chemical structure of L-Ascorbic acidAttack of ascorbic enol on proton to give 1,3-diketone
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Ascorbic acid

Ascorbic acid is an organic acid with antioxidant properties. Its appearance is white to light yellow crystals or powder. It is water soluble. The L-enantiomer of ascorbic acid is commonly known as vitamin C. In 1937 the Nobel Prize for chemistry was awarded to Walter Haworth for his work in determining the structure of ascorbic acid (shared with Paul Karrer, who received his award for work on vitamins), and the prize for Physiology or medicine that year went to Albert Szent-Györgyi for his studies of the biological functions of L-ascorbic acid. more...

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Chemistry

Acidity


The hydroxyls (OH) next to the bottom double bond are enols. One enol loses an electron pair, becoming an oxonium group (=OH+), by creating a double bond to the carbon. Simultaneously, the carbon-carbon double bond (between the enols) transfers its electrons to form a double bond to the next (two-oxygen) carbon. To give way, the double bond electrons of the carbonyl are received by the carbonyl's oxygen, to produce an enolate. The oxonium promptly deprotonates to produce a carbonyl, and this loss of protons gives ascorbic acid its acidity. The overall reaction is enol deprotonation to produce an enolate, where the negative charge of the resulting enolate counterion is delocalized over the system of carbonyl (C=O) and the double bond (C=C). This delocalization makes the counterion more stable and less likely to regain the proton.

Tautomerism

Ascorbic acid also rapidly interconverts into two unstable diketone tautomers by proton transfer, although it is the most stable in the enol form. The proton of the enol is lost, and reacquired by electrons from the double bond, to produce a diketone. This is an enol reaction. There are two possible forms, 1,2-diketone and 1,3-diketone.

Uses

Ascorbic acid is easily oxidized and so is used as a reductant in photographic developer solutions (among others) and as a preservative.

Exposure to oxygen, metals, light and heat destroy ascorbic acid, so it must be stored in dark and cold and not in a metal containment.

The oxidized form of ascorbic acid is known as dehydroascorbic acid.

The L-enantiomer of ascorbic acid is also known as vitamin C (the name "ascorbic" comes from its property of preventing and curing scurvy). Primates (including humans) and a few other species in all divisions of the animal kingdom, notably the guinea pig, have lost the ability to synthesise vitamin C and must obtain it in their food.

Ascorbic acid and its sodium, potassium, and calcium salts are commonly used as antioxidant food additives. These compounds are water soluble and thus cannot protect fats from oxidation: for this purpose, the fat-soluble esters of ascorbic acid with long-chain fatty acids (ascorbyl palmitate or ascorbyl stearate) can be used as food antioxidants.

The relevant European food additive E numbers are: E300 ascorbic acid, E301 sodium ascorbate, E302 calcium ascorbate, E303 potassium ascorbate, E304 fatty acid esters of ascorbic acid (i) ascorbyl palmitate (ii) ascorbyl stearate.

Antioxidant mechanism

Ascorbate acts as an antioxidant by being itself available for energeticaly favourable oxidation. Oxidants (scientifically referred to as reactive oxygen species) such as the hydroxyl radical (formed from hydrogen peroxide), contain an unpaired electron and thus are highly reactive and damaging to humans and plants at the molecular level. This is due to their interaction with nucleic acid, proteins and lipids. Reactive oxygen species can 'abstract' a hydrogen from ascorbate, which becomes monodehydroascorbate and soon gains another electron to become dehydroascorbate. The reactive oxygen species are reduced to water while the oxidized forms of ascorbate are relatively stable and unreactive, and do not cause cellular damage.

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Ascorbic acid from lime juice - Nutrient Intake
From Nutrition Research Newsletter, 9/1/03 by O Garcia

In poor rural Mexican communities, 80-85% of the population consumes a diet based on maize tortillas, beans, green vegetables, and fruit. In the typical Mexican rural diet, <64% of the total energy comes from carbohydrates, maize provides 40% of the total protein and 45% of the energy, and the intake of meat, fish, and poultry is very low. This type of diet is associated with poor iron bioavailability, anemia, and deficiencies of iron and other micronutrients. In rural Mexico, iron deficiency affects 10-70% of individuals in different age and population groups, although iron intake overall is higher than recommended. A potential approach to improving iron status is to make iron more available for absorption. Ascorbic acid (AA) is the main dietary enhancer of iron absorption apart from meat, fish, and poultry, but the intake of AA-rich foods is low in rural Mexico. The median AA intake of 33 mg/d in non-pregnant, non-lactating (NPNL) women is derived from the locally produced alcoholic beverage pulque (a lime beverage known as agua de limon), red and green tomatoes, potatoes, chili peppers, wild greens, cactus, other citrus fruit, and mangoes when in season.

