Cytotoxic effect of CdSe quantum dots on mouse embryonic development
Abstract
Aim: The aim of this study was to examine the cytotoxic effect of quantum dots (QD), a novel luminescent material, on early post-implantation embryonic development.
Methods: Mouse blastocysts were incubated in medium with or without CdSe-core QD (250 or 500 nmol/L) for 24 h. Cell apoptosis was analyzed by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling assay and Annexin V/propidium iodide staining, and proliferation was investigated by dual differential staining. Pre-implantation and post-implantation development was assessed by in vitro and in vivo analyses, respectively.
Results: The apoptotic staining analysis showed that CdSe-core QD induced apoptosis in mouse blastocysts in a dose-dependent manner. Pretreatment of blastocysts with CdSe-core QD inhibited cell proliferation, primarily in the inner cell mass. CdSecore QD also inhibited post-implantation embryonic development; fewer CdSecore QD-pretreated blastocysts reached the later stages of development compared to the controls. The pre-implantation development of morulas into blastocysts was also inhibited by CdSe-core QD. Furthermore, CdSe-core QD at 500 nmol/L were associated with resorption of post-implantation blastocysts and a decrease in fetal weight. The cytotoxicity of CdSe QD in embryonic development was significantly reduced by the addition of a ZnS coating.
Conclusion: Our results show that CdSe-core QD induce apoptosis in mouse blastocysts, inhibit cell proliferation, retard early post-implantation blastocyst development, and increase early-stage blastocyst death in vitro and in vivo.
Keywords:
Methods: Mouse blastocysts were incubated in medium with or without CdSe-core QD (250 or 500 nmol/L) for 24 h. Cell apoptosis was analyzed by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling assay and Annexin V/propidium iodide staining, and proliferation was investigated by dual differential staining. Pre-implantation and post-implantation development was assessed by in vitro and in vivo analyses, respectively.
Results: The apoptotic staining analysis showed that CdSe-core QD induced apoptosis in mouse blastocysts in a dose-dependent manner. Pretreatment of blastocysts with CdSe-core QD inhibited cell proliferation, primarily in the inner cell mass. CdSecore QD also inhibited post-implantation embryonic development; fewer CdSecore QD-pretreated blastocysts reached the later stages of development compared to the controls. The pre-implantation development of morulas into blastocysts was also inhibited by CdSe-core QD. Furthermore, CdSe-core QD at 500 nmol/L were associated with resorption of post-implantation blastocysts and a decrease in fetal weight. The cytotoxicity of CdSe QD in embryonic development was significantly reduced by the addition of a ZnS coating.
Conclusion: Our results show that CdSe-core QD induce apoptosis in mouse blastocysts, inhibit cell proliferation, retard early post-implantation blastocyst development, and increase early-stage blastocyst death in vitro and in vivo.