Toxicity mechanism of silver nanoparticles to Chlamydomonas reinhardtii: photosynthesis, oxidative stress, membrane permeability, and ultrastructure analysis

Silver nanoparticles (Ag-NPs) are widely used in daily life and inevitably discharged into the aquatic environment, causing increasingly serious pollution. Research on the toxicity of Ag-NPs is still in infancy, little information is available on the relationships between oxidative stress and antioxidant, as well as damaging degrees of Ag-NPs to cellular structural components of Chlamydomonas reinhardtii (C. reinhardtiii). In the present study, we revealed the toxicity mechanism of C. reinhardtii under Ag-NPs stress using flow cytometry (FCM), metabolic methods, and transmission electron microscopy. The results showed that the chloroplasts were damaged and the synthesis of photosynthetic pigments was inhibited under Ag-NPs stress, which inhibited the growth of C. reinhardtii. Meanwhile, Ag-NPs also caused C. reinhardtii to produce excessive reactive oxygen species (ROS), increased malondialdehyde content and changed the permeability of cell membrane, resulting in the acceleration of internalization of Ag-NPs. The decrease of cell size and intracellular chlorophyll autofluorescence was observed with FCM. To deal with the induced excessive ROS that could lead to lethal and irreversible structure damage, C. reinhardtii activated antioxidant enzymes including superoxide dismutase and peroxidase. This study provides new information for better understanding the potential toxicity risks of Ag-NPs in the aquatic environment.

Automated summary

Silver nanoparticles have toxic effects on algal cells, damaging chloroplasts, inhibiting growth, and inducing excessive ROS production and changes in cell membrane permeability. To counteract excessive ROS, algae activate antioxidant enzymes.