Canesi Laura, Ciacci Caterina, Betti Michele, Fabbri Rita, Canonico Barbara, Fantinati Andrea, Marcomini Antonio, Pojana Giulio
Dipartimento di Biologia, Università di Genova, Genova, Italy.
Environ Int. 2008 Nov;34(8):1114-9. doi: 10.1016/j.envint.2008.04.002. Epub 2008 May 19.
The potential for human and ecological toxicity associated with nanomaterials is a growing area of investigation. In mammalian cells, nanoparticles have been shown to induce inflammation and oxidative stress, and changes in cell signalling and gene expression. As the nanotechnology industries increase production, nanoscale products and by products will enter the aquatic environment, posing a possible threat to aquatic organisms. In particular, filter-feeding organisms may represent a unique target group for nanoparticle toxicology. In this work, the effects of commercial nanosized carbon black (NCB) on the immune cells, the hemocytes, of the bivalve mollusc Mytilus, and the possible mechanisms involved were investigated. The results demonstrate that NCB (1, 5, and 10 microg/ml), did not induce significant lysosomal membrane destabilization, as evaluated by the NR retention time assay. A concentration-dependent uptake of NCB by hemocytes was observed and it was associated by a rapid increase in extracellular lysozyme release, extracellular oxyradical production, and nitric oxide (NO) release. Moreover, at the highest concentration tested, NCB induced significant changes in mitochondrial parameters (decrease mitochondrial mass/number and membrane potential), as evaluated by flow cytometry. The effects of NCB were mediated by rapid activation of the stress-activated MAPKs (Mitogen Activated Protein Kinases) p38 and JNKs, that play a key role in immune and inflammatory responses. The results demonstrate that in mussel hemocytes like in mammalian cells NCB exposure can induce inflammatory processes, and indicate that bivalve immunocytes can represent a suitable model for investigating the effects and modes of action of nanoparticles in the cells of aquatic invertebrates.
与纳米材料相关的对人类和生态的潜在毒性是一个不断发展的研究领域。在哺乳动物细胞中，纳米颗粒已被证明会引发炎症和氧化应激，并导致细胞信号传导和基因表达的变化。随着纳米技术产业产量的增加，纳米级产品和副产品将进入水生环境，对水生生物构成潜在威胁。特别是滤食性生物可能是纳米颗粒毒理学的一个独特目标群体。在这项工作中，研究了商业纳米级炭黑（NCB）对双壳贝类贻贝免疫细胞（血细胞）的影响以及可能涉及的机制。结果表明，通过NR保留时间测定法评估，NCB（1、5和10微克/毫升）未诱导明显的溶酶体膜不稳定。观察到血细胞对NCB的浓度依赖性摄取，并且伴随着细胞外溶菌酶释放、细胞外氧自由基产生和一氧化氮（NO）释放的迅速增加。此外，通过流式细胞术评估，在测试的最高浓度下，NCB诱导了线粒体参数的显著变化（线粒体质量/数量和膜电位降低）。NCB的作用是由应激激活的丝裂原活化蛋白激酶（MAPKs）p38和JNKs的快速激活介导的，它们在免疫和炎症反应中起关键作用。结果表明，在贻贝血细胞中，如同在哺乳动物细胞中一样，接触NCB可诱导炎症过程，并表明双壳贝类免疫细胞可作为研究纳米颗粒在水生无脊椎动物细胞中的作用和作用方式的合适模型。
