Toxicity of vanadium during development of sea urchin embryos: bioaccumulation, calcium depletion, ERK modulation and cell-selective apoptosis
| Autor: | Roberto Chiarelli, Rosaria Scudiero, Valeria Memoli, Maria Carmela Roccheri, Chiara Martino |
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| Přispěvatelé: | Chiarelli, R, Scudiero, R, Memoli, V, Roccheri, Mc, Martino, C, Chiarelli R., Scudiero R., Memoli V., Roccheri M.C., Martino C. |
| Jazyk: | angličtina |
| Rok vydání: | 2022 |
| Předmět: |
Embryo
Nonmammalian Organic Chemistry Apoptosis Vanadium General Medicine calcium uptake vanadium bioaccumulation Paracentrotus lividus embryos stress cell-selective apoptosis cellselective apoptosis Bioaccumulation vanadium bioaccumulation calcium uptake Paracentrotus lividus sea urchin embryos stress cell selective apoptosis Catalysis Computer Science Applications Inorganic Chemistry Paracentrotus Animals Calcium Settore BIO/06 - Anatomia Comparata E Citologia Physical and Theoretical Chemistry Molecular Biology Spectroscopy |
| Zdroj: | International Journal of Molecular Sciences; Volume 23; Issue 11; Pages: 6239 |
| Popis: | Vanadium toxicology is a topic of considerable importance as this metal is widely used in industrial and biomedical fields. However, it represents a potential emerging environmental pollutant because wastewater treatment plants do not adequately remove metal compounds that are subsequently released into the environment. Vanadium applications are limited due to its toxicity, so it is urgent to define this aspect. This metal is associated with sea urchin embryo toxicity as it perturbs embryogenesis and skeletogenesis, triggering several stress responses. Here we investigated its bioaccumulation and the correlation with cellular and molecular developmental pathways. We used cytotoxic concentrations of 1 mM and 500 μM to perform quantitative analyses, showing that vanadium accumulation interferes with calcium uptake during sea urchin development and provokes a disruption in the biomineralization process. At the end of the whole treatment, the accumulation of vanadium was about 14 and 8 μg for embryos treated respectively with 1 mM and 500 μM, showing a dose-dependent response. Then, we monitored the cell signaling perturbation, analyzing key molecular markers of cell survival/cell death mechanisms and the DNA fragmentation associated with apoptosis. This paper clarifies vanadium’s trend to accumulate directly into embryonic cells, interfering with calcium uptake. In addition, our results indicate that vanadium can modulate the ERK pathway and activate a cell-selective apoptosis. These results endorse the sea urchin embryo as an adequate experimental model to study metal-related cellular/molecular responses. |
| Databáze: | OpenAIRE |
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