Arterial Tortuosity Syndrome reveals function of dehydroascorbic acid in collagen and elastin synthesis: Implications for skin care.

Some investigations in Arterial Tortuosity Syndrome (ATS) suggest that impaired intracellular transport of the oxidized form of vitamin C (dehydroascorbic acid, DHAA) is at the core of the pathogenesis. Lack of vitamin C for lysyl- and prolyl-hydroxylase activity may explain the defects in collagen and elastin formation found in ATS, and draws strong parallels between ATS and scurvy. Topically applied vitamin C has a well-established basis in the field of skin care, and part of its benefit is attributed to proper collagen formation in the skin.