing machine, and
Knife
Chemicals Required:
Potassium iodide
Iodine crystals
Soluble starch
Distilled water
This method determines the vitamin C concentration in a solution by a redox titration using
iodine. Vitamin C, more properly called ascorbic acid, is an essential antioxidant needed by the
human body (see additional notes). As the iodine is added during the titration, the ascorbic acid
is oxidised to dehydroascorbic acid, while the iodine is reduced to iodide ions.
Due to this reaction, the iodine formed is immediately reduced to iodide as long as there is any
ascorbic acid present. Once all the ascorbic acid has been oxidised, the excess iodine is free to
react with the starch indicator, forming the blue-black starch-iodine complex. This is the
endpoint of the titration.
The method is suitable for use with vitamin C tablets, fresh or packaged fruit juices and solid
fruits and vegetables. This method is more straight forward than the alternative method using
potassium iodate, but as the potassium iodate solution is more stable than the iodine as a primary
standard, the alternative method is more reliable.
Page | 7
PREPARATION AND PROCEDURE FOR ESTIMATION OF VITAMIN C
Preparation of chemicals
Pipette 2ml of the original solution(OS) in a conical flask and the add 98ml of distilled
water to it to attain the dilute sample solution(SS) i.e., 50 times.
Pipette 20ml of the SS into a 250ml conical flask and then add about 150ml of distilled
water to it followed by addition of 3ml starch indicator solution(SI).
Titrate the SS with 0.005 mol l -1 iodine solution. The end point of the titration is
identified as the first permanent trace of a dark blue black color due to the starch iodide
complex.
Repeat the titration with further aliquots of SS until you obtain concordant results.
AA + I2 → 2 I− + Dehydroascorbic Acid
The vitamin C concentrations, obtained through redox titration method are discussed and
tabulated.
Page | 8
Vitamin C concentration
It is evident from the present findings that concentration of vitamin C varies from 4.00 mg/100g
to 89.446 mg/100mL (Table I).
Page | 9
6.6 8.8 2.2 2.2
8.8 11.2 2.4
11.2 13.4 2.2
Page | 10
30.2 32.4 2.2
Page | 11
30.6 32.6 2.0 2.0
32.6 34.6 2.0
34.6 36.6 2.0
Page | 12
19.0 20.4 1.4
CALCULATION
AA + I2 → 2 I− + Dehydroascorbic Acid
As iodine solution is taken as the standard solution, it is taken as 0.005 mol l-1.
=2
N = CV
Page | 13
NAA = 2N
M = NAA * MAA
1. For Lemon,
The weight of the given sample was measured before and after extracting the juice i.e.,
OS.
Weight of the sample before extracting the juice = 26.18g
Weight of the sample after extracting the juice = 11.44g
Original solution(OS) = 26.18g - 11.44g = 15.0g
N = CV
2. For Lime,
The weight of the given sample was measured before and after extracting the juice i.e.,
OS.
Weight of the sample before extracting the juice = 113.39g
Weight of the sample after extracting the juice = 90.0g
Original solution(OS) = 113.39g - 90.0g = 23.39g
Page | 14
N = CV
= 0.005 *2.0 /1000
= 0.01/1000 mol
Then, NAA = 2N
= 2* 0.01/1000 mol
Finally, M = NAA * MAA
= 2* 0.01/1000 * 176.12
= 3.52mg
So, 23.39g of OS of Lime contains 3.52mg of AA.
So, 100g OS of Lime will contain = 3.52/23.39 * 100
= 15.05mg
3. For Tomato,
The weight of the given sample was measured before and after extracting the juice i.e.,
OS.
Weight of the sample before extracting the juice = 74.76g
Weight of the sample after extracting the juice = 54.70g
Original solution(OS) = 74.76g – 54.70g = 17.06g
N = CV
= 0.005 *1.6 /1000
= 0.008/1000 mol
Then, NAA = 2N
= 2* 0.008/1000 mol
Finally, M = NAA * MAA
= 2* 0.008/1000 * 176.12
= 2.81mg
So, 17.06g of OS of Tomato contains 2.81mg of AA.
So, 100g OS of Tomato will contain = 2.81/17.06 * 100
= 16.57mg
4. For Orange,
Page | 15
The weight of the given sample was measured before and after extracting the juice i.e.,
OS.
