February 14, 2024 | Yandong Bai, Yongmei Li, Yuemei Li, and Lijie Tian
Cerium oxide nanoparticles (CeO₂ NPs) exhibit catalytic activities due to the redox transitions between Ce³⁺ and Ce⁴⁺ ions, enabling them to mimic various enzyme functions, including superoxide dismutase (SOD), catalase (CAT), peroxidase, and oxidase activities. These properties allow CeO₂ NPs to act as antioxidants, scavenging reactive oxygen species (ROS) and reactive nitrogen species (RNS), and are used in biomedical applications such as disease diagnosis and treatment. The review discusses the catalytic mechanisms and enzyme-like activities of CeO₂ NPs, highlighting their potential in treating diseases related to oxidative damage, including brain, bone, nerve, and vascular disorders. CeO₂ NPs can neutralize harmful radicals like the hydroxyl radical (·OH) through the Fenton reaction, reducing oxidative stress and cellular damage. They also exhibit phosphatase-like activity, dephosphorylating phosphoproteins and playing roles in signal transduction and cell regulation. In brain disease treatment, CeO₂ NPs have shown promise in reducing oxidative damage and neuroinflammation, as demonstrated by studies on Alzheimer's and Parkinson's diseases. For bone diseases, CeO₂ NPs can prevent ionizing radiation-induced bone loss and promote bone formation. They also display anti-inflammatory effects by modulating the AMPK signaling pathway and reducing inflammatory cytokines. In vascular therapy, CeO₂ NPs can enhance therapeutic effects by catalyzing ROS and improving endothelial function. Additionally, CeO₂ NPs are effective in treating acute injuries, such as lung and liver damage, and in wound healing by promoting tissue regeneration and reducing inflammation. The review emphasizes the importance of nanoparticle size, surface modifications, and environmental factors in determining the biological activity and toxicity of CeO₂ NPs. While CeO₂ NPs show great potential in biomedical applications, their clinical use requires further research to address toxicity and long-term safety concerns.Cerium oxide nanoparticles (CeO₂ NPs) exhibit catalytic activities due to the redox transitions between Ce³⁺ and Ce⁴⁺ ions, enabling them to mimic various enzyme functions, including superoxide dismutase (SOD), catalase (CAT), peroxidase, and oxidase activities. These properties allow CeO₂ NPs to act as antioxidants, scavenging reactive oxygen species (ROS) and reactive nitrogen species (RNS), and are used in biomedical applications such as disease diagnosis and treatment. The review discusses the catalytic mechanisms and enzyme-like activities of CeO₂ NPs, highlighting their potential in treating diseases related to oxidative damage, including brain, bone, nerve, and vascular disorders. CeO₂ NPs can neutralize harmful radicals like the hydroxyl radical (·OH) through the Fenton reaction, reducing oxidative stress and cellular damage. They also exhibit phosphatase-like activity, dephosphorylating phosphoproteins and playing roles in signal transduction and cell regulation. In brain disease treatment, CeO₂ NPs have shown promise in reducing oxidative damage and neuroinflammation, as demonstrated by studies on Alzheimer's and Parkinson's diseases. For bone diseases, CeO₂ NPs can prevent ionizing radiation-induced bone loss and promote bone formation. They also display anti-inflammatory effects by modulating the AMPK signaling pathway and reducing inflammatory cytokines. In vascular therapy, CeO₂ NPs can enhance therapeutic effects by catalyzing ROS and improving endothelial function. Additionally, CeO₂ NPs are effective in treating acute injuries, such as lung and liver damage, and in wound healing by promoting tissue regeneration and reducing inflammation. The review emphasizes the importance of nanoparticle size, surface modifications, and environmental factors in determining the biological activity and toxicity of CeO₂ NPs. While CeO₂ NPs show great potential in biomedical applications, their clinical use requires further research to address toxicity and long-term safety concerns.