TOXICITY INDUCED BY GADOLINIUM IONS ON DEVELOPING SEA URCHIN EMBRYOS

TOXICITY INDUCED BY GADOLINIUM IONS ON DEVELOPING SEA URCHIN EMBRYOS C. Martino,1,2 R. Chiarelli,1 C. Costa,2 D. Koop,3 R. Scudiero,4 M. Byrne,3 V. Matranga,2 M.C. Roccheri1 1Department of Biological, Chemical and Pharmaceutical Sciences and Technologies, University of Palermo, Italy; 2Institute of Biomedicine and Molecular Immunology "A. Monroy", CNR, Palermo, Italy; 3Department of Anatomy and Histology, F13, University of Sydney, NSW, Australia; 4Department of Biology, University of Naples Federico II, Italy E-mail: chiara.martino@unipa.it Pharmaceuticals are a class of emerging environmental contaminants. Gadolinium (Gd) is a metal of the lanthanide series of the elements whose chelates are commonly employed as contrast agents for magnetic resonance imaging, and subsequently released into the aquatic environment. We investigated the effects of exposure to sublethal Gd concentrations on the development of four phylogenetically and geographically distant species: two Mediterranean species, Paracentrotus lividus and Arbacia lixula, and two species living in the East coast of Australia, Heliocidaris tuberculata and Centrostephanus rodgersii. Measures of the Gd and Ca content inside embryos by ICPMS showed a time- and dose-dependent increase in Gd, in parallel with a reduction in Ca, suggesting that Gd competes with Ca for binding to the Ca channels. In all the four species, we observed a general delay of embryo development at 24h postfertilization, and a strong inhibition of skeleton growth at 48 h, with species-specific threshold levels of sensitivity. Further experiments were carried out on P. lividus embryos. Removal of Gd after 24 h caused partial recovery of embryo development 48 h post fertilization. We detected an increase of the LC3 autophagic marker at 24 and 48 h, while confocal microscopy studies confirmed the increased number of autophagosomes and autophagolysosomes. In contrast, immunofluorescence studies showed no apoptotic induction.