Weight of the sample before extracting the juice = 143.27g
Weight of the sample after extracting the juice = 130.65g
Original solution(OS) = 143.27g - 130.65g = 12.61g
N = CV
= 0.005 *2.2 /1000
= 0.011/1000 mol
Then, NAA = 2N
= 2* 0.011/1000 mol
Finally, M = NAA * MAA
= 2* 0.011/1000 * 176.12
= 3.87mg
So, 12.61g of OS of Orange contains 3.87mg of AA.
So, 100g OS of Orange will contain = 3.87/12.61 * 100
= 30.72mg
Page | 16
So, 15.60g of OS of Green grapes contains 3.87mg of AA.
So, 100g OS of Green grapes will contain = 3.87/15.60 * 100
= 24.82g
Then, NAA = 2N
= 2* 0.011/1000 mol
Finally, M = NAA * MAA
= 2* 0.011/1000 * 176.12
= 3.87mg
So, 18.40g of OS of Purple grapes contains 3.87mg of AA.
7. For Pomegranate,
The weight of the given sample was measured before and after extracting the juice i.e.,
OS.
Weight of the sample before extracting the juice = 184.30g
Weight of the sample after extracting the juice = 169.05g
Original solution(OS) = 184.30g – 169.05g = 15.25g
N = CV
Page | 17
= 0.005 *1.0 /1000
= 0.005/1000 mol
Then, NAA = 2N
= 2* 0.005/1000 mol
Finally, M = NAA * MAA
= 2* 0.005/1000 * 176.12
= 1.76mg
So, 15.25g of OS of Pomegranate contains 1.76mg of AA.
So, 100g OS of Pomegranate will contain = 1.76/15.25 * 100
= 11.54mg
8. For Apple,
The weight of the given sample was measured before and after extracting the juice i.e.,
OS.
Weight of the sample before extracting the juice = 118.55g
Weight of the sample after extracting the juice = 30.52g
Original solution(OS) = 118.55g – 30.52g = 88.02g
N = CV
= 0.005 *2.0 /1000
= 0.01/1000 mol
Then, NAA = 2N
= 2* 0.01/1000 mol
Finally, M = NAA * MAA
= 2* 0.01/1000 * 176.12
= 3.52mg
So, 88.02g of OS of Apple contains 3.52mg of AA.
So, 100g OS of Apple will contain = 3.52/88.02 * 100
= 4.00mg
9. For Basil,
Page | 18
The weight of the given sample was measured before and after extracting the juice i.e.,
OS.
Weight of the sample before extracting the juice = 12.69g
Weight of the sample after extracting the juice = 2.04g
Original solution(OS) = 12.69g – 2.04g = 10.65g
N = CV
= 0.005 *2.4 /1000
= 0.012/1000 mol
Then, NAA = 2N
= 2* 0.012/1000 mol
Finally, M = NAA * MAA
= 2* 0.012/1000 * 176.12
= 4.22mg
So, 10.653g of OS of Basil contains 4.22mg of AA.
So, 100g OS of Basil will contain = 4.22/10.653 * 100
= 39.66mg
Page | 19
So, 8.48g of OS of Carrot contains 2.81mg of AA.
So, 100g OS of Carrot will contain = 2.81/8.48 * 100
= 39.66mg
Page | 20
= 0.013/1000 mol
Then, NAA = 2N
= 2* 0.013/1000 mol
Finally, M = NAA * MAA
= 2* 0.013/1000 * 176.12
= 4.57mg
So, 6.76g of OS of Bittergourd contains 4.57mg of AA.
So, 100g OS of Bittergourd will contain = 4.57/9.86 * 100
= 35.69mg
Page | 21
Weight of the sample before extracting the juice = 8.99g
Weight of the sample after extracting the juice = 3.42g
Original solution(OS) = 8.99g – 3.42g = 5.57g
N = CV
= 0.005 *2.0 /1000
= 0.01/1000 mol
Then, NAA = 2N
= 2* 0.01/1000 mol
Finally, M = NAA * MAA
= 2* 0.01/1000 * 176.12
= 3.52mg
So, 5.57g of OS of Coriander leaves contains 3.52mg of AA.
