Vanadium induces calcium depletion and cell selective apoptosis during development of sea urchin embryos

Abstract

Vanadium (V) is a metal widely distributed in soil, water and air. It has recently received growing interest because its compounds are often used in different applications, from industry to medicine.1 Here, using atomic absorption spectrometry, we demonstrate the predisposition of V to accumulate directly into embryonic cells, interfering with Ca uptake. At the morphological level, we observed dose- and time-dependent effects on phenotypes and on skeletal malformations. At the molecular level, V-exposed embryos showed the activation of the cellular stress response, inducing Hsp 60 and Hsp 70 synthesis and the activation of autophagy and apoptosis. The Hsps-mediated stress response to V appeared to counteract the damage induced by low (50 nM and 100 nM) and intermediate (500 nM and 1 µM) concentrations, while high cytotoxic doses (500 µM and 1 mM) induced more marked cell death mechanisms starting at 24 h of development, when the control embryos reached the gastrula stage.2 Only few cells showed nuclei with apoptotic DNA fragmentation, particularly in the ectodermal layer. Mesodermal and endodermal cells did not appear to be involved in this process of selective apoptosis.3 Microscopic fluorescence inspections indicated that primary mesenchyme cells (PMCs) were not involved in apoptotic processes, therefore their inability to carry on the skeletogenesis could be due to the Ca depletion. These results allow us to elect the sea urchin embryo as a suitable experimental model for studying the metal-correlated cellular/molecular responses.4,5