Effect of arsenic trioxide on apoptosis and mitochondrial transmembrane potential of Marek disease cancer cells

Abstract

Objective To investigate the mechanism of apoptosis induced by arsenic trioxide(As2O3) on MDCC-MSB1 cancer cell line in vitro. Methods MDCC-MSB1 cells were divided into 4 groups, treated with 0 (control group), 2, 4 or 8 μmoL/L of As2O3. At 48 h following the treatment, MTr assay was applied to detect the inhibitory effect of As2O3 on MDCC-MSB1. Morphological changes of apoptosis were observed by fluorescence microscopy. Apoptosis was examined by DNA Ladder. Changes of mitochondrial transmembrane potential were examined by Rhodamin 123 dye and flow cytometry. Results Inhibition ratio was 0, (5.34±3.02)%, (10.78± 0.55)% and (20.02±3.24)% respectively, along with the dosages of As2O3, the differences between the groups were statistically significant(P<0.01). Morphologic changes of apoptosis were observed by DNA ladder of agarose gel electrophoresis. Apoptosis rates were significandy increased from 3.200±0.459, 11.543±0.391, 17.206±0.636 to 21.343±0.620, and the differences between the groups were statistically significant(P<0.01). DNA ladder of experimental group was detected, Intact cell membrane, and mitochondrial transmembrane potential Pl-/Rh123- decreased apoptotic cells percentage was significantly increased from (1.06±0.14)%, (4.63±0.04)%, (9.62±0.07)% to (10.39±0.10)%, respective to doses of 0, 2,4, and 8 μmol of As2O3. The differences between the groups were statistically significant(P<0.01). Conclusions As2O3 can induce apoptosis in MDCC-MSB1 cells by decreasing the mitochondrial transmembrane potential. Key words: Arsenic; Apoptosis; Membrane potential, mitochondrial