Abstract
Both oxidative stress and neurotoxicity are huge challenges to human health, and effective methods and agents for resisting these adverse effects are limited, especially in vivo. It is shown here that, compared to large graphene oxide (GO) nanosheets, GO quantum dots (GOQDs), as nanozymes, efficiently reduce reactive oxygen species (ROS) and H2O2 in 1‐methyl‐4‐phenyl‐pyridinium ion (MPP+)‐induced PC12 cells. In addition, GOQDs exert neuroprotective effects in a neuronal cell model by decreasing apoptosis and α‐synuclein. GOQDs also efficiently diminish ROS, apoptosis, and mitochondrial damage in zebrafish treated with MPP+. Furthermore, GOQDs‐pretreated zebrafish shows increased locomotive activity and Nissl bodies in the brain, confirming that GOQDs ameliorate MPP+‐induced neurotoxicity, in contrast to GO nanosheets. GOQDs contribute to neurotoxic amelioration by increasing amino acid metabolism, decreasing tricarboxylic acid cycle activity, and reducing steroid biosynthesis, fatty acid biosynthesis, and galactose metabolic pathway activity, which are related to antioxidation and neurotransmission. Meanwhile, H2O2 decomposition and Fenton reactions suggest the catalase‐like activity of GOQDs. GOQDs can translocate into zebrafish brains and exert catalase‐mimicking activity to resist oxidation in the intracellular environment. Unlike general nanomaterials, biocompatible GOQDs demonstrate their high potential for human health by reducing oxidative stress and inhibiting neurotoxicity.
Highlights
Increasing amino acid metabolism, decreasing tricarboxylic acid cycle activity, a decreased susceptibility to denaturaand reducing steroid biosynthesis, fatty acid biosynthesis, and galactose metabolic pathway activity, which are related to antioxidation and neurotransmission
Our recent study showed that graphene oxide (GO) nanosheets translocated into the brains of zebrafish and induced oxidative stress and neurotoxicity.[5b]. Compared with GO, GO quantum dots (GOQDs) protected PC12 cells and larval zebrafish from neurotoxicity; the underlying mechanisms are shown in Figure S10 (Supporting Information)
Increased locomotive activity and Nissl bodies were observed in the brains of GOQDs-pretreated larvae and further confirmed that the GOQDs mitigated neurotoxicity
Summary
Increasing amino acid metabolism, decreasing tricarboxylic acid cycle activity, a decreased susceptibility to denaturaand reducing steroid biosynthesis, fatty acid biosynthesis, and galactose metabolic pathway activity, which are related to antioxidation and neurotransmission. H2O2 decomposition and Fenton reactions suggest the catalase-like activity of GOQDs. GOQDs can translocate into zebrafish brains tion; and an ability to mimic the cellular matrix in natural tissues or body fluid, in a manner that is similar to enzymes and proteins, for therapeutic applications.[3]. Biocompatible GOQDs demonstrate their high potential for human health by reducing oxidative stress and inhibiting neurotoxicity. Neurotoxicity has severe influences on human health and has ified GO has attracted considerable attention in the clinic due pathological features, such as memory disorders, learning ability to the enzyme-like activities and biocompatibility of modified decline, behavioral dysfunction, and cognitive dysfunction.[1] GO.[6] GO quantum dots (GOQDs), which are smaller versions of GO, combine the virtues of GO and QDs and have fluores-
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