Vitamin C contributing to the more severe symptoms of scurvy. More generally, the biochemical role of vitamin C is to act as an antioxidant (a reducing agent) by donating electrons to various enzymatic and non-enzymatic reactions. Doing so converts vitamin C to an oxidized state - either as semidehydroascorbic acid or dehydroascorbic acid. These compounds can be restored to a reduced state by glutathione and NADPH-dependent enzymatic mechanisms. In plants, vitamin C is a substrate for ascorbate peroxidase. This enzyme utilizes ascorbate to neutralize toxic hydrogen peroxide (HO) by converting it to water (HO). Scurvy is a disease resulting from a deficiency
Vitamin A deficiency reference point for the extent of deficiency (with mortality increasing with severity of the eye disease). In a longitudinal study of preschool Indonesian children, susceptibility to disease increased nine times when severe VAD was present. The reason for the increased infection rate in vitamin A deficient populations is the T-killer cells require retinoids to proliferate correctly. Retinoic acid binds the promoter region of specific genes, so activates the transcription process and cell replication. A vitamin A-deficient diet will have a very limited surplus of retinol, so cell proliferation and replication will be suppressed, contributing to a reduced number of T-cells