Numakawa Tadahiro, Matsumoto Tomoya, Numakawa Yumiko, Richards Misty, Yamawaki Shigeto, Kunugi Hiroshi
Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo 187-8502, Japan.
J Toxicol. 2011;2011:405194. doi: 10.1155/2011/405194. Epub 2011 May 31.
Oxidative stress is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. Low levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are important for maintenance of neuronal function, though elevated levels lead to neuronal cell death. A complex series of events including excitotoxicity, Ca(2+) overload, and mitochondrial dysfunction contributes to oxidative stress-mediated neurodegeneration. As expected, many antioxidants like phytochemicals and vitamins are known to reduce oxidative toxicity. Additionally, growing evidence indicates that neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and estrogens significantly prevent neuronal damage caused by oxidative stress. Here, we review and discuss recent studies addressing the protective mechanisms of neurotrophic factors and estrogen within this system.
氧化应激参与了神经退行性疾病的发病机制，如阿尔茨海默病、帕金森病和亨廷顿病。低水平的活性氧（ROS）和活性氮（RNS）对于维持神经元功能很重要，不过水平升高会导致神经元细胞死亡。一系列复杂事件，包