Naturally occurring 1,8-dihydroxyanthraquinones are under consideration as 
possible carcinogens. Here we wanted to elucidate a possible mechanism of their 
genotoxicity. All three tested anthraquinones, emodin, aloe-emodin, and 
danthron, showed capabilities to inhibit the non-covalent binding of 
bisbenzimide Hoechst 33342 to isolated DNA and in mouse lymphoma L5178Y cells 
comparable to the topoisomerase II inhibitor and intercalator m-amsacrine. In a 
cell-free decatenation assay, emodin exerted a stronger, danthron a similar and 
aloe-emodin a weaker inhibition of topoisomerase II activity than m-amsacrine. 
Analysis of the chromosomal extent of DNA damage induced by these anthraquinones 
was performed in mouse lymphoma L5178Y cells. Anthraquinone-induced mutant cell 
clones showed similar chromosomal lesions when compared to the topoisomerase II 
inhibitors etoposide and m-amsacrine, but were different from mutants induced by 
the DNA alkylator ethyl methanesulfonate. These data support the idea that 
inhibition of the catalytic activity of topoisomerase II contributes to 
anthraquinone-induced genotoxicity and mutagenicity.