Vitamin C: prospective functional markers for defining optimal nutritional status

Abstract

Most species of plants and animals synthesize ascorbic acid, but human subjects cannot, making vitamin C an essential component of our diet. Relationships between vitamin C intake and status, and between status and health are not yet clear. There is evidence, however, that higher intake of vitamin C is associated with lower risk of disease, supporting the concept that optimal intake is needed for optimal vitamin C status, and that both factors are required for optimal health. Vitamin C has low toxicity in healthy subjects, but a clear definition of optimal status and the dietary intake required to meet and maintain this status is needed before a change in the current recommended intake can be considered. Available evidence suggests that intake of 200 mg vitamin C/d saturates tissues and maintains fasting plasma levels above the proposed threshold (50 μmol/l) for minimum risk of CHD. However, the issue of whether or not these levels produce ‘optimal vitamin C status’ awaits the clear and accepted definition of the term. This definition in turn awaits the development of reliable functional markers capable of assessing the effects of varying levels of vitamin C nutriture. In the present paper the relationship between intake and body stores of vitamin C and the role of vitamin C in human health are reviewed briefly. The requirements of a reliable functional marker of human vitamin C status are defined, three classes of functional markers (molecular, biochemical and physiological) are described, and possible candidate markers are examined.

Factors influencing blood concentration of retinol, α-tocopherol, vitamin C, and β-carotene in the French participants of the SU.VI.MAX trial

“…Serum vitamins are not considered as good markers of deficiency, and this is particularly true for retinol (Tanumihardjo, 2004), vitamin E (Lehmann, 1988), and C (Benzie, 1999). Indeed, retinol deficiency should be diagnosed by MRDR or RDR tests, a-tocopherol in erythrocyte is a better marker of deficiency, and vitamin C concentration in leukocytes is also more reliable to assess tissue concentrations than simple serum concentrations (Sauberlich, 1975(Sauberlich, , 1999.…”

Oxidation of LDL by Myeloperoxidase and Reactive Nitrogen Species

“…65 Vitamin C also protects against LDL lipid peroxidation initiated by MPO-derived tyrosyl radicals. 50,66 This is likely due to vitamin C's scavenging of these radicals (reaction 10) or possibly preventing their formation by MPO, because the rate constants of the reaction of vitamin C and tyrosine with compounds I and II are comparable 63,64 and because their extracellular concentrations are similar (20 to 80 mol/L versus 25 to 150 mol/L, respectively).…”

“…50,66 This is likely due to vitamin C's scavenging of these radicals (reaction 10) or possibly preventing their formation by MPO, because the rate constants of the reaction of vitamin C and tyrosine with compounds I and II are comparable 63,64 and because their extracellular concentrations are similar (20 to 80 mol/L versus 25 to 150 mol/L, respectively). 52,65 In addition, because tyrosyl radical-mediated lipid peroxidation is presumably mediated via an ␣-tocopheroxyl radical intermediate, 58 vitamin C could also be acting as a co-antioxidant in this system (see reaction 9). Thus, vitamin C appears to provide efficient antioxidant protection from HOCl-and MPO-mediated damage to LDL in vitro by a number of mechanisms (reactions 7 through 10).…”

Dietary antioxidants for chronic periodontitis prevention and its treatment: a review on current evidences from animal and human studies

“…As ascorbate, it is an enzymatic cofactor in a range of essential metabolic reactions in all animals and plants 43,44 , but this vitamin is also known to act as antioxidant in living organisms 44 .…”