So, 100g OS of Coriander leaves will contain = 3.52/5.57 * 100
= 63.22mg
Page | 22
= 33.62g
Page | 23
Then, NAA = 2N
= 2* 0.012/1000 mol
Finally, M = NAA * MAA
= 2* 0.012/1000 * 176.12
= 4.22mg
So, 8.30g of OS of Green pea contains 4.22mg of AA.
So, 100g OS of Green pea will contain = 4.22/8.30 * 100
= 50.87mg
= 2* 0.01/1000 * 176.12
= 3.52mg
So, 9.79g of OS of brinjal contains 3.52mg of AA.
So, 100g OS of brinjal will contain = 3.52/9.79 * 100
= 35.95mg
Page | 24
Weight of the sample before extracting the juice = 97.53g
Weight of the sample after extracting the juice = 86.87g
Original solution(OS) = 97.53g– 86.87g = 10.66g
N = CV
= 0.005 *2.2 /1000
= 0.011/1000 mol
Then, NAA = 2N
= 2* 0.011/1000 mol
Finally, M = NAA * MAA
= 2* 0.011/1000 * 176.12
= 3.87mg
So, 10.66g of OS of Pumpkin contains 3.87mg of AA.
So, 100g OS of Pumpkin will contain = 3.87/10.66 * 100
= 36.34mg
Page | 25
So, 100g OS of Papaya will contain = 3.87/8.53 * 100
= 45.41mg
Page | 26
Then, NAA = 2N
= 2* 0.008/1000 mol
Finally, M = NAA * MAA
= 2* 0.008/1000 * 176.12
= 2.817mg
So, 9.16g of OS of Onion contains 2.81mg of AA.
So, 100g OS of Onion will contain = 2.81/9.16 * 100
= 30.75mg
= 2* 0.009/1000 * 176.12
= 3.170mg
So, 7.33g of OS of Cabbage contains 3.17mg of AA.
So, 100g OS of Cabbage will contain = 3.17/7.33 * 100
= 43.20mg
Page | 27
Weight of the sample before extracting the juice = 17.10g
Weight of the sample after extracting the juice = 11.13g
Original solution(OS) = 17.10g– 11.13g = 5.96g
N = CV
= 0.005 *1.4 /1000
= 0.007/1000 mol
Then, NAA = 2N
= 2* 0.007/1000 mol
Finally, M = NAA * MAA
= 2* 0.007/1000 * 176.12
= 2.46mg
So, 5.964g of OS of Beans contains 2.46mg of AA.
= 41.33mg
Page | 28
So, 14.62g of OS of cauliflower contains 4.22mg of AA.
So, 100g OS of cauliflower will contain = 4.22/14.62 * 100
= 50.79mg
Page | 29
Then, NAA = 2N
= 2* 0.009/1000 mol
Finally, M = NAA * MAA
= 2* 0.009/1000 * 176.12
= 3.17
So, 3.54g of OS of Tamarind contains 3.17mg of AA.
So, 100g OS of Tamarind will contain = 3.17/3.54 * 100
= 89.44mg
Page | 30
Figure 2: Iodine Solution Figure 3: Starch Soution
Figure 4: Sample
Solution Figure5:
Redox Titration
Page | 31
Figure 6: Micropipette
CONCLUSION
The present study aims to “Determine the concentration of vitamin C by titration from given
sample solution by redox titration using iodine solution”. This was undertaken after going
through various literatures that mention about analysis of vitamin C content. During the review
of literatures it was found that lots of reports are available on vitamin C estimation but detail
study on these edible fruits and vegetables were not there. Therefore, this study was attempted on
vitamin C content of lemon, lime, tomato, orange, grapes(green and purple), pomegranate, apple,
AA Concentration (mg/100g)
basil, carrot, radish, bittergourd, garlic, coriander, potato, green chilli, green pea, brinjal,
pumpkin, papaya, cucumber, onion, cabbage, beans, cauliflower, kiwi and tamarind.
The objective of the study is to analyze the quantity of vitamin C present mg/100g among the
above edible animal fruits and vegetables.
