Editing Vitamin C (section)

===Pharmacodynamics===
Pharmacodynamics includes enzymes for which vitamin C is a cofactor, with function potentially compromised in a deficiency state, and any enzyme cofactor or other physiological function affected by administration of vitamin C, orally or injected, in excess of normal requirements. At normal physiological concentrations, vitamin C serves as an [[enzyme]] [[substrate (biochemistry)|substrate]] or [[cofactor (biochemistry)|cofactor]] and an [[electron donor]] antioxidant. The enzymatic functions include the synthesis of [[collagen]], [[carnitine]], and [[neurotransmitter]]s; the synthesis and [[catabolism]] of [[tyrosine]]; and the metabolism of [[microsome]]s. In nonenzymatic functions it acts as a reducing agent, donating electrons to oxidized molecules and preventing oxidation in order to keep iron and copper atoms in their reduced states.<ref name=PKIN2020VitC/> At non-physiological concentrations achieved by intravenous dosing, vitamin C may function as a [[pro-oxidant]], with therapeutic toxicity against cancer cells.<ref name="Bottger2021">{{cite journal |vauthors=Böttger F, Vallés-Martí A, Cahn L, Jimenez CR |title=High-dose intravenous vitamin C, a promising multi-targeting agent in the treatment of cancer |journal=J Exp Clin Cancer Res |volume=40 |issue=1 |pages=343 |date=October 2021 |pmid=34717701 |pmc=8557029 |doi=10.1186/s13046-021-02134-y |doi-access=free |url=}}</ref><ref name="Park2018">{{cite journal |vauthors=Park S, Ahn S, Shin Y, Yang Y, Yeom CH |title=Vitamin C in cancer: a metabolomics perspective |journal=Front Physiol |volume=9 |issue= |pages=762 |date=2018 |pmid=29971019 |pmc=6018397 |doi=10.3389/fphys.2018.00762 |doi-access=free |url=}}</ref>

Vitamin C functions as a cofactor for the following [[enzyme]]s:<ref name=PKIN2020VitC/>
* Three groups of enzymes ([[prolyl-3-hydroxylase]]s, [[P4HA1|prolyl-4-hydroxylase]]s, and [[lysyl hydroxylase]]s) that are required for the [[hydroxylation]] of [[proline]] and [[lysine]] in the synthesis of [[collagen]]. These reactions add [[hydroxide|hydroxyl groups]] to the amino acids [[proline]] or [[lysine]] in the collagen molecule via [[prolyl hydroxylase]] and [[lysyl hydroxylase]], both requiring vitamin C as a [[cofactor (biochemistry)|cofactor]]. The role of vitamin C as a cofactor is to oxidize prolyl hydroxylase and lysyl hydroxylase from Fe{{sup|2+}} to Fe{{sup|3+}} and to reduce it from Fe{{sup|3+}} to Fe{{sup|2+}}. Hydroxylation allows the collagen molecule to assume its triple [[helix]] structure, and thus vitamin C is essential to the development and maintenance of [[granulation tissue|scar tissue]], [[blood vessel]]s, and [[cartilage]].
* Two enzymes ([[trimethyllysine dioxygenase|ε-N-trimethyl-L-lysine hydroxylase]] and [[gamma-butyrobetaine dioxygenase|γ-butyrobetaine hydroxylase]]) are necessary for synthesis of [[carnitine]]. Carnitine is essential for the transport of [[fatty acid]]s into [[mitochondria]] for [[Adenosine triphosphate|ATP]] generation.
* [[Hypoxia-inducible factor-proline dioxygenase]] enzymes (isoforms: [[EGLN1]], [[EGLN2]], and [[EGLN3]]) allows cells to respond physiologically to low concentrations of oxygen.
* [[Dopamine beta-hydroxylase]] participates in the biosynthesis of [[norepinephrine]] from [[dopamine]].
* [[Peptidylglycine alpha-amidating monooxygenase]] amidates [[peptide hormone]]s by removing the glyoxylate residue from their c-terminal glycine residues. This increases peptide hormone stability and activity.

As an antioxidant, ascorbate scavenges reactive oxygen and nitrogen compounds, thus neutralizing the potential tissue damage of these [[free radical]] compounds. Dehydroascorbate, the oxidized form, is then recycled back to ascorbate by endogenous antioxidants such as [[glutathione]].<ref name=DRItext />{{rp|pages=98–99}} In the eye, ascorbate is thought to protect against photolytically generated free-radical damage; higher plasma ascorbate is associated with lower risk of cataracts.<ref name="pmid30878580"/> Ascorbate may also provide antioxidant protection indirectly by regenerating other biological antioxidants such as [[α-tocopherol]] back to an active state.<ref name=DRItext />{{rp|pages=98–99}} In addition, ascorbate also functions as a non-enzymatic reducing agent for mixed-function oxidases in the microsomal drug-metabolizing system that inactivates a wide variety of substrates such as drugs and environmental carcinogens.<ref name=DRItext />{{rp|pages=98–99}}