Abstract
Artemisinin (ART) and its biogenetic precursors artemisinic acid (AA) and dihydroartemisinic acid (DHAA) are important traditional medicinal herb compounds with tumor growth inhibition properties. Herein, we have studied the cytotoxicity of ART, AA, and DHAA on different cancer cell lines (H1299, A431, and HCT 116) and investigated in detail their binding mechanisms with ctDNA by using spectroscopy, cyclic voltammetry, and computational methods. The UV absorbance, cyclic voltammetry, DNA helix melting, competition binding, and circular dichroism studies suggested that the complex formation of ART–ctDNA and AA–ctDNA occurs through groove binding. However, in the case of DHAA–ctDNA interaction, electrostatic interaction plays a major role. The thermodynamic parameters, viz., ΔG0, ΔH0, and ΔS0 were calculated, which showed the involvement of hydrogen bonds and van der Waals interactions for drug–ctDNA interaction. FTIR and molecular docking results suggested that ART, AA, and DHAA were bound to the A–T rich region in the minor groove of ctDNA.
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