Gadolinium-induced stress response causes a time-dependent miss-expression of regulative and structural genes involved in the development of the sea urchin P. lividus

Gadolinium (Gd) is a lanthanide metal whose chelates are commonly used as contrast agents for magnetic resonance imaging. Due to its release into the oceans and to the noxious environmental effects, Gd is now considered an emerging pollutant. In this study, we used the sea urchin embryo as a developmental model, in order to assess the Gd toxic effects. After fertilization, the embryo exposure to 20microM of Gd for 24h and 48h was inspected under microscope for recording morphological defects. Effects as expression of the LC3II autophagic marker and presence of autophagosomes, were evalueted by Western Blotting and CLSM analyses, while potential molecular effects were investigated by analyzing the temporal expression of candidates genes involved in the skeletogenesis, on three regulation hierarchical levels, by comparative One step RT-PCR. Our results indicate that Gd-exposed embryos reveal a dose-dependent inhibition of skeleton elongation and patterning without impairments of other territories, as well as an increase of both autophagosomes and LC3II levels, indicating an activated autophagic process as a cell survival strategy. In addition, we found a mis-regulated expression of genes analyzed among transcription factors, growth factors and effectors coding for skeletal matrix proteins, indicating altered signaling interactions in Gd-exposed embryos. Further studies are needed to investigate on gene regulatory networks involved in the skeleton malformations caused by Gd.