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Ascorbic Acid

C6H8O6 organic

Properties

StateSolid at room temperature
ColorWhite to pale yellow crystalline powder
SolubilitySoluble in water (33 g/100 mL at 20 °C)
Melting Point190 °C (decomposes)

About Ascorbic Acid

Ascorbic acid is the vitamin most humans get from food because we lost the ability to make it ourselves — about 60 million years ago, the primate lineage that includes humans, other apes, and guinea pigs accumulated an inactivating mutation in the L-gulonolactone oxidase gene that catalyzes the last step of vitamin C biosynthesis. Most other mammals still produce their own; we need a couple of pieces of citrus a day. Chemically, ascorbic acid is a five-membered lactone with a 2,3-enediol functionality that's responsible for both its biological role and its industrial usefulness. The enediol is easily oxidized to the diketone (dehydroascorbate), which is why ascorbic acid is such a strong reducing agent and why it works as an antioxidant in food preservation: it preferentially gets oxidized by ambient oxygen, sparing the food it's been added to. The pKa1 of 4.17 puts it in the realm of weak organic acids; the second proton (pKa2 = 11.6) doesn't typically come off under physiological conditions. In the body, ascorbic acid is the obligatory cofactor for prolyl hydroxylase and lysyl hydroxylase, the enzymes that hydroxylate proline and lysine residues in collagen — without those modifications, collagen triple helices don't form properly, and the resulting weak connective tissue produces the bleeding gums, loose teeth, and poor wound healing of scurvy.

Where you'll encounter it

If you take a vitamin C supplement, eat citrus fruit, or drink orange juice, the molecule doing the work is ascorbic acid. In a food-science context, it's the antioxidant added to commercial guacamole, pre-cut apple slices, and cured meats — the orange-red fading of cut apple flesh that ascorbic acid prevents is enzymatic browning catalyzed by polyphenol oxidase, and the ascorbic acid sacrificially reduces the oxidized phenolic intermediates back to colorless form. In a pharmacy, the standard cold-and-flu effervescent tablets are ascorbic acid plus sodium bicarbonate, which gives the fizzy CO2 release on dissolution. The historical context — James Lind's 1747 controlled trial showing that citrus cured scurvy in British sailors — is one of the earliest examples of a randomized clinical trial, predating the formal methodology by two centuries.

Common Uses

  • Dietary supplement and antiscorbutic for vitamin C deficiency
  • Food antioxidant preventing enzymatic browning (E300)
  • Effervescent-tablet cold-and-flu pharmaceutical formulations
  • Reducing agent in dough conditioners and cured-meat preservation
  • Bench reductant for selective metal-ion redox chemistry

Safety Information

Very low toxicity — excess intake is excreted in urine within hours, and the practical upper limit before gastrointestinal upset (loose stools, mild cramping) is around 2 grams per day for most adults. Megadose use can rarely contribute to oxalate kidney stones in susceptible individuals, since one of the metabolic byproducts is oxalic acid. Generally safe at the doses found in food and standard supplements.

This safety summary is for educational reference only and may not be complete. It is not a substitute for Safety Data Sheets (SDS), medical advice, or professional chemical safety guidance. Always consult appropriate SDS and qualified professionals before handling chemicals.

Constituent Elements

Frequently Asked Questions

What is the molar mass of ascorbic acid?
176.124 g/mol. Sum 6(12.011) for the carbons, 8(1.008) for the hydrogens, and 6(15.999) for the oxygens, giving 176.12. The molar mass is useful for converting between the international-unit dosing on supplement labels and the milligram dosing in clinical literature: 1 mg of ascorbic acid is about 5.7 µmol, which is roughly the daily dietary requirement to prevent scurvy.
Why do humans need vitamin C from food?
Humans, other great apes, guinea pigs, and a few species of bats and fish carry an inactivating mutation in the gene for L-gulonolactone oxidase, the final enzyme of the four-step ascorbic-acid biosynthesis pathway. The mutation is ancestral in primates — it happened in our shared ancestor about 60 million years ago. Without that enzyme, the pathway stops at L-gulonolactone instead of reaching ascorbic acid, so we rely on dietary intake. The gene fragment is still detectable in our genome as a pseudogene, frozen at the point where it was disabled.
How does vitamin C prevent scurvy?
It's the obligate cofactor for prolyl-4-hydroxylase and lysyl hydroxylase, two enzymes that hydroxylate specific residues in newly synthesized collagen polypeptides. The hydroxyl groups are essential for the cross-links that hold the collagen triple helix together; without them, the resulting collagen is structurally defective. Defective collagen weakens connective tissue throughout the body — most visibly in gums, blood vessels, and skin — which gives scurvy its characteristic bleeding-gum, loose-tooth, slow-wound-healing presentation.