Different reactivity to glutathione but similar tumor cell toxicity of chalcones and their quinolinone analogues

Resumo

Non-enzyme catalyzed nucleophilic addition of reduced glutathione (GSH) onto two open-chain sulfonamide chalcones and two quinolinone-chalcone hybrids were studied to investigate the relationship between tumor cell cytotoxic activities and GSH-reactivities of the compounds. The consumption of the chalcones or the quinolinone-chalcone hybrids due to conjugation with GSH was evaluated by analytical high-performance liquid chromatography, and the formed diastereomeric adducts were identified by liquid chromatography–mass spectrometry. When the reaction was conducted with the open-chain chalcones, the equilibria were shifted towards formation of the respective GSH-conjugates. On the other hand, the cyclic chalcone derivatives with the quinolinone moiety were found to equilibrate to mixtures containing predominantly the reactants despite the strong electron withdrawing group present in the B-ring of the compounds. The observed opposite behavior can be rationalized by reduced thiol-reactivity of the quinolinone-chalcone hybrids and fast decomposition of their GSH-conjugates. A combined X-ray diffraction and theoretical approach were used to explain the observed difference in the reactivities towards GSH. However, structural differences did not influence tumor cell (SF-295, PC-3 and HCT-116) cytotoxicity of the evaluated compounds. Accordingly, the altered GSH-reactivity seems to be not a determining factor in the tested tumor cell cytotoxic activity of the investigated compounds.

Descrição

Palavras-chave

Chalcones, Quinolinone, Glutathione, Michael reaction, Tumor cell cytotoxicity

Citação

D’OLIVEIRA, Giulio D. C. et al. Different reactivity to glutathione but similar tumor cell toxicity of chalcones and their quinolinone analogues. Medicinal Chemistry Research, [s. l.], v. 28, p. 1448-1460, 2019. DOI: 10.1007/s00044-019-02384-8. Disponível em: https://link.springer.com/article/10.1007/s00044-019-02384-8. Acesso em: 17 ago. 2023.