RESUMO
Using Saccharomyces cerevisiae as an experimental model, the potential toxicological effects of Fe3O4 nanoparticles (Fe3O4-NPs) were investigated following exposure to 0-600â¯mg/L for 24â¯h. Results revealed that cell proliferation was significantly inhibited by Fe3O4-NPs with an IC50 value of 326.66â¯mg/L. Mortality showed a concentration-dependent increase, and the highest concentration in this study (600â¯mg/L) resulted in 22.30% mortality. In addition, Effects on proliferation and mortality were accounted for Fe3O4-NPs rather than iron ion released from Fe3O4-NPs. Scanning and transmission electron microscope observation showed that Fe3O4-NPs extensively attached on the cell surfaces, causing cells to deform and shrink. Moreover, Fe3O4-NPs could be internalized in S. cerevisiae cells via endocytosis and then be distributed in cytoplasm and vesicles. The data of uptake kinetics demonstrated that the maximal accumulation (4.898â¯mg/g) was reached at 15â¯h. Besides, percentage of late apoptosis/necrosis was observably increased (pâ¯<â¯0.01) at 600â¯mg/L (15.80%), and the expression levels of apoptosis-related genes (SOD, Yca1 and Nuc1) were dramatically increased following exposure to Fe3O4-NPs for 24â¯h. As expected, mitochondrial transmembrane potential was significantly decreased (pâ¯<â¯0.01) at 50-600â¯mg/L, and biomarkers of oxidative stress (ROS, CAT and SOD) were also markedly changed following exposure. Altogether, the combined results so far indicated Fe3O4-NPs could induce S. cerevisiae cell apoptosis that mediated by mitochondrial impairment and oxidative stress.
