4.6 Article

Impact of denticity of chromone/chromene thiosemicarbazones in the ruthenium(II)-DMSO complexes on their cytotoxicity against breast cancer cells

Journal

APPLIED ORGANOMETALLIC CHEMISTRY
Volume 36, Issue 7, Pages -

Publisher

WILEY
DOI: 10.1002/aoc.6750

Keywords

apoptosis; cell cycle arrest; chromone; chromene thiosemicarbazone; denticity; Ru(II)-DMSO

Funding

  1. Department of Science and Technology, Government of India [IF160449]
  2. Fondo Nacional de Ciencia y Tecnologia [3200391, 11170840]
  3. Ministry of Education, Government of India

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Denticity of ligands plays a significant role in the cytotoxicity of metal complexes. This study evaluated the impact of ligand denticity in the Ru(II)-DMSO complexes on the cytotoxicity of cancer cells. Results showed that the complex with a tridentate chromone ligand exhibited better anticancer activity compared to the one with a bidentate chromene ligand. The stable nature of the tridentate system and the higher reactivity of the chloride ligand in the tridentate species were attributed to the observed differences in cytotoxicity. The complex demonstrated selective cytotoxicity against breast cancer cells and lower toxicity against normal cells, indicating its effective anticancer potential.
Denticity plays a prominent role in the cytotoxicity of metal complexes. The impact of ligand denticity of chromone/chromene thiosemicarbazones (TSCs) in the Ru(II)-DMSO complexes on the cytotoxicity of cancer cells was evaluated. Ru(II)-DMSO complex containing tridentate chromone TSC (D1) exhibited better in vitro anticancer activity than the one with bidentate chromene TSC (D2). Using the optimized structures of the complexes, the reason behind the same was attributed to the thermodynamically stable nature of the tridentate system. Hydrolysis study of the complexes showed the kinetically labile nature of the chloride ligand in the tridentate species with respect to the bidentate counterpart. The selective cytotoxicity of complex D1 against breast cancer cells and its less toxicity against normal cells demonstrated the effective anticancer potential of the complex. Further, the binding efficacy of the complexes against DNA and BSA, along with imaging and flow cytometry experiments, warranted the effective cell death induced by the complexes against breast cancer cells via apoptosis.

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