Harnessing redox reactions for anticancer effects: A copper(II) Schiff base complex induces apoptosis in HepG2 liver cancer cells via ROS generation.

This study uncovers the potential of a copper(II) Schiff base complex, CuL, to access the Cu(I) oxidation state and generate reactive oxygen species (ROS), highlighting its significance in eventual therapeutic applications. UV-vis absorption spectroscopy was used to follow the redox stability of the metal complex, also in the presence of reducing agents, such as ascorbic acid and glutathione, and of the copper(I) chelator, bathocuproine disulfonate. Utilizing human tumor cell lines HepG2 (hepatocarcinoma cells), we assessed its efficacy in reducing cell viability, increasing the sub-G/G cell fraction, and initiating apoptotic pathways. Cell viability assays demonstrated a dose-dependent cytotoxicity with pronounced effects at sub-micromolar concentrations. Flow cytometry revealed significant ROS production, followed by mitochondrial membrane potential dissipation, and caspase activation, underscoring CuL's mechanism of action. These findings position CuL as a promising candidate for cancer therapy, providing insights into copper complexes' therapeutic application through oxidative stress and apoptosis modulation.