Chalcones are essential intermediate compounds in the flavonoids biosynthesis, and they are easily found in arboreal or smaller plants. Many works have demonstrated anti-inflammatory, analgesic and antitumoral activities for several chalcones. Our objective was to study the antitumoral activity as well as the mechanism of action of eleven chalcones chemically derived from 3,4- (metilenodioxibenzaldeide).

Murine L-1210 lymphoblastic leukemia cells were used. The cells were incubated with the chalconas at 1, 10 and 100 µM for 24 hours. The cellular viability was evaluated by the MTT method, and the apoptosis was analysed by DNA fragmentation in agarose gel 1,5% electrophoresis, stained with ethidium bromide. The lipoperoxidation was evaluated through TBARS assay and total intracellular glutathione (GSH) levels were measured using the Tietze method.

We observed that 100µM of the compounds 3-(1,3-benzodioxol-5-yl)- 1-phenylprop-2-en-1-one (A), 3-(1,3-benzodioxol-5-yl)-1-(2,5-dimethoxyphenyl)prop-2-en-1-one (B), 3-(1,3-benzodioxol-5-yl)-1-(4-hydroxy-3- methoxyphenyl)prop-2-en-1-one (C) and 3-(1,3-benzodioxol-5-yl)-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one (D) reduced the number of viable cells in 78 ± 0,94%, 81 ± 1,7%, 83,4 ± 1,1% and 76 ± 1,1%, respectively, when compared with the control (100% of viable cells) and all of them promoted DNA fragmentation. Only the compound B produced lipid peroxidation and just the compound C have depleted 87,5 ± 0,46% of GSH intracellular level.

Our results showed that the synthetic chalcones named A, B, C and D caused apoptosis in L-1210 Lymphoblastic leukemia cells, chalcone B cause the peroxidation of the membrane and chalcone C depleted total intracellular GSH levels suggest alterations in cellular redox state that regulate apoptosis sensitivity.