What is the difference between vitamin a and c

The bioavailability to humans of ascorbic acid from oranges, orange juice and cooked broccoli is similar to that of synthetic ascorbic acid. J Nutr ; 6. Gregory JF 3rd. Ascorbic acid bioavailability in foods and supplements. Nutr Rev ; Yung, S. Ascorbic acid absorption in humans: a comparison among several dosage forms. Journal of Pharmaceutical Sciences. Kondo Y. Bioavailability of vitamin C from mashed potatoes and potato chips after oral administration in healthy Japanese men. Uchida E. Absorption and excretion of ascorbic acid alone and in acerola Malpighia emarginata juice: Comparison in healthy Japanese subjects.

Carter B. Absorption of folic acid and ascorbic acid from nutrient comparable beverages. Guarnieri S. Orange juice vs vitamin C: Effect on hydrogen peroxide-induced DNA damage in mononuclear blood cells. Nelson E. Comparative bioavailability of folate and vitamin C from a synthetic and a natural source.

Am J Clin Nutr. Gruenwald J, Graubaum HJ et al. Adv Ther. Vinson, J. Comparative bioavailability to humans of ascorbic acid alone or in a citrus extract. American Journal of Clinical Nutrition. Synthetic or food-derived vitamin C-are they equally bioavailable? Uchida E, Kondo Y, et al. Absorption and excretion of ascorbic acid alone and in acerola Malpighia emarginata juice: comparison in healthy Japanese subjects.

Biol Pharm Bull. A randomized steady-state bioavailability study of synthetic versus natural kiwifruit-derived vitamin C. Jones E, Hughes RE. The influence of bioflavonoids on the absorption of vitamin C. Johnston, C. Comparison of the absorption and excretion of three commercially available sources of vitamin C. Vitamin B is a set of water-soluble vitamins.

It is found in foods such as yeast, cereal, legumes, peas, nuts, pork, and beef and fish. Both vitamins can be used under the supervision of a physician to treat a variety of nutritional deficiencies. However, if taken as supplements when they are not needed can be harmful, so it is important to first discuss your need for these vitamins with your physician.

Maybe you could use a little help learning about vitamin A. To compound the situation, a variety of vitamin A- and vitamin C-related metabolites and isomers are also found in vivo. Vitamin A is a generic term that includes a number of preformed retinoids e. During absorption, distribution and metabolism, retinol and retinyl esters are predominant while retinoic acids and retinal carotenoids are cleaved to retinal play essential roles in vitamin A's biological activities in maintaining cell growth, differentiation and night vision and retinyl esters for vitamin A storage The bioactive form of vitamin C is ascorbic acid AA and its anion, ascorbate , needed as a scavenger against free radicals and as a cofactor in a number of enzymes required for the biosynthesis of, for example, collagen, carnitine and neurotransmitters.

Specific attention in the present study has been given to the different vitamin A and C compounds found in supplements and their oxidative effects related to DNA. Not included in the present study due to it being less accessible for purchase.

A key site of radical and oxidative attack of DNA is at the 8-position of guanine G , the base most susceptible to oxidation due to its low redox potential. Antioxidants have the ability to scavenge radicals and protect biomolecules such as lipids, proteins and DNA against oxidative damage, avoiding oxidative stress.

In addition to their scavenging properties, some antioxidants can promote antioxidant enzymes or even repair existing DNA damage by, e. On the contrary, their ability to react with electrons also enables antioxidants to act as pro-oxidants—causing oxidative stress opposed to preventing it 9 , The aim of the present study was to investigate whether vitamin A and C compounds, respectively, permitted in supplements differ in their potencies to cause chemical pro-oxidant effects on dG as well as DNA damage, formamido pyrimidine DNA glycosylase FPG -sensitive sites oxidative lesions and cytotoxicity.

In addition to these compounds, retinal and DHAA were also included as these might be formed as degradation products and are found in vivo. Vitamin solutions were freshly prepared for each experiment. Ascorbic acid 6-palmitate AA6P was also dissolved in an equivalent amount of ethanol, while all other C vitamins were dissolved in a buffer or supplemented RPMI only.

RP and AA6P were dissolved in ethanol due to lower solubility. It could be the case that the relatively low solubility could affect the outcome of the assays, but, on the other hand, visually it was observed that they were solubilised. Hoffmann-La Roche, Basel, Switzerland. In order to minimise oxidation of dG, the buffer and dG solution were kept on ice during the mixing and until exposure. New calibration curves for 8-oxodG and dG using standards were generated on each day of analysis.

Vitamin solutions and standards were eluted for 20 min using the HPLC eluent 0. The EC-chromatograms were smoothed using the Stavinsky-Golaz method. At the time of splitting, 0. The trypan blue stain penetrates damaged cell membranes allowing discrimination between damaged unviable and intact viable cells. Cells were also treated with the enzyme FPG, enabling FPG-sensitive sites to be identified including oxidised purines such as 8-oxoguanine.

Cells were mixed with 0. Slides were washed and equilibrated in enzyme buffer 0. DNA was then unwinded in alkaline solution 0. The slides were neutralised in EDTA twice, and milli-Q-water once, 5 min in each, dried overnight and fixated in methanol for 5 min, all at room temperature. The FPG was diluted in enzyme buffer before use.

Electrophoresis was performed at 1. All incubations performed in solutions were carried out in dark and on ice, unless otherwise stated. For FPG-sensitive sites, the photosensitiser Ro Ro and visible light, giving rise predominately to 8-oxoguanine 17 , was used as positive control.

Exposures were terminated by centrifugation as above, and the cells were resuspended in PBS. The same steps as for vitamin-exposed cells were then followed see above.

Fifty cells were assessed in duplicates for each run i. The presence of 0. Therefore, controls with supplemented medium only were used throughout the comet assay experiments. For each vitamin, four to six independent experiments were conducted for dG studies, four for cytotoxicity analysis five to seven for AA6P and three to four for comet assay runs.

The normal plasma level of retinol is in the range of 2—2. In acetate buffer with 0. At the two highest concentrations, retinol acetate RA also induced a significant increase in 8-oxodG formation. Either acetate buffer containing 0.

Retinol still caused an increase in 8-oxodG formation when compared to control, while retinal no longer did. The control value for retinol also changed significantly between the different buffers but not for any of the other controls. The mean value of dG oxidation caused by CA also increased several fold, the amount did, however, vary between runs and the increase was not statistically significant. None of the control values differed between the two buffers.

In comparison to the acetate buffer containing 0. Dose—response studies were therefore carried out for the vitamin compounds exceeding this limit.

The effect of A vitamin A and B vitamin C compounds on the viability of HL cells after h exposure, as determined by trypan blue staining. Neither did any of the vitamin compounds cause FPG-sensitve sites, with one exception. Cutting-edge techniques meet innovative natural ingredients in this collection of smoothing skincare. Sustainably grown, organic botanicals are at the heart of this luxurious range of holistic, high performance skin care.

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