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RESEARCH PRODUCT
Cadmium induces an apoptotic response in sea urchin embryos.
Anna Maria RinaldiMaria AgnelloSimone FilostoRosaria ScudieroMaria Carmela Roccherisubject
Embryo NonmammaliancadmiumImmunocytochemistrychemistry.chemical_elementWestern blotApoptosisDNA FragmentationEmbryo developmentCleavage (embryo)BiochemistryGel electrophoresiParacentrotus lividusIn Situ Nick-End LabelingIn Situ Nick-End LabelingAnimalssea urchin embryoCadmiumbiologyCaspase 3Stress proteinMicrofilament ProteinsCell BiologyOriginal Articlesbiology.organism_classificationMolecular biologyLaminschemistryApoptosisSea UrchinsDNA fragmentationCarrier ProteinsIntracellulardescription
Cadmium is a heavy metal toxic for living organisms even at low concentrations. It does not have any biological role, and since it is a permanent metal ion, it is accumulated by many organisms. In the present paper we have studied the apoptotic effects of continuous exposure to subacute/sublethal cadmium concentrations on a model system: Paracentrotus lividus embryos. We demonstrated, by atomic absorption spectrometry, that the intracellular amount of metal increased during exposure time. We found, using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, that long treatments with cadmium triggered a severe DNA fragmentation. We demonstrated, by immunocytochemistry on whole-mount embryos, that treatment with cadmium causes activation of caspase-3 and cleavage of death substrates alpha-fodrin and lamin A. Incubating the embryos since fertilization with Z-DEVD FMK, a caspase-3 inhibitor, we found, by immunocytochemistry, that cleavage by caspase-3 and cleavage of death substrates were inactivated.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2007-03-01 |