The photodynamic therapy (PDT) has been outstanding as a promising alternative 
for treating different carcinomas. However, the lack of detailed knowledge on 
the mechanisms of action prevents exploitation of the therapy full potential. 
Herein we shall evaluate not only the photodynamic efficiency but the mechanism 
of cell death triggered by the photoactivated erythrosine in oropharyngeal 
cancer cells (HEp-2). Cytotoxic assays were performed by MTT at distinct 
concentrations (10-3 to 10-6 mol/L) and incubation time (3, 24 and 48 h) of 
erythrosine in HEp-2 in vitro culture. In addition to the cytotoxic effect, the 
mechanisms of cell death were evaluated by flow cytometry following the annexin 
V/propidium iodide double staining protocol. Erythrosine was incorporated by 
HEp-2 cells in a dose- and time-dependent pathway. The incubation of erythrosine 
in dark has not shown any significant effect over the culture until 24 h and 
1.25×10-6 mol/L concentration, from which a small portion (<25% and 
statistically significant) of the cell population have undergone apoptosis. On 
the other hand, 50% of cell viability is reduced mainly by necrosis when 10, 
3.75 and 1.9×10-6 mol/L of erythrosine concentrations at 3, 24 and 48 h of 
incubation are photoactivated, respectively. Bioinspired models of tumor 
membrane based on Langmuir monolayers of 2-dioleoyl-sn-glycero-3-phosphocholine 
(DOPC) and 1,2-dioleoyl-sn-glycero-3-phospho-L-serine (DOPS) mixture reveled 
that electrostatic interactions with the lipid head groups are the main driving 
forces allowing the erythrosine adsorption. Furthermore, light-induced 
hydroperoxidation significantly increased the surface area of the monolayers, 
which might be the origin of the necrotic pathway triggered in HEp-2 cells.