Effect of anthraquinone derivatives on lipid peroxidation in rat heart mitochondria: structure-activity relationship

J Nat Prod. 1995 Sep;58(9):1365-71. doi: 10.1021/np50123a005.

Abstract

Lipid peroxidation was induced in rat heart mitochondria with FeSO4 and the inhibitory effects of various anthraquinone derivatives were compared. Oxygen consumption and malondialdehyde formation were used to quantitate the amount of lipid peroxidation. Emodin [2], alizarin [13], and alizarin complexone [14] significantly inhibited lipid peroxidation; their potency as inhibitors of lipid peroxidation was higher than that of alpha-tocopherol. Structure-activity analysis showed that two hydroxyl groups arranged in either the ortho- or meta-position in the C ring of the anthraquinone nucleus are required for such derivatives to inhibit lipid peroxidation. The diphenyl-p-picrylhydrazyl test showed that alizarin [13] and alizarin complexone [14] are free-radical scavengers while emodin [2] is not. The mechanism for emodin [2] to inhibit lipid peroxidation is most likely due to inhibition on the propagation of lipid peroxyl radicals in the mitochondrial membrane.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anthraquinones / chemistry
  • Anthraquinones / pharmacology*
  • Antioxidants / chemistry
  • Antioxidants / pharmacology
  • Free Radical Scavengers / chemistry
  • Free Radical Scavengers / pharmacology
  • In Vitro Techniques
  • Lipid Peroxidation / drug effects*
  • Male
  • Mitochondria, Heart / drug effects*
  • Mitochondria, Heart / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Structure-Activity Relationship

Substances

  • Anthraquinones
  • Antioxidants
  • Free Radical Scavengers