Antioxidant properties of xanthones from Calophyllum brasiliense: prevention of oxidative damage induced by FeSO₄

BMC Complement Altern Med. 2013 Oct 11;13:262. doi: 10.1186/1472-6882-13-262.


Background: Reactive oxygen species (ROS) are important mediators in a number of degenerative diseases. Oxidative stress refers to the imbalance between the production of ROS and the ability to scavenge these species through endogenous antioxidant systems. Since antioxidants can inhibit oxidative processes, it becomes relevant to describe natural compounds with antioxidant properties which may be designed as therapies to decrease oxidative damage and stimulate endogenous cytoprotective systems. The present study tested the protective effect of two xanthones isolated from the heartwood of Calophyllum brasilienses against FeSO₄-induced toxicity.

Methods: Through combinatory chemistry assays, we evaluated the superoxide (O₂·⁻), hydroxyl radical (OH·), hydrogen peroxide (H₂O₂) and peroxynitrite (ONO⁻) scavenging capacity of jacareubin (xanthone III) and 2-(3,3-dimethylallyl)-1,3,5,6-tetrahydroxyxanthone (xanthone V). The effect of these xanthones on murine DNA and bovine serum albumin degradation induced by an OH· generator system was also evaluated. Additionally, we investigated the effect of these xanthones on ROS production, lipid peroxidation and glutathione reductase (GR) activity in FeSO₄-exposed brain, liver and lung rat homogenates.

Results: Xanthone V exhibited a better scavenging capacity for O₂·⁻, ONOO⁻ and OH· than xanthone III, although both xanthones were unable to trap H₂O₂. Additionally, xanthones III and V prevented the albumin and DNA degradation induced by the OH· generator system. Lipid peroxidation and ROS production evoked by FeSO₄ were decreased by both xanthones in all tissues tested. Xanthones III and V also prevented the GR activity depletion induced by pro-oxidant activity only in the brain.

Conclusions: Altogether, the collected evidence suggests that xanthones can play a role as potential agents to attenuate the oxidative damage produced by different pro-oxidants.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Brain Chemistry / drug effects
  • Calophyllum / chemistry*
  • DNA Damage / drug effects
  • Ferrous Compounds / toxicity*
  • Glutathione Reductase / metabolism
  • Kidney / chemistry
  • Kidney / drug effects
  • Lipid Peroxidation / drug effects
  • Liver / chemistry
  • Liver / drug effects
  • Male
  • Oxidation-Reduction / drug effects
  • Oxidative Stress / drug effects*
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species / metabolism
  • Xanthones / pharmacology*


  • Antioxidants
  • Ferrous Compounds
  • Reactive Oxygen Species
  • Xanthones
  • ferrous sulfate
  • Glutathione Reductase