Chen · Proceedings of the National Academy of Sciences of the United States of America 2007 · Preclinical animal experiment · n=?

Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo.

Cited 670 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Preclinical animal pharmacokinetic and mechanistic study in rats

PubMed 17502596 · doi:10.1073/pnas.0702854104 · record verified 2026-08-30

What was done

Rats received parenteral (intravenous or intraperitoneal) or oral ascorbate at doses equivalent to human pharmacologic dosing (approximately 0.25 to 0.5 mg per gram body weight). Concentrations of ascorbate in blood and extracellular fluid were measured, ascorbate radical was quantified by electron paramagnetic resonance, and hydrogen peroxide generation was tracked using a peroxyxanthone probe.

What was found

Baseline ascorbate levels of 50 to 100 microM in blood and extracellular fluid increased to peak concentrations >8 mM after intravenous injection and approached 3 mM after intraperitoneal injection, compared to <150 microM after oral gavage. In blood, ascorbate radical was undetectable after oral dosing and remained <50 nM after parenteral dosing. In extracellular fluid after parenteral dosing, ascorbate radical concentrations were 4- to 12-fold higher than in blood (reaching up to 250 nM). Extracellular hydrogen peroxide was detected only after parenteral administration and only when extracellular ascorbate radical concentrations exceeded 100 nM.

Why it matters

This paper demonstrates in vivo that pharmacologic parenteral ascorbate selectively generates hydrogen peroxide and ascorbate radical in extracellular fluid while sparing blood. This mechanistic evidence supports evaluating high-dose intravenous ascorbate as a prooxidant therapeutic strategy.

Limits

The study was conducted entirely in rats, and human extracellular kinetics may differ. The total sample size (number of animals) is not reported in the abstract. The study evaluated pharmacokinetic and radical markers rather than clinical efficacy or tumor response endpoints.

Cited by