Wang Xuezi, Dong Baolin, Gan Qi, Li Jianjun, Wu Peng, Guan Yupeng, Wang Jiancheng
Scientific Research Center, The Seventh Affiliated Hospital Sun Yat-Sen University Shenzhen P. R. China.
School of Medicine Sun Yat-Sen University Shenzhen P. R. China.
FASEB Bioadv. 2025 Sep 3;7(8):e70041. doi: 10.1096/fba.2025-00093. eCollection 2025 Aug.
Oxidative stress is characterized by an imbalance between the production and elimination of free radicals, where the rate of free radical generation surpasses the rate of their removal. This imbalance can lead to tissue and organ damage, contributing to the pathogenesis of various diseases. The nervous system, due to its high oxygen consumption, is particularly susceptible to oxidative stress. Numerous neurotoxins can induce neurotoxicity through oxidative stress, thereby contributing to the onset of neurodegenerative diseases, such as Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis. Furthermore, neurotoxicity can exacerbate oxidative stress by disrupting mitochondrial metabolism and impairing the activity of antioxidant enzymes, thereby intensifying neurotoxic effects. This review examines the mechanisms underlying the interaction between oxidative stress and neurotoxicity and explores strategies to mitigate neurotoxicity by reducing oxidative stress, with the aim of informing future clinical approaches for the treatment of neurodegenerative diseases.
氧化应激的特征是自由基产生与清除之间的失衡,即自由基生成速率超过其清除速率。这种失衡会导致组织和器官损伤,促进各种疾病的发病机制。神经系统由于其高氧消耗,特别容易受到氧化应激的影响。许多神经毒素可通过氧化应激诱导神经毒性,从而导致神经退行性疾病的发生,如帕金森病、阿尔茨海默病、亨廷顿病和肌萎缩侧索硬化症。此外,神经毒性可通过破坏线粒体代谢和损害抗氧化酶的活性来加剧氧化应激,从而增强神经毒性作用。本综述探讨了氧化应激与神经毒性之间相互作用的潜在机制,并探索了通过降低氧化应激来减轻神经毒性的策略,旨在为未来治疗神经退行性疾病的临床方法提供参考。