EFFECTS OF VANADIUM DURING DEVELOPMENT OF SEA URCHIN EMBRYOS IN A CLIMATE CHANGE PROSPECTIVE

The increasing industrial use of vanadium (V), as well as its pos- sible pharmaceutical use in various diseases, has intensified its environmental release, making it an emerging pollutant. Biological effects of metal pollution can be modified by higher seawater temperatures1,2. Paracentrotus lividus embryos exposed to V show altered phenotypes, skeletal absence or malformations, cell stress response mediated by HSPs, autophagy and apoptosis, and modulation of metal related proteolytic activities.3,4,5 Here, we have extended our V-toxicity studies to determine embryo response to two different temperature increases: +3° (21°C) and +6° (24°C) with respect to the physiological developmental tem- perature (18°C). These temperatures agree with near-future (2100) temperature projections for ocean warming and current marine heatwaves events for the Mediterranean Sea (IPCC, 2019). At 24 h and 48 h development accelerates in a temperature-dependent manner. V-exposed embryos showed alternative developmental phenotypes. Rising temperature caused an increased V intake in embryo cells and a reduction in intracellular calcium. Zymography assays showed that embryos modulated proteolytic activities and the levels of several metalloproteinases. The cytoprotection trig- gered by temperature increase was tested by HSP60 and HSP70 levels. HSPs acted primarily during early development (8 h) and it was mainly mediated by HSP60. The activation of cell-selective apoptosis resulted as a last defense strategy, probably to in part defend the development program. Our results indicate that sea urchin embryos can activate different defense strategies to over- come the negative effects of V exposure on embryo development. The effects of global warming could be met up to a thermotolerant threshold. However, the negative synergistic effects may become irreversible.