Doxorubicin inhibits oxidation of 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonate) (ABTS) by a lactoperoxidase/H2O2 system by reacting with ABTS-derived radical

Krzysztof J. Reszka, Bradley E. Britigan

Research output: Contribution to journalArticle

17 Scopus citations


The effect of doxorubicin on oxidation of 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonate) (ABTS) by lactoperoxidase and hydrogen peroxide has been investigated. It was found that: (1) oxidation of ABTS to its radical cation (ABTS{radical dot}+) is inhibited by doxorubicin as evidenced by its induction of a lag period, duration of which depends on doxorubicin concentration; (2) the inhibition is due to doxorubicin hydroquinone reducing the ABTS{radical dot}+ radical (stoichiometry 1: 1.8); (3) concomitant with the ABTS{radical dot}+ reduction is oxidation of doxorubicin; only when the doxorubicin concentration decreases to a near zero level, net oxidation of ABTS could be detected; (4) oxidation of doxorubicin leads to its degradation to 3-methoxysalicylic acid and 3-methoxyphthalic acid; (5) the efficacy of doxorubicin to quench ABTS{radical dot}+ is similar to the efficacy of p-hydroquinone, glutathione and Trolox C. These observations support the assertion that under certain conditions doxorubicin can function as an antioxidant. They also suggest that interaction of doxorubicin with oxidants may lead to its oxidative degradation.

Original languageEnglish (US)
Pages (from-to)164-171
Number of pages8
JournalArchives of Biochemistry and Biophysics
Issue number2
StatePublished - Oct 15 2007


  • ABTS
  • Anthracyclines
  • Doxorubicin
  • EPR
  • Glutathione
  • Hydroquinone
  • Inactivation
  • Lactoperoxidase
  • Oxidation
  • Trolox C

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology

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