Significance
Graphene oxide (GO) has attracted considerable interests in biomedical fields, which also resulted in numerous safety risks to human bodies. It is urgently required to establish a paradigm for accurately evaluating their adverse effects in biological systems. This study thoroughly explored the neurotoxicity of GO in PC12 cells. We found GO triggered an increased autophagic response and the impairment of autophagic flux, which was functionally involved in cell apoptosis. Inhibitionofexcessive accumulation of autophagic cargo attenuated apoptotic cell death. Our findings highlight deep considerations on the regulation mechanism of autophagy-lysosomes-apotosis-axis, which will contribute to a better understanding of the neurotoxicity of graphene-family nanomaterials, and provide a new insight in the treatment of cancer cells at nanoscale levels.
Statement of significance
Graphene oxide (GO) has attracted considerable interests in biomedical fields, which also resulted in numerous safety risks to human bodies. It is urgently required to establish a paradigm for accurately evaluating their adverse effects in biological systems. This study thoroughly explored the neurotoxicity of GO in PC12 cells. We found GO triggered an increased autophagic response and the impairment of autophagic flux, which was functionally involved in cell apoptosis. Inhibitionofexcessive accumulation of autophagic cargo attenuated apoptotic cell death. Our findings highlight deep considerations on the regulation mechanism of autophagy-lysosomes-apotosis-axis, which will contribute to a better understanding of the neurotoxicity of graphene-family nanomaterials, and provide a new insight in the treatment of cancer cells at nanoscale levels.