Vitamin C deficiency: more than just a nutritional disorder |
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Authors: | Joris R Delanghe Michel R Langlois Marc L De Buyzere Na Na Jin Ouyang Marijn M Speeckaert Mathieu A Torck |
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Institution: | Department of Clinical Chemistry, University Hospital Ghent, De Pintelaan 185, B 9000, Ghent, Belgium, Joris.Delanghe@ugent.be. |
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Abstract: | Although vitamin C deficiency and scurvy are generally considered as pure nutritional disorders, only a minority of the vitamin C concentration is determined by food intake. In the presence of transition metals (iron and copper), the antiscorbutic factor shifts from an antioxidant to a pro-oxidant function. Haptoglobin (Hp) is a plasma α-2 glycoprotein characterized by 3 common phenotypes (Hp 1-1, Hp 2-1 and Hp 2-2). Its free hemoglobin (Hb)-binding capacity prevents Hb-driven oxidative damage. When the antioxidant capacity of Hp is insufficient, its role is taken over by hemopexin (heme-binding protein) and by vitamin C (free radical scavenger). The Hp 2-2 phenotype has a lower capacity to inhibit oxidation and vitamin C depletion. In this article, two consequences of this major finding are tackled. The Hp polymorphism is an important non-nutritional modifying factor in the pathogenesis of vitamin C deficiency and scurvy, which may explain the success of long-range human migration by the natural selection of some populations characterized by high Hp 1 allele frequencies. Moreover, we propose tailoring the recommended dietary allowance (RDA) values of vitamin C, taking into consideration the Hp phenotype dependency. |
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Keywords: | Haptoglobin Polymorphism Scurvy Vitamin C |
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