Abstract
Quercetin - based rhodium(III) complex, [(RhL2ClH2O)-L-III], L is quercetin, was synthesized via the direct interaction between the polyphenolic natural product (3,3',4',5,7-pentahydroxylflavone) and RhCl3 3H(2)O. Characterization of the pure isolated metal complex by analytical, electrolytic conductance, TGA and spectroscopic techniques demonstrated the stoichiometric ratio 1:2 metal to ligand. The final structure of [(RhL2ClH2O)-L-III] was confirmed using PXRD-structural analysis by processing the XRD data of microcrystalline powder by the relevant computer program Expo 2014. The mimetic catalytic activity of superoxide dismutase (SOD) was studied and the obtained results showed that [(RhL2ClH2O)-L-III] has mid activity compared to other SOD mimics. By analogy with the work of the original-SOD and its functional models, a mechanism for SOD-mimicking catalytic activity of the newly synthesized rhodium(III) complex has been proposed. The binding of the Rh(III) chelate to DNA was tested, and spectroscopic investigations indicated the successful binding of the metal complex to DNA by the groove/electrostatic binding pattern with intrinsic binding constants K-b of 2.76 x 10(6) M-1 . In addition, the quercetin - based Rh-III exhibits relatively higher DPPH scavenger power than the free quercetin. The in vitro data indicated the efficient anti-proliferative activities of the current rhodium(III) complex compared with cis-platin with increased safety on normal cells. In addition, our data revealed that the studied Rh-III complex could prevent cancer cell replication with increasing the p53 levels, inhibit both Bcl2 and MMP9, then activating caspase 9, which then cleaves caspase 3, leading to apoptosis triggering. Apoptosis activation led to cell cycle arrest at the pre-G1 phase and decreased Hela cell proliferation, which appeared in the decreased G2/M phase. Ongoing biological assays indicate that the current Rh(III) complex is a promising anti-proliferative agent with minimal toxicity to normal cells.(c) 2022 Elsevier B.V. All rights reserved.