Esculetin modulates cytotoxicity induced by oxidants in NB4 human leukemia cells

- Esculetin (100 μM), a polyphenolic antioxidant compound, induces apoptosis on human NB4 cells.
- Since apoptosis involves redox imbalance, co-treatments with esculetin and oxidants are assayed.
- Esculetin (100 μM) prevents the increase of apoptosis and the superoxide anion production promotes by t-BHP.
- H2O2 potentiates cell death acting synergistically with esculetin.
- Increases of apoptosis by H2O2 plus esculetin may be related to increments of O2−.

Esculetin is a polyphenolic compound with cytoprotective properties. We previously demonstrated the induction of apoptosis by esculetin in NB4 human leukemia cells, as a model, by a mechanism not well understood. To analyse the antioxidant activity of esculetin on apoptosis, we have studied the influence of co-treatments of esculetin at a concentration of 100 μM with exogenous ROS donors, namely tert-butyl-hydroperoxide and hydrogen peroxide, on NB4 cells. Esculetin (100 μM) exerts a protective effect on cell viability and death necrosis or late apoptosis caused by the oxidant t-BHP whereas it potentiates decrease of cell viability and cell death caused by H2O2. In the first case, the O2− scavenging activity of esculetin (100 μM) could be implicated. In the last one, cytotoxicity by apoptosis induction seems to be related to the increase in O2−, among other possible mechanisms. These results contribute to the study of the antitumor properties of esculetin by regulation of redox balance in leukemia cells.