Ascorbic Acid

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forms

Back 1

ascorbic acid and dehydroascorbate (oxidized form): vitamers (both equally active)

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synthesis

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derived from glucose in the liver of mammals and the kidney of birds

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missing enzyme

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we can't synthesize ascorbic acid b/c we don't have L-gulonolactone oxidase (we've been missing this for about 40million years)

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absorption

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actively transported. when we lost the ability to synthesize ascorbic acid, we gained the ability to actively transport it.

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active transporters

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SVCT I and II (sodium-dependent vit C transporter): high affinity driven by Na+ gradient; low affinity for dehydroascorbic acid; no affinity for intermediates of synthetic pathway.

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SVCT I

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expressed in intestine, kidney, and liver epithelial cells

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SVCT II

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expressed in osteoblasts, neurons, anterior pituitary, pancreas, and retina (tissues w/ a high need for vit C)

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transport in plasma

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present as ascorbate complexed to albumin

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transport into cells

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(1) as ascorbic acid via SVCT2 (2) as dehydroascorbate via facilitative glucose transporters (Glut 1 and 2) - reduced to ascorbate via dehydroascorbate reductase, high glucose interferes with dehydroascorbate uptake

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high levels of blood glucose

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impairs absorption of ascorbic acid. in uncontrolled diabetes can't take up enough ascorbate. SVCT not sufficient to uptake ascorbic acid.

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excretion

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mainly in urine: 25% as ascorbate/dehydroascorbate, 25% as diketogulonic acid, 50% as oxaloate. in deficiency, excretion of ascorbate/dehydroascorbate decreases

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high vit C intake

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will excrete high levels of oxalate = kidney stones

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reabsorption

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in kidney proximal tubule (over certain plasma [ ] saturate uptake mechanism in kidney and is secreted

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function of vit C

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reductant in hydroxylation reactions - only reduced form can do this. oxidized form needs to be converted back to reduced form (ascorbic acid) in order to act as a reductant. hydroxylase reactions.

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monooxygenases

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transfer of 1 oxygen to product. e.g. - dopamine b-hydroxylase: norepi synthesis and peptidyl glycine hydroxylase (a-amidation rxn). uses copper.

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a-amidation reaction

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activation of peptide hormones and hormone releasing factors; attach amino group to C-terminal end (carboxyl end) - if this doesn't happen, will be inactive

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dioxygenase

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prolyl & lysyl hydroxylases: hydroxylation of collagen/elastin, posttranslational modification (critical that this happens, if collagen not hydroxylated can't carry out collagen crosslinking and don't have stable collagen structure, collagen broken down). requires a-ketoglutarate and reductant (ascorbate). uses iron.

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ex. dioxygenase

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proline -> hydroxyproline (a-ketoglutarate -> succinate) ascorbate used sporadically - occasionally the ferrous iron oxidizes to ferric iron. use ascorbate to reduce iron back to ferrous iron.

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other metabolic functions

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carnitine synthesis (required for transport of fatty acids into mito for b-oxidation); tyrosine metabolism

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vit C and histamine

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ascorbate required for degradation of histamine to aspartate. histamine increases with ascorbate deficiency.

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high histamine

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associated with capillary fragility (classic sign of scurvy)

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histamine and colds

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histamine release early event in allergic response and colds - false believe that vit C breaksdown histamine which alleviates cold symptoms

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deficiency

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scurvy: impaired wound healing, edema and hemorrhage in skin, mucous membranes, and muscles; weakening of collagenous structures in bone, cartilage, teeth; lethary, fatigue, muscle atrophy; hysteria, depression

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assessment

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no functional test exists; plasma ascorbate concentrations are most reliable and tecnhically feasible (shows linear relationship to dietary intake, drop rapidly during deficiency)

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sources

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citrus, berries, green leafy veggies, potatoes. highly susceptible to loss on storage (oxidative damage)

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toxicity

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non-toxic but increase in oxalate w/ possibility of increased kidney stones