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首页> 外文期刊>Environmental toxicology and chemistry >SILVER NANOPARTICLES AND DISSOLVED SILVER ACTIVATE CONTRASTING IMMUNE RESPONSES AND STRESS-INDUCED HEAT SHOCK PROTEIN EXPRESSION IN SEA URCHIN
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SILVER NANOPARTICLES AND DISSOLVED SILVER ACTIVATE CONTRASTING IMMUNE RESPONSES AND STRESS-INDUCED HEAT SHOCK PROTEIN EXPRESSION IN SEA URCHIN

机译：银纳米颗粒和溶解的银活化剂对免疫反应的响应和应力诱导的热激蛋白在海胆蛋白中的表达

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Using immune cells of sea urchin Strongylocentrotus droebachiensis in early development as a model, the cellular protective mechanisms against ionic and poly(allylamine)-coated silver nanoparticle (AgNPs; 14 +/- 6 nm) treatments at 100 mu g L-1 were investigated. Oxidative stress, heat shock protein expression, and pigment production by spherulocytes were determined as well as AgNP translocation pathways and their multiple effects on circulating coelomocytes. Sea urchins showed an increasing resilience to Ag over time because ionic Ag is accumulated in a steady way, although nanoAg levels dropped between 48 h and 96 h. A clotting reaction emerged on tissues injured by dissolved Ag (present as chloro-complexes in seawater) between 12 h and 48 h. Silver contamination and nutritional state influenced the production of reactive oxygen species. After passing through coelomic sinuses and gut, AgNPs were found in coelomocytes. Inside blood vessels, apoptosis-like processes appeared in coelomocytes highly contaminated by poly(allylamine)-coated AgNPs. Increasing levels of Ag accumulated by urchins once exposed to AgNPs pointed to a Trojan-horse mechanism operating over 12-d exposure. However, under short-term treatments, physical interactions of poly(allylamine)-coated AgNPs with cell structures might be, at some point, predominant and responsible for the highest levels of stress-related proteins detected. The present study is the first report detailing nano-translocation in a marine organism and multiple mechanisms by which sea urchin cells can deal with toxic AgNPs. (C) 2016 SETAC
机译：以海胆Strongylocentrotus droebachiensis早期发育的免疫细胞为模型，研究了离子和聚（烯丙胺）涂层的银纳米颗粒（AgNPs; 14 +/- 6 nm）处理在100μg L-1下的细胞保护机制。 。测定了氧化应激，热休克蛋白的表达和由球细胞产生的色素，以及AgNP易位途径及其对循环内皮细胞的多重影响。海胆随着时间的推移显示出对Ag的增强抵抗力，因为离子Ag以稳定的方式积累，尽管纳米Ag含量在48 h至96 h之间下降。在12小时至48小时之间，被溶解的银（在海水中以氯络合物形式存在）损伤的组织上出现了凝结反应。银污染和营养状态影响了活性氧的产生。经过鼻窦和肠腔后，在内皮细胞中发现了AgNPs。在血管内部，被聚（烯丙胺）包被的AgNPs高度污染的内皮细胞中出现了类似凋亡的过程。一旦暴露于AgNPs，海胆累积的Ag水平就会增加，这表明特洛伊木马机制在暴露12天后会起作用。然而，在短期治疗下，聚（烯丙胺）包被的AgNPs与细胞结构的物理相互作用在某些时候可能是主要的，并负责检测到的最高水平的应激相关蛋白。本研究是第一份报告，详细介绍了海洋生物中的纳米易位以及海胆细胞可以处理有毒AgNP的多种机制。 （C）2016年SETAC

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