Low Dose and Long Term Toxicity of Sodium Arsenite Caused Caspase Dependent Apoptosis Based on Morphology and Biochemical Character

objective: although arsenite is toxic it is currently recommended for the treatment of malignancies.inthisstudythe effectsofsub-micromolarconcentrationsof sodiumarsenite onthe viability,morphologyandmechanism of celldeath of ratbone marrow mesenchymalstem cells (bmcs) over 21 days was investigated.materials and methods: in this experimental study, bmcs were extracted in dulbecco’s modified eagles medium (dmem) containing 15% of fetal bovine serum (fbs) and expandedtill the 3 passage. the cells were treated with 1, 10, 25, 50, 75 and 100 nm of sodiumarsenitefor21daysandtheviabilityofthecellsestimatedusing3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium(mtt)andtrypanbluestaining.cellswerethentreatedwiththeselecteddose(25nm)ofsodiumarsenitetodeterminetheircolonyformingability(cfa)and populationdoublingnumber(pdn). morphology ofthe cells wasstudied usingflorescentdyes,andtheintegrityofthednawasinvestigatedusingthecometassayandagarosegelelectrophoresis.theterminaldeoxynucleotidyltransferasedutpnickendlabeling(tunel)andthecaspase3assaywerethenappliedtounderstandthemechanismrdof cell death. data was analyzed using one way anova, tukey test.results: a significant reduction of viability, pdn and cfa was found following treat-ment of bmcs with 25 nm sodium arsenite (p < 0.05). cytoplasm shrinkage and a significant decrease in the diameter of the nuclei were also seen. comet assay and agarose gel electrophoresis revealed dna breakage, while positive tunel and activatedcaspase 3 confirmed the apoptosis.conclusion: a low concentration of sodium arsenite (25 nm) caused reduction of viability due to induction of apoptosis. therefore, long term exposure to low dose of this chemical may have unwanted effects on bmcs.