Vitamin C concentration of lemon is 18.78 mg/100g, lime is 15.05 mg/100g, tomato is 16.57
Basil
mg/100g, orange is 30.70 mg/100g, green grapes is 24.82 mg/100g, purple grapes is 21.05
Garlic
Tamarind
mg/100g, pomegranate is 11.54 mg/100g, apple is 4.00 mg/100g, basil is 39.66 mg/100g, carrot
Kiwi
is 33.21 mg/100g, radish is 35.69 mg/100g, bittergourd is 67.66 mg/100g, garlic is 41.01
AA Concentration (mg/100g)
Cauliflower
mg/100g, coriander is 63.22 mg/100g, potato is 33.62 mg/100g, green chilli is 45.59 mg/100g,
Beans
Cabbage
green pea is 50.87 mg/100g, brinjal is 35.95 mg/100g, pumpkin is 36.34 mg/100g, papaya is
Onion
45.41 mg/100g, cucumber is 24.24 mg/100g, onion is 30.75 mg/100g, cabbage is 43.20 mg/100g,
Cucumber
Papaya
beans is 41.33 mg/100g,cauliflower is 50.79 mg/100g, kiwi is 22.26 mg/100g, tamarind is 89.44
Pumpkin
mg/100g. Brinjal
SAMPLES USED
GreenPea
It is evident from the present findings that concentration of vitamin C varies from 4.00 mg/100g
GreenChilli
Potato
to 89.446 mg/100g. Coriander
Bittergourd
Vitamin C concentration was found to be highest in Tamarind and lowest in Apple.
Radish
Carrot
Apple
Pomegranate
Purplegrapes
Greengrapes
Page | 32
Orange
Tomato
Lime
Lemon
100
0
90
50
40
10
80
70
60
30
20
CONC. OFAA(mg/100g)
REFERENCES
Anderson D, Phillips BJ, Yu T, Edwards AJ, Ayesh R, Butterworth KR. The effect of vitamin C
supplementation on biomarkers of oxygen radical generated damage in human volunteers with
low or high cholesterol levels. Environ Mol Mutagen. 1997;30:161–174. (PubMed)
Anon. Ascorbic acid and catabolism of cholesterol. Nutr Rev 1973;31:154. (PubMed)
Bendich A, Cohen M. Ascorbic acid safety: analysis factors affecting iron absorption. Toxicol
Lett. 1990;51:189–190. (PubMed)
Block G, Patterson B, Subar A. Fruit, vegetables, and cancer prevention: a review of the
epidemiological evidence. Nutr Cancer. 1992;18:1–29. (PubMed)
Cameron E, Campbell A. The orthomolecular treatment of cancer. II. Clinical trial of high-dose
ascorbic acid supplements in advanced human cancer. Chem Biol Interact. 1974;9:285–
315. (PubMed)
Chinoy NJ. Ascorbic acid turn over in animal and human tissue. J Anim Morphol Physiol. 1978;
(Silver Jubilee Volume):69–85.
Page | 33
Dakhale GN, Khanzode SD, Khanzode SS, Saoji A. Supplementation of vitamin C with atypical
antipsychotics reduces oxidative stress and improves the outcome of
schizophrenia. Psychopharmacology. 2005;182:494–498. (PubMed)
Dixon SJ, Wilson JX. Adaptive regulation of ascorbate transport in osteoblastic cells. J Bone
Miner Res. 1992;7:675–681. (PubMed)
Dunitz JD. Linus Carl Pauling. 28 February 1901–19 August 1994. Biographical Memoirs of
Fellows of the Royal Society. 1996;42:316–8. (PubMed)
Gajawat S, Sancheti G, Goyal PK. Vitamin C against concomitant exposure to heavy metal and
radiation: a study on variations in hepatic cellular counts. Asian J Exp Sci. 2005;19(2):53–58.
Gaur GS, Dixit AK. Comparative study of vitamin C on serum lipid profile in healthy male and
female human subjects. J Sci Res. 2012;4(3):775–781.
Gowri S, Patel K, Prakash J, Srinivasan K. Influence of amla fruits (Emblica officinalis) on the
bio-availability of iron from staple cereals and pulses. Nutr Res. 2001;21(12):1483–1492.
Harding AH, Wareham NJ, Bingham SA, Khaw K, Luben R, Welch A, et al. Plasma vitamin C
level, fruit and vegetable consumption, and the risk of new-onset type 2 diabetes mellitus: the
European prospective investigation of cancer—Norfolk prospective study. Arch Intern
Med. 2008;168(14):1493–1499. (PubMed)
Haworth WN, Hirst EL. Synthesis of ascorbic acid. J Soc Chem Ind (Lond) 1933;52:645–647.
