The intracellular antioxidant balance of HL-60 cells and its implication in apoptosis induced by quinoidal compounds

Abstract

The quinoidal structure is the most widespread chemical structure in nature. Many of recently used anthracyclic neoplastic compounds have a quinoidal structure, which is a good substrate for the enzymes reducing them in one electron way with subsequent production of ROS (reactive oxygen species). It has been suggested that ROS may act as a second messenger regulating the activity of redox-sensitive enzymes and Ca2+ signaling involved in the induction of apoptosis. We found that 2-mercaptoethanol (2-ME) and N-acetyl-L-cysteine (NAC) were the best inhibitors of apoptosis: direct quenching of free radicals and protection of SH- group were most effective for the HL-60 cell line. Butylhydroxytoluene (BHT) and N, N’-diphenyl-p-phenylene diamine (DPPD), lipid soluble antioxidants show another critical point for apoptosis in HL-60 cells, which is lipid peroxidation. We also found that fetal bovine serum affected the induction of apoptosis by anthracyclic and anthracyclic antitumor compounds in HL-60 cells, probably through the penetration, efflux and accumulation of anthraquinones. The exact mechanism of this phenomenon needs more experimental data. Our findings contribute to the understanding of the intracellular conditions of apoptosis induction in the HL-60 cell line. Keywords: leukemic cells, antioxidants, ROS, apoptosis