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Mitochondrial impairment and oxidative stress mediated apoptosis induced by α-Fe2O3 nanoparticles in Saccharomyces cerevisiae

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Abstract

In this study, the potential toxicity of α-Fe2O3-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 IC50 and LC50 values were 352 and 541 mg L−1, respectively. Toxic effects were attributed to α-Fe2O3-NPs rather than iron ions released from the NPs. α-Fe2O3-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-Fe2O3-NPs were rapidly internalized in S. cerevisiae, and the accumulated NPs induced cell apoptosis mediated by mitochondrial impairment and oxidative stress.

Graphical abstract: Mitochondrial impairment and oxidative stress mediated apoptosis induced by α-Fe2O3 nanoparticles in Saccharomyces cerevisiae

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Publication details

The article was received on 28 Apr 2017, accepted on 17 Jul 2017 and first published on 18 Jul 2017


Article type: Paper
DOI: 10.1039/C7TX00123A
Citation: Toxicol. Res., 2017, Advance Article
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    Mitochondrial impairment and oxidative stress mediated apoptosis induced by α-Fe2O3 nanoparticles in Saccharomyces cerevisiae

    S. Zhu, F. Luo, B. Zhu and G. Wang, Toxicol. Res., 2017, Advance Article , DOI: 10.1039/C7TX00123A

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