Abstract
Electrochemical methods are considered useful tools for simulations of biological redox reactions. The activities of quinones depend on their bioreduction. Biologically active pterocarpanquinones LQB-149 (nitroderivative), 150 and 151 (bromo and chloroderivatives, respectively) were electrochemically investigated by cyclic voltammetry, differential pulse voltammetry, and in situ UV-Vis spectroelectrochemistry, in aprotic media (N,N-dimethylformamide (DMF) + tetra-N-butylammonium (TBAPF6)). The data obtained regarding their reduction mechanisms, positive reactivity with oxygen and analysis of the electrogenerated intermediates were useful in explaining their biological outcomes. The appearance of bands at 397 and 480 nm, for the halogenated compounds, suggests the generation of transient quinonemethides (QM), electrophilic intermediates related to their activity. As an additional proof for the intermediacy of QM, in the redox processes, chemical reduction of LQB-150, in the presence of hexanethiol was performed and led to a thioalkylated quinone. For the nitroderivative, a broad band appeared at 432 nm, corresponding to the generation of the nitroradical anion, giving rise to a dianion diradical, after reduction at the second wave potential. Computational data correlate well with electrochemical experiments. Homogeneous electron transfer to oxygen, yielding reactive oxygen species, the generation of electrophilic species and the radical reactivity, explain partially the mechanism of biological action.
Highlights
The solution was stirred at room temperature under argon and the reaction was monitored periodically by using thin layer chromatography (TLC; eluent: Hex/EtOAc 7:3)
The solvent was removed under reduced pressure and the residue was purified by using column chromatography, to afford compound 1 as a yellow solid (6.0 mg, 0.012 mmol, 57%)
DMF was chosen as an aprotic organic solvent for electrochemical studies, because it can mimic the nonpolar environment in the cell, where lipid peroxidation, one of the causes of membrane fragmentation, normally occurs.[23]
Summary
They can create a variety of hazardous effects in vivo including acute cytotoxicity, immunotoxicity, and carcinogenesis, and, in contrast, can induce cytoprotection and be relevant medicines against several diseases.[1] The molecular pathways related to this bioactivity/toxicity of quinones include oxidative stress (OS) enhancement, bioreductive alkylation through the Several pterocarpanquinones, hybrid quinones prepared from pterocarpans (flavonoids) and lapachol had been. LQB‐118 is a potent anticancer pterocarpanquinone, and its biological activities and mechanisms of action have been extensively reported.[4,5] This pterocarpanquinone is a developing and orally active pterocarpanquinone agent that effectively induces the programmed cell death of prostate cancer cells, through quinone reduction and reactive oxygen species (ROS) generation. The inhibition of superoxide dismutase 1 (SOD1) expression enhances LQB‐118 activity, presumably by impairing the cellular antioxidant response.[6,7] This molecule presents antiparasitic profile.[5,8]
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