Effect of vitamin C deficiency on fetal and neonatal development and aging.

Abstract

Vitamin C (L-ascorbic acid) is a water-soluble vitamin that functions as an electron donor to reduce the reactive oxygen species. Vitamin C is also a cofactor for numerous biosynthetic enzymes such as prolyl and lysyl hydroxylase for procollagen hydroxylation. Vitamin C is synthesized mainly in the liver of most mammalian species including mice and rats. However, humans, primates, and guinea pigs are unable to synthesize vitamin C in vivo. To clarify the relationships between vitamin C and aging, we developed SMP30/GNL knockout mice which unable to synthesize vitamin C in vivo and found that these knockout mice were shorter in life-span than the wild-type mice when fed vitamin C low diet (about 2.5% a day of vitamin C). Moreover, we also found that an absence or low intake of vitamin C during pregnancy induced multiple abnormalities in the developing tissues of SMP30/GNL knockout mice. Therefore, a diet that supplies an adequate amount of vitamin C is essential to avoid a life-shortening deficiency and to provide optimal conditions for fetal and neonatal health.