Hulse JD, Ellis SR, Henderson LM. Carnitine biosynthesis-beta hydroxylation of trimethyllysine
by an α-ketoglutarate dependent mitochondrial dioxygenase. J Biol Chem. 1978;253:1654–
1659. (PubMed)
Johnson CS. Biomarkers for establishing a tolerable upper intake level for vitamin C. Nutr
Rev. 1999;57:71–77. (PubMed)
Page | 34
Kallner AB, Hartmann D, Horning DH. Steady state turnover and body pool of ascorbic acid in
man. Am J Clin Nutr. 1979;32:530–539. (PubMed)
Khaw KT, Bingham S, Welch A, Luben R, Wareham N, Oakes S, Day N. Relation between
plasma ascorbic acid and mortality in men and women in EPIC-Norfolk prospective study: a
prospective population study: European prospective investigation into cancer and
nutrition. Lancet. 2001;357:657–663.(PubMed)
Leibovitz B, Siegel BV. Ascorbic acid, neutrophil function, and the immune response. Int J Vit
Nutr Res. 1978;48(2):159–164. (PubMed)
Levin M. New concepts in the biology and biochemistry of ascorbic acid. New Engl J
Med. 1986;31:892–902. (PubMed)
Levine M, Conry-Cantilena C, Wang Y, Welch RW, Washko PW, Dhariwal KR, et al. Vitamin
C pharmacokinetics in healthy volunteers: evidence for a recommended dietary allowance. Proc
Natl Acad Sci USA. 1996;93:3704–3709. (PMC free article) (PubMed)
Li Y, Schellhorn Herb E. New developments and novel therapeutic perspectives for vitamin C. J
Nutr. 2007;137:2171–2184. (PubMed)
Loria CM, Klag MJ, Caulfield LE, Whelton PK. Vitamin C status and mortality in US
adults. Am J Clin Nutr. 2000;72:139–145. (PubMed)
MacDonald L, Thumser AE, Sharp P. Decreased expression of the vitamin C transporter SVCT1
by ascorbic acid in a human intestinal epithelial cell line. Br J Nutr. 2002;87(20):97–
100. (PubMed)
Malo C, Wilson JX. Glucose modulates vitamin C transport in adult human small intestinal brush
border membrane vesicles. J Nutr. 2000;130:63–69. (PubMed)
Mathur V, Murdia A, Hakim AA, Suhalka ML, Shaktawat GS, Kothari LK. Male infertility and
the present status of its management by drugs. J Postgrad Med. 1979;25:90–96. (PubMed)
Page | 35
Naidu AK, Vitamin C. In human health and disease is still a mystery? An overview. Nutr
J. 2003;2:7.(PMC free article) (PubMed)
Naziroğlu M, Butterworth PJ, Sonmez TT. Dietary vitamin C and E modulates antioxidant levels
in blood, brain, liver, muscle, and testes in diabetic aged rats. Int J Vit Nutr
Res. 2011;81(6):347–357.(PubMed)
Nelson EW, Lane H, Fabri PJ, Scott B. Demonstration of saturation kinetics in the intestinal
absorption of vitamin C in man and the guinea pig. J Clin Pharmacol. 1978;18:325–
335. (PubMed)
Sharma P, Pramod J, Sharma PK, Chaturvedi SK, Kothari LK. Effect of vitamin C
administration on serum and aortic lipid profile of guinea pigs. IJMR. 1988;87:28. (PubMed)
Steinmetz KA, Potter JD. Vegetables, fruit, and cancer prevention: a review. J Am Diet
Assoc. 1996;96:1027–1039. (PubMed)
Page | 36
Stevenson NR, Brush MK. Existence and characteristic of Na+ dependent active transport of
ascorbic acid in guinea pigs. Am J Clin Nutr. 1969;22:318. (PubMed)
Takanga H, Mackenzie B, Hediger MA. Sodium dependent ascorbic acid transporter family
SLC23. Pflugers Arch. 2004;447:677–682. (PubMed)
Vaney N, Sharma P, Pramod J, Varandami J, Kothari LK. Leucocyte ascorbic acid and blood
lipids in normocholesterolemic men receiving different amounts of vitamin
C. Vitaminologia. 1988;4:47–48.
Page | 37