GLYCEROL (GLY) INHIBITS HEPATOCELLULAR CARCINOMA CELL PROLIFERATION BY REACTIVE OXYGEN SPECIES (ROS) GENERATION

CAPIGLIONI, AM; LORENZETTI, MF; QUIROGA, AD; PARODY, JP; CARRILLO, MC; MARINELLI, RA; CEBALLOS. MP; ALVAREZ, ML

Congreso; LXI REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC); 2016

In previous studies our group reported antiproliferative and proapoptoticeffects of GLY administration in an in vivo preneoplasicmodel. We postulate GLY as a possible ROS inductor that worksas a signaling molecule after its metabolization to GLY phospha te(GlyP). Aim: To begin to study the antiproliferative mechanisms ofGLY using hepatocarcinoma HepG2 cells. Methods and Results:MTT assay was used to determine the effects of GLY on HepG2cell line proliferation. The dose-response curve revealed that cellproliferation was diminished in a dose dependent manner (IC50=0.5% v/v). The primary cellular metabolite of GLY is GlyP. Toanalyze this metabolic fate of GLY, HepG2 cells were incubatedat 37 0C for 72 h with 0.5% and 1% GLY and GlyP generationwas measured by a colorimetric reaction. GlyP levels showed a47.5%* and 21.0%* increase in cells treated with GLY 0.5% and1%, respectively, compared to control cells. It has been reportedthat subsequent GlyP metabolism induces ROS generation. Todetermine the possible occurrence of this phenomenon, after 72h of treatment, cells were incubated 30 min with 2′,7'-Dichlorofluoresceindiacetate (DCF-DA). Inside the cells, DCF-DA moleculeswere hydrolyzed by esterases, and reacted with intracellular ROS,producing a fluorescent product that can be measured fluorometrically.GLY caused a raise of 20%* in ROS production at bothconcentrations tested (*p