OBJECTIVES: Emodin is a bioactive anthraquinone that has diverse biological effects. It is also known as a biosynthetic precursor of hypericin. The purpose of this study was to assess mechanisms of potential genotoxic and antioxidant effects of emodin. We also investigated the potential genotoxic effect of photoactivated emodin. METHODS: Potential genotoxicity was determined by the alkaline comet assay and the Ames test. The potential DNA protectivity of emodin was determined by the DNA-topology assay. On purpose to clarify molecular mechanism of its DNA protectivity against Fe(2+)-induced DNA breaks, three different assays were used (Reducing power-, DPPH- and Fe(2+)-chelating assay). RESULTS: Using the alkaline comet assay and the Ames test we confirmed the genotoxic effect of both non-photoactivated and photoactivated emodin in a dose-dependent manner. Genotoxicity of photoactivated emodin did not differ from that obtained with non-photoactivated one. The DNA-topology assay revealed a DNA-protective activity of emodin. In the reducing power and DPPH assays emodin exhibited weak antioxidant activities. We did not observe any chelating activity of emodin in the Fe(2+)-chelating assay. CONCLUSIONS: We found out that emodin exhibited dual activities. On one side it was genotoxic inducing primary DNA lessions (determined by the comet assay) as well as gene mutations (determined by the Ames test). On the other side it exhibited DNA-protective activity (determined by the DNA-topology assay). Molecular mechanism underlying this DNA protective effect can be attributed to its free radicals scavenging and reducing activities.
OBJECTIVES: Emodin is a bioactive anthraquinone that has diverse biological effects. It is also known as a biosynthetic precursor of hypericin. The purpose of this study was to assess mechanisms of potential genotoxic and antioxidant effects of emodin. We also investigated the potential genotoxic effect of photoactivated emodin. METHODS: Potential genotoxicity was determined by the alkaline comet assay and the Ames test. The potential DNA protectivity of emodin was determined by the DNA-topology assay. On purpose to clarify molecular mechanism of its DNA protectivity against Fe(2+)-induced DNA breaks, three different assays were used (Reducing power-, DPPH- and Fe(2+)-chelating assay). RESULTS: Using the alkaline comet assay and the Ames test we confirmed the genotoxic effect of both non-photoactivated and photoactivated emodin in a dose-dependent manner. Genotoxicity of photoactivated emodin did not differ from that obtained with non-photoactivated one. The DNA-topology assay revealed a DNA-protective activity of emodin. In the reducing power and DPPH assays emodin exhibited weak antioxidant activities. We did not observe any chelating activity of emodin in the Fe(2+)-chelating assay. CONCLUSIONS: We found out that emodin exhibited dual activities. On one side it was genotoxic inducing primary DNA lessions (determined by the comet assay) as well as gene mutations (determined by the Ames test). On the other side it exhibited DNA-protective activity (determined by the DNA-topology assay). Molecular mechanism underlying this DNA protective effect can be attributed to its free radicals scavenging and reducing activities.