One of the main target organs for the lanthanides(Ln) is bone. Previous studies revealed that ytterbium(Yb) produced damage to the skeletal system in vivo. But the effects of Yb3+ on bone marrow stromal cells(BMSCs) in vitro had not been reported. In this paper, cell viability, apoptosis, mitochondrial membrane potential(MMP), reactive oxygen species(ROS) and lactate dehydrogenase(LDH) were measured in order to study the effects of Yb3+ on BMSCs. The results indicated that Yb3+ displayed a slight positive effect on the BMSCs viability at concentrations of 1×10–6, 1×10–5, and 1×10–4 mol/L, but turned to decrease the viability of BMSCs at the highest concentration of 1×10–3 mol/L for 24, 48 and 72 h. Yb3+ at 1×10–3 mol/L promoted apoptosis of BMSCs, increased the levels of ROS and LDH, and decreased MMP in BMSCs. It suggested that the precipitate of Yb PO4 might decrease the viability of BMSCs. Yb3+ induced the apoptosis of BMSCs via mitochondrial pathway. The results might be useful for more rational application of Yb-based compounds in the future.
As lanthanide-doped sodium yttrium flouride(NaYF_4)nanoparticles have great potential inbiomedical applications,their biosafety is important and has attracted significant attention.In the present work,three different sized NaYF_4:Eu^(3+)nanoparticles have been prepared.Liver BRL 3 A cell was used as a cell model to evaluate their biological effects.Cell viability and apoptosis assays were used to confirm the cytotoxicity induced by NaYF_4:Eu^(3+)NPs.Apart from the elevated malondialdehyde(MDA),the decrease of superoxide dismutase(SOD),glutathione peroxidase(GSH-PX)and catalase(CAT)activity indicated reactive oxygen species(ROS)generation,which were associated with oxidative damage.The decrease of mitochondrial membrane potential(MMP)value demonstrated the occurrence of mitochondria damage.Then,release of cytochrome c from mitochondria and activation of caspase-3 confirmed that NaYF_4:Eu^(3+)NPs induced apoptosis was mitochondria damage-dependent.
