Background: Evidence has been provided of the anti-proliferative activity of citalopram against some
Objective: The apoptotic impact of citalopram, an antidepressant, against liver hepatocellular carcinoma cell line
HepG2 was investigated in relation to the oxidative pathway and nuclear factor (NF)κB activation.
Method: The cytotoxic effects of citalopram on HepG2 cells were determined by MTT assay. Reactive oxygen
species (ROS) formation and cytochrome c release were measured following treatment with citalopram.
Apoptosis analysis and Bax and Bcl-2 mRNA and protein levels were also determined.
Results: The cytotoxic effects of different concentrations of citalopram on HepG2 cells were observed as a
reduction in cell viability and an increase in ROS formation. Citalopram caused an increase in mitochondrial
Bax levels and a decrease in Bcl2 levels and also caused cytochrome c release. Moreover, DAPI staining
and flow cytometry assays revealed citalopram-induced apoptosis in HepG2 cells. Oxidant scavengers and Bay
11-7082 (an irreversible inhibitor of NFκB activation) prevented the citalopram-associated cell death, increased
BAX and decreased Bcl2.
Conclusion: Outcomes from current study suggest that citalopram might exhibit apoptotic effect against
hepatocellular carcinoma cell line by induction of cell death through cytochrome c release and ROS-dependent
activation of NFκB.