Subject(s)
Clonal Evolution , Enhancer of Zeste Homolog 2 Protein/genetics , Leukemia, Myeloid, Acute/pathology , Myelodysplastic Syndromes/genetics , Phosphoproteins/genetics , RNA Splicing Factors/genetics , Aged, 80 and over , Bone Marrow/pathology , DNA Mutational Analysis , Disease Progression , Female , Humans , Leukemia, Myeloid, Acute/genetics , Leukocyte Count , Mutation , Myelodysplastic Syndromes/blood , Myelodysplastic Syndromes/diagnosis , Myelodysplastic Syndromes/pathologyABSTRACT
Several authors have demonstrated the chemoprotective and anti-carcinogenic role of selenium. However, the therapeutic potential of selenium in myelodysplastic syndrome (MDS) as single agent and as co-adjuvant of the current therapies has not been previously studied. Sodium selenite and selenomethionine, alone and in combination with cytarabine, induce a decrease in cell viability in a time-, dose- and administration-dependent manner inducing cell death by apoptosis in F36P cells (MDS cell line). These compounds increased superoxide production and induced mitochondrial membrane depolarization. The increase in BAX/BCL-2 ratio and in the activated caspase 3 expression levels, the decrease in mitochondria membrane potential, as well as the increase in superoxide production, supports the mitochondria contribution on selenium-induced apoptosis. These findings suggest that selenium may offer a new therapeutic approach in myelodysplastic syndrome in monotherapy and/or as co-adjuvant therapy to conventional anti-carcinogenic.
