IntroductionNanomaterials such as silver nanoparticles (AgNPs) have gained widespread application across various fields. However, the large-scale production and application of AgNPs have raised concerns about their distribution in the environment and potential pollution issues.MethodsThis study investigates the toxic effects of AgNPs on the diatom Phaeodactylum tricornutum by employing electron microscopy for cellular observation, quantifying apoptotic cell numbers, and measuring antioxidant indicators. The research examines how varying concentrations of AgNPs induce stress in P. tricornutum and the specific mechanisms of the toxic effect.ResultsThe findings reveal that AgNPs induce apoptosis in P. tricornutum cells by triggering a mitochondria-mediated pathway, marked by a decrease in mitochondrial membrane potential and the activation of caspase enzymes. Additionally, AgNP exposure results in an overproduction of reactive oxygen species (ROS) within the algal cells, leading to lipid peroxidation of the cell membrane and a consequent increase in malondialdehyde (MDA) levels. This oxidative stress response induces the upregulation of antioxidant enzyme activities in an attempt to mitigate the excessive ROS.DiscussionROS is identified as the primary factor responsible for inducing mitochondria-mediated apoptosis. The research results will provide a theoretical basis for understanding the toxic effects and mechanisms of AgNPs on marine microalgae.

中文翻译：

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AgNPs暴露下ROS诱导的三角鳍指依赖性细胞凋亡的机制


简介纳米银纳米颗粒 （AgNP） 等纳米材料已在各个领域得到广泛应用。然而，AgNPs 的大规模生产和应用引发了人们对其在环境中的分布和潜在污染问题的担忧。方法本研究采用电子显微镜进行细胞观察，定量凋亡细胞数量，并测量抗氧化指标，探讨 AgNPs 对硅藻 Phaeodactylum tricornutum 的毒性作用。该研究考察了不同浓度的 AgNPs 如何诱导三角 P. tricornutum 的应激以及毒性作用的具体机制。结果研究结果显示，AgNPs 通过触发线粒体介导的途径诱导三角 P. 细胞凋亡，其特征是线粒体膜电位降低和 caspase 酶激活。此外，AgNP 暴露导致藻类细胞内活性氧 （ROS） 过量产生，导致细胞膜脂质过氧化，从而导致丙二醛 （MDA） 水平增加。这种氧化应激反应诱导抗氧化酶活性上调，以试图减轻过量的 ROS。DiscussionROS 被确定为负责诱导线粒体介导的细胞凋亡的主要因子。研究结果将为理解 AgNPs 对海洋微藻的毒性作用和机制提供理论依据。