Mitochondrial impairment and oxidative stress mediated apoptosis induced by α-Fe2O3nanoparticles in Saccharomyces cerevisiae

In this study, the potential toxicity of α-Fe 2 O 3 -NPs was investigated using a unicellular eukaryote model, Saccharomyces cerevisiae ( S. cerevisiae ). The results showed that cell viability and proliferation were significantly decreased ( p < 0.01) following exposure to 100-600 mg L -1 for 24 h. The IC 50 and LC 50 values were 352 and 541 mg L -1 , respectively. Toxic effects were attributed to α-Fe 2 O 3 -NPs rather than iron ions released from the NPs. α-Fe 2 O 3 -NPs were accumulated in the vacuole and cytoplasm, and the maximum accumulation (3.95 mg g -1 ) was reached at 12 h. About 48.6% of cells underwent late apoptosis/necrosis at 600 mg L -1 , and the mitochondrial transmembrane potential was significantly decreased ( p < 0.01) at 50-600 mg L -1 . Biomarkers of oxidative stress [reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)] and the expression of apoptosis-related genes (Yca1, Nma111, Nuc1 and SOD) were significantly changed after exposure. These combined results indicated that α-Fe 2 O 3 -NPs were rapidly internalized in S. cerevisiae , and the accumulated NPs induced cell apoptosis mediated by mitochondrial impairment and oxidative stress.