Pulque is the main source of AA for NPNL rural Mexican women in the present study, as well as the third most important source of nonheme iron. The amount of pulque consumed is the main predictor of a lower risk of anemia and iron deficiency. There are no reported long-term, community-level efficacy trials of the effects of adding AA from local food sources to meals high in poorly available, nonheme iron. The current study reports the long-term (8 months) effect of increasing AA intake from agua de limon on the iron status of iron-deficient, rural Mexican women by using a dose that had first been proven, with the use of iron isotopes, to double iron absorption in similar women.

Two rural Mexican populations were randomly assigned to an AA or a placebo group, each with 18 iron-deficient women. The AA group was given 500 ml limeade containing 25 mg AA twice a day, 6 d/wk, for 8 months. The placebo group was given a lime-flavored beverage free of AA or citric acid. Beverages were consumed within 30 min of two main daily meals. Data were collected on morbidity (3 times/wk), dietary intake (on 6 d), socioeconomic status, parasites (twice), medical history, and response to treatment. Blood samples at 0, 2, 4, 6, and 8 months were analyzed for hemoglobin, plasma AA, plasma ferritin, transferrin receptors, and C-reactive protein.

AA intake was significantly higher in the AA group, but nonheme iron, heme iron, and phytic acid intakes did not differ significantly. Plasma AA was significantly higher in the AA group at 2, 4, 6, and 8 months. There were no final differences between groups in hemoglobin, plasma ferritin, or transferrin receptor concentrations or in the ratio of transferrin receptors to plasma ferritin after control for initial concentrations. Increasing dietary AA by 25 mg at each of thetwo meals/d did not improve iron status in iron-deficient women consuming diets high in phytate and nonheme iron. The lack of improvement in iron stores was not due to noncompliance or failure of the intended intake of AA. Women in both communities had a high intake of nonheme iron and phytate, and the subjects consumed the limeade with the meals that were highest in iron and phytate. No parasites were detected that could interfere with iron absorption. It is therefore probable that other factors had a stronger influence on iron status than did AA intake. Although there was no significant difference in the measured intakes of nonheme or heme iron between the groups, the researchers had no control over the subjects diets except for the dose of AA.

The results of this study do not necessarily mean that increased AA intake should not be encouraged. There are several situations in which higher intakes of the vitamin would likely improve iron status. One is a situation in which meals contain substantial amounts of fortifying iron, at least in the form of ferrous sulfate. It has been estimated that a 6:1 (by wt) ratio of AA to iron is required to usefully increase the absorption of soluble nonheme iron, whereas a ratio closer to 12:1 may be needed if the foods are high in phytic or phenolic acid, as they are in rural Mexico. The ratios in this study were 10:1 in the AA group and 5:1 in the control group. The effect of AA on iron absorption is dose related. In conclusion, increasing AA intake as limeade did not improve the iron status of iron-deficient women consuming diets high in phytate and nonheme iron in rural Mexico. Because of the lack of efficacy and the paucity of local food sources that can adequately increase AA intake, the researchers conclude that this food-based intervention is not practical or effective for improving the iron status of women in these communities, at least once they already have become iron depleted. Iron fortification or supplementation is required. It is possible, however, that AA could produce a detectable increase in iron stores in some other situations.

O Garcia, M Diaz, J Rosado, L Allen. Ascorbic acid from lime juice does not improve the iron status of iron-deficient women in rural Mexico. Am J Clin Nutr 78:267273. (August 2003) [Correspondence: LH Allen, Department of Nutrition, Meyer Hall, One Shields Avenue, University of California, Davis, CA 95616-8669. E-mail: lhallen@ucdavis.edu.]

COPYRIGHT 2003 Frost & Sullivan
COPYRIGHT 2003 Gale Group

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