Updated: 13-05-2025
Vitamin C is a cofactor in at least eight enzymatic reactions, including several collagen synthesis reactions that, when dysfunctional, cause the most severe symptoms of scurvy.
In animals, these reactions are especially important in wound-healing and in preventing bleeding from capillaries.
Ascorbate may also act as an antioxidant against oxidative stress.
The fact that the enantiomer D-ascorbate (not found in nature) has identical antioxidant activity to L-ascorbate yet far less vitamin activity underscores the fact that most of L-ascorbate’s function as a vitamin relies not on its antioxidant properties but upon stereospecific enzymic reactions.
“Ascorbate” without the letter for the enantiomeric form is always presumed to be L-ascorbate.
Vitamin C Deficiency Diseases
Scurvy is a disease resulting from vitamin C deficiency.
Humans and certain animals require vitamin C in their diets for the synthesis of collagen.
In infants, scurvy is sometimes referred to as Barlow’s disease.
Other eponyms for scurvy include Moeller’s disease and Cheadle’s disease.
The chemical name for vitamin C, ascorbic acid, is derived from the Latin name for scurvy, scorbutus, which also provides the adjective scorbutic.
Typical symptoms of scurvy are initially fatigue, followed by the formation of spots on the skin, spongy gums, and bleeding from the mucous membranes.
Spots are most abundant on the thighs and legs, and a person may look pale, feel depressed, and be partially immobilised.
As scurvy advances, there can be open, suppurating wounds, loss of teeth, yellow skin, fever, neuropathy, and finally death from bleeding.
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