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5.0 affects the differential pulse voltammetric curves observed for CC. The characteristic peak of curcumin at 0.3 V significantly decreased, and a new peak appeared at 0.0 V as observed for the Cu(II)–CC system. In addition, the voltammogram of curcumin at HMDE in the cathodic scan [31] is shown that optimum deposition potential is -0.8 V and deposition time is 60 s for reduction peak at -1.0 V and -1.6 V. Using the same conditions and appropriate concentrations of the metal and curcumin, reaction between those was followed. In the presence of an appropriate amount of Cu(II), the DPV signals differ from those of CC. As a result of the reaction between curcumin and Cu(II) (Fig. 2) the characteristic peak of curcumin at -1.0 V significantly decreased , and the peak at -1.6 V disappeared. The results show that there is an interaction between curcumin and copper(II), with the possible formation of a complex between the metal and this ligand, Cu(II)-CC complex. 3.2 Damage of calf thymus DNA by curcumin and Cu(II) Cu(II)-CC complex generated changes in calf thymus DNA. The reaction between dsDNA and Cu(II)-CC complex was assessed by recording the characteristic peak of DNA at +1.02 V. This peak corresponds to the oxidation of guanine residues [35]. As a result of this interaction, the characteristic peak of dsDNA decreased. The increased DNA damage by Cu(II)-CC complex was observed in the presence of various concentrations of the transition metal ions, copper(II) (140 mg L-1 dsDNA and 5 μM CC) (the results aren’t shown). The most probable mechanism for DNA damage by Cu(II)-CC complex appears to involve both the hydroxyl radical as well as singlet oxygen [34]. Furthermore, DNA was incubated with increasing concentrations of Cu(II) (1–20 M) in the presence of 5 M curcumin at room temperature in relation to different incubation time. 7PDF Image | Electroanalytical dsDNA and curcumin vs copper
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