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钒对海胆胚胎的毒性作用。

Toxic effects induced by vanadium on sea urchin embryos.

机构信息

Department of Biological, Chemical and Pharmaceutical Sciences and Technologies (STEBICEF), University of Palermo, Viale Delle Scienze Building 16, Palermo, 90128, Italy.

出版信息

Chemosphere. 2021 Jul;274:129843. doi: 10.1016/j.chemosphere.2021.129843. Epub 2021 Feb 3.

Abstract

Vanadium, a naturally occurring element widely distributed in soil, water and air, has received considerable interest because its compounds are often used in different applications, from industry to medicine. While the possible medical use of vanadium compounds is promising, its potential harmful effects on living organisms are still unclear. Here, for the first time, we provide a toxicological profile induced by vanadium on Paracentrotus lividus sea urchin embryos, reporting an integrated and comparative analysis of the detected effects reflecting vanadium-toxicity. At the morphological level we found a dose-dependent induction of altered phenotypes and of skeletal malformations. At the molecular levels, vanadium-exposed embryos showed the activation of the cellular stress response, in particular, autophagy and a high degree of cell-selective apoptosis in a dose-dependent manner. The stress response mediated by heat shock proteins seems to counteract the damage induced by low and intermediate concentrations of vanadium while the high cytotoxic concentrations induce more marked cell death mechanisms. Our findings, reporting different mechanisms of toxicity induced by vanadium, contribute to increase the knowledge on the possible threat of vanadium for marine organisms and for both environmental and human health.

摘要

钒是一种广泛分布于土壤、水和空气中的天然存在的元素,由于其化合物常用于从工业到医学等不同领域,因此引起了相当大的关注。虽然钒化合物的可能医学用途很有前景,但它对生物体的潜在有害影响尚不清楚。在这里,我们首次提供了关于钒对海胆胚胎的毒性特征,报告了对反映钒毒性的检测到的影响进行的综合和比较分析。在形态学水平上,我们发现了表型改变和骨骼畸形的剂量依赖性诱导。在分子水平上,暴露于钒的胚胎表现出细胞应激反应的激活,特别是自噬和细胞选择性凋亡,呈剂量依赖性。热休克蛋白介导的应激反应似乎可以抵消低浓度和中浓度钒引起的损伤,而高细胞毒性浓度则诱导更明显的细胞死亡机制。我们的研究结果报告了钒诱导的不同毒性机制,有助于增加对钒对海洋生物以及对环境和人类健康可能构成的威胁的认识。

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