Editing Vitamin C (section)

===Pharmacokinetics===
Ascorbic acid is absorbed in the body by both active transport and passive diffusion.<ref>{{cite journal |vauthors=Lykkesfeldt J, Tveden-Nyborg P |title=The pharmacokinetics of vitamin C |journal=Nutrients |volume=11 |issue=10 |date=October 2019 |page=2412 |pmid=31601028 |pmc=6835439 |doi=10.3390/nu11102412 |doi-access=free |url=}}</ref> Approximately 70%–90% of vitamin C is active-transport absorbed when intakes of 30–180&nbsp;mg/day from a combination of food sources and moderate-dose dietary supplements such as a multi-vitamin/mineral product are consumed. However, when large amounts are consumed, such as a vitamin C dietary supplement, the active transport system becomes saturated, and while the total amount being absorbed continues to increase with dose, absorption efficiency falls to less than 50%.<ref name=NIH2021 /> Active transport is managed by Sodium-Ascorbate Co-Transporter proteins (SVCTs) and Hexose Transporter proteins (GLUTs). [[SLC23A1|SVCT1]] and [[SLC23A2|SVCT2]] import ascorbate across plasma membranes.<ref name="Savini_2008">{{cite journal | vauthors = Savini I, Rossi A, Pierro C, Avigliano L, Catani MV | title = SVCT1 and SVCT2: key proteins for vitamin C uptake | journal = Amino Acids | volume = 34 | issue = 3 | pages = 347–55 | date = April 2008 | pmid = 17541511 | doi = 10.1007/s00726-007-0555-7 | s2cid = 312905 }}</ref> The Hexose Transporter proteins [[GLUT1]], [[GLUT3]] and [[GLUT4]] transfer only the oxydized dehydroascorbic acid (DHA) form of vitamin C.<ref name="pmid9228080">{{cite journal | vauthors = Rumsey SC, Kwon O, Xu GW, Burant CF, Simpson I, Levine M | title = Glucose transporter isoforms GLUT1 and GLUT3 transport dehydroascorbic acid | journal = The Journal of Biological Chemistry | volume = 272 | issue = 30 | pages = 18982–9 | date = July 1997 | pmid = 9228080 | doi = 10.1074/jbc.272.30.18982 | doi-access = free | title-link = doi }}</ref><ref name=Linster2007 /> The amount of DHA found in plasma and tissues under normal conditions is low, as cells rapidly reduce DHA to ascorbate.<ref name="pmid12729925">{{cite journal | vauthors = May JM, Qu ZC, Neel DR, Li X | title = Recycling of vitamin C from its oxidized forms by human endothelial cells | journal = Biochimica et Biophysica Acta (BBA) - Molecular Cell Research | volume = 1640 | issue = 2–3 | pages = 153–61 | date = May 2003 | pmid = 12729925 | doi = 10.1016/S0167-4889(03)00043-0 | doi-access =  | title-link = doi }}</ref>

SVCTs are the predominant system for vitamin C transport within the body.<ref name="Savini_2008" /> In both vitamin C synthesizers (example: rat) and non-synthesizers (example: human) cells maintain ascorbic acid concentrations much higher than the approximately 50 micromoles/liter (μmol/L) found in plasma. For example, the ascorbic acid content of pituitary and adrenal glands can exceed 2,000&nbsp;μmol/L, and muscle is at 200–300&nbsp;μmol/L.<ref name=Padayatty2016>{{cite journal | vauthors = Padayatty SJ, Levine M | title = Vitamin C: the known and the unknown and Goldilocks | journal = Oral Diseases | volume = 22 | issue = 6 | pages = 463–93 | date = September 2016 | pmid = 26808119 | pmc = 4959991 | doi = 10.1111/odi.12446 }}</ref> The known coenzymatic functions of ascorbic acid do not require such high concentrations, so there may be other, as yet unknown functions. A consequence of all this high concentration organ content is that plasma vitamin C is not a good indicator of whole-body status, and people may vary in the amount of time needed to show symptoms of deficiency when consuming a diet very low in vitamin C.<ref name=Padayatty2016 />

Excretion (via urine) is as ascorbic acid and metabolites. The fraction that is excreted as unmetabolized ascorbic acid increases as intake increases. In addition, ascorbic acid converts (reversibly) to DHA and from that compound non-reversibly to 2,3-diketogulonate and then oxalate. These three metabolites are also excreted via urine. During times of low dietary intake, vitamin C is reabsorbed by the kidneys rather than excreted. This salvage process delays onset of deficiency. Humans are better than guinea pigs at converting DHA back to ascorbate, and thus take much longer to become vitamin C deficient.<ref name=PKIN2020VitC/><ref name=Linster2007 />