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 fat malabsorption such as pancreatitis, cystic fibrosis, tropical sprue, and biliary obstruction. Other causes of vitamin A deficiency are inadequate intake, fat malabsorption, or liver disorders. Deficiency impairs immunity and hematopoiesis and causes rashes and typical ocular effects (e.g., xerophthalmia, night blindness). Along with poor diet, a large amount of infection and disease is present in many developing communities. Infection is very draining on vitamin A reserves and this vitamin A deficit leaves the individual more susceptible to infection; increased documentation of xerophthalmia has been seen after an outbreak of measles and the varying stages of xerophthalmia become a good