Graphene oxide disrupted mitochondrial homeostasis through inducing intracellular redox deviation and autophagy-lysosomal network dysfunction in SH-SY5Y cells.

Graphene oxide (GO) nanomaterials have significant advantages for drug delivery and electrode materials in neural science, however, their exposure risks to the central nervous system (CNS) and toxicity concerns are also increased. The current studies of GO-induced neurotoxicity remain still ambiguous, let alone the mechanism of how complicated GO chemistry affects its biological behavior with neural cells. In this study, we characterized the commercially available GO in detail and investigated its biological adverse effects using cultured SH-SY5Y cells. We found that ultrasonic processing in medium changed the oxidation status and surface reactivity on the planar surface of GO due to its hydration activity, causing lipid peroxidation and cell membrane damage. Subsequently, ROS-disrupted mitochondrial homeostasis, resulting from the activation of NOX2 signaling, was observed following GO internalization. The autophagy-lysosomal network was initiated as a defensive reaction to obliterate oxidative damaged mitochondria and foreign nanomaterials, which was ineffective due to reduced lysosomal degradation capacity. These sequential cellular responses exacerbated mitochondrial stress, leading to apoptotic cell death. These data highlight the importance of the structure-related activity of GO on its biological properties and provide an in-depth understanding of how GO-derived cellular redox signaling induces mitochondrion-related cascades that modulate cell functionality and survival.

Nanoscaffolds in promoting regeneration of the peripheral nervous system.

The ability to surgically repair peripheral nerve injuries is urgently needed. However, traditional tissue engineering techniques, such as autologous nerve transplantation, have some limitations. Therefore, tissue engineered autologous nerve grafts have become a suitable choice for nerve repair. Novel tissue engineering techniques derived from nanostructured conduits have been shown to be superior to other successful functional neurological structures with different scaffolds in terms of providing the required structures and properties. Additionally, different biomaterials and growth factors have been added to nerve scaffolds to produce unique biological effects that promote nerve regeneration and functional recovery. This review summarizes the application of different nanoscaffolds in peripheral nerve repair and further analyzes how the nanoscaffolds promote peripheral nerve regeneration.

Central neurotoxicity induced by the instillation of ZnO and TiO2 nanoparticles through the taste nerve pathway.

AIM: To explore whether nanoparticles (NPs) can be transported into the CNS via the taste nerve pathway. MATERIALS & METHODS: ZnO and TiO2 NPs were tongue-instilled to male Wistar rats. Toxicity was assessed by Zn/Ti biodistribution, histopathological examination, oxidative stress assay, quantitative reverse-transcriptase PCR analysis, learning and memory capabilities. RESULTS: ZnO NPs and TiO2 NPs significantly deposited in the nerves and brain, respectively. The histopathological examination indicated a slight injury in the cerebral cortex and hippocampus. Ultrastructural changes and an imbalanced oxidative stress were observed. The Morris water maze results showed that the learning and memory of rats were impaired. CONCLUSION: NPs can enter the CNS via the taste nerve translocation pathway and induce a certain adverse effect.