Search for: All records

Three new organotin( iv ) carboxylate compounds were synthesized and structurally characterized by elemental analysis and FT-IR and multinuclear NMR ( 1 H, 13 C, 119 Sn) spectroscopy. Single X-ray crystallography reveals that compound C2 has a monoclinic crystal system with space group P 2 1 / c having distorted bipyramidal geometry defined by C 3 SnO 2 . The synthesized compounds were screened for drug-DNA interactions via UV-Vis spectroscopy and cyclic voltammetry showing good activity with high binding constants. Theoretical investigations also support the reactivity of the compounds as depicted from natural bond orbital (NBO) analysis using Gaussian 09. Synthesized compounds were initially evaluated on two cancer (HeLa and MCF-7) cell lines and cytotoxicity to normal cells was evaluated using a non-cancerous (BHK-21) cell line. All the compounds were found to be active, with IC 50 values less than that of the standard drug i.e. cisplatin. The cytotoxic effect of the most potent compound C2 was confirmed by LDH cytotoxicity assay and fluorescence imaging after PI staining. Apoptotic features in compound C2 treated cancer cells were visualized after DAPI staining while regulation of apoptosis was observed by reactive oxygen species generation, binding of C2 with DNA, a change in mitochondrial membrane potential and expression of activated caspase-9 and caspase-3 in cancer cells. Results are indicative of activation of the intrinsic pathway of apoptosis in C2 treated cancer cells. 

Three triorganotin (IV) cyclopentane carboxylates were synthesized and structurally characterized by in solid state by Fourier‐transform infrared spectroscopy and single crystal diffraction, and in solution by NMR (¹H,¹³C, and¹¹⁹Sn) spectroscopy. The complexes were tested for their anticancer activity against MCF‐7 and HeLa cells along with normal BHK‐21 cells. As revealed by MTT assay, complex2was identified as the most potent derivative with an IC₅₀value of 2.59 and 0.051 μM against HeLa and MCF‐7 cells, respectively. The results were compared with cisplatin as reference drug. Fluorescent microscopic studies using 4′,6‐diamidino‐2‐phenylindole (DAPI) and propidium iodide (PI) staining confirmed the occurrence of apoptosis in HeLa cells treated with the most active complex2. The complex2also triggered the release of lactate dehydrogenase (LDH) in treated HeLa and MCF‐7 cells whereas a luminescence assay displayed a remarkable increase in the activity of caspase‐9 and ‐3. Moreover, flow cytometric results revealed that complex2caused G0/G1 arrest in the treated HeLa cells. The complexes were further screened for DNA binding studies through UV‐vis spectroscopy and cyclic voltammetry. The high activity of complex2was attributed to its higher Lewis acidity as indicated by natural bond orbital (NBO) analysis. Theoretical modelling and molecular docking studies were also conducted to study the reactivity of complexes againstVEGFR 2 Kinase.