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Characterization of the genotoxicity of anthraquinones in mammalian cells

S O Mueller1, H Stopper

  • 1Department of Toxicology, University of Würzburg, 97078, Würzburg, Germany. mueller1@niehs.nih.gov

Biochimica Et Biophysica Acta
|August 6, 1999
PubMed

Insights

Naturally occurring anthraquinones like emodin may cause cancer by damaging DNA. These compounds inhibit topoisomerase II, an enzyme crucial for DNA replication, leading to genotoxicity and mutagenicity.

Area of Science:

  • Biochemistry
  • Toxicology
  • Genetics

Background:

  • Naturally occurring 1,8-dihydroxyanthraquinones are suspected carcinogens.
  • Understanding the genotoxic mechanisms of these compounds is crucial.

Purpose of the Study:

  • To elucidate the genotoxicity mechanism of emodin, aloe-emodin, and danthron.
  • To investigate their interaction with DNA and topoisomerase II activity.

Main Methods:

  • Assessing inhibition of bisbenzimide Hoechst 33342 binding to DNA.
  • Evaluating topoisomerase II activity using a cell-free decatenation assay.
  • Analyzing chromosomal DNA damage in mouse lymphoma L5178Y cells.

Main Results:

  • Anthraquinones inhibited DNA binding similarly to known topoisomerase II inhibitors.
  • Emodin, danthron, and aloe-emodin showed varying degrees of topoisomerase II inhibition.
  • Induced chromosomal lesions resembled those from topoisomerase II inhibitors, not DNA alkylators.

Conclusions:

  • Topoisomerase II inhibition is a likely mechanism for anthraquinone genotoxicity.
  • These findings contribute to understanding the carcinogenic potential of these natural compounds.

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