摘要
So far, potential chronic risks of silver nanoparticles (AgNPs) on organisms remain largely unknown, especially molecular-level alterations at the environmentally relevant concentrations. In this study, Chlamydomonas reinhardtii ( C. reinhardtii ) is used as the model organism to investigate chronic toxic effects of 100 μg/L and 50 mg/L AgNPs for 120 d. Physiological studies showed that AgNPs attached on cell surface and internalized into algal cells, inducing the increase in cell permeability, the decline in cell size and granularity, the damage in photosynthetic systems, and the production of reactive oxygen species (ROS). The damage in photosynthetic systems was reflected in the decline in the photosynthetic activity ( F v / F m ), photosynthetic efficiency ( F v / F 0 ), and fluorescence intensities of Peridinin-Chlorophyll Protein Complex and Allophycocyanin. C. reinhardtii attempted to increase the absorption (ABS/RC), dissipation (Dl 0 /RC) and trapping (TR 0 /RC) of light energy for adapting AgNPs stress. In addition, the accumulation of glutathione (GSH), ascorbate (ASC), and the irreversible cell apoptosis was observed in 50 mg/L AgNPs group. Transcriptomics showed that most of genes involved in photosynthetic systems (e.g. photo-oxidation, light harvesting, and chlorophyll synthesis) were down regulated, providing evidence for chloroplast as the main target of AgNPs toxicity. The up-regulation of some genes, involved in ASC and aldarate metabolism, and GSH metabolism, showed self-adaptive capacity of C. reinhardtii to eliminate ROS under long-term exposure to AgNPs. Phagocytosis and endocytosis were the main pathways of the internalization of AgNPs. This study provided valuable data for potential chronic risks of nanoparticles in aquatic environment.
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