Acutely induced cell mortality in the unicellular green alga Chlamydomonas reinhardtii (Chlorophyceae) following exposure to acrylic resin nanoparticles
Acutely induced cell mortality in the unicellular green alga Chlamydomonas reinhardtii (Chlorophyceae) following exposure to acrylic resin nanoparticles
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DOI：
10.1111/jpy.12798
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发表时间：
2018-11
影响因子：
2.9
通讯作者：
D. Widyaningrum;Daisuke Iida;Yuma Tanabe;Y. Hayashi;Sari Dewi Kurniasih;T. Ohama
中科院分区：
文献类型：
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作者：
D. Widyaningrum;Daisuke Iida;Yuma Tanabe;Y. Hayashi;Sari Dewi Kurniasih;T. Ohama
纳米颗粒具有独特的性质，使其在工业和医疗技术行业中具有吸引力，但也可能对生物有害，因此了解它们的分子作用机制至关重要。我们考察了三种不同大小的聚氰基丙烯酸异丁酯纳米粒子(IBCA-NPs)对单细胞绿藻衣藻的影响。我们发现，暴露于IBCA-NPs后，莱茵梭子蟹立即表现出异常的游泳行为。此外，1小时后，大部分细胞停止游泳，10%-30%的细胞被台盼蓝染色，表明这些细胞的质膜已严重受损。细胞超微结构观察显示，细胞壁遭到严重破坏，许多IBCA-NPs定位于细胞壁与质膜之间的间隙，有的甚至位于细胞质内。对三种不同细胞壁条件的莱茵隐杆线虫的比较进一步表明，在没有细胞壁的情况下，细胞死亡率增加得更快。有趣的是，如果总表面积相同，无论IBCA-NP大小如何，细胞死亡率随时间的变化基本上是相同的。此外，对IBCA-NPs轨迹的直接观察表明，第一个触发因素是它们与细胞壁的接触，这很可能伴随着细胞壁表面吸附的蛋白质的失活或移除。细胞死亡伴随着活性氧的过量产生，在恒光下生长的细胞中比在黑暗中更容易检测到这种情况。
Nanoparticles have unique properties that make them attractive for use in industrial and medical technology industries but can also be harmful to living organisms, making an understanding of their molecular mechanisms of action essential. We examined the effect of three different sized poly(isobutyl‐cyanoacrylate) nanoparticles (iBCA‐NPs) on the unicellular green alga Chlamydomonas reinhardtii. We found that exposure to iBCA‐NPs immediately caused C. reinhardtii to display abnormal swimming behaviors. Furthermore, after one hour, most of the cells had stopped swimming and 10%–30% of cells were stained with trypan blue, suggesting that these cells had severely impaired plasma membranes. Observation of the cyto‐ultrastructure showed that the cell walls had been severely damaged and that many iBCA‐NPs were located in the space between the cell wall and plasma membrane, as well as inside the cytosol in some cases. A comparison of three strains of C. reinhardtii with different cell wall conditions further showed that the cell mortality ratio increased more rapidly in the absence of a cell wall. Interestingly, cell mortality over time was essentially identical regardless of iBCA‐NP size if the total surface area was the same. Furthermore, direct observation of the trails of iBCA‐NPs indicated that the first trigger was their contact with the cell wall, which is most likely accompanied by the inactivation or removal of adsorbed proteins from the cell wall surface. Cell mortality was accompanied by the overproduction of reactive oxygen species, which was detected more readily in cells grown under constant light rather than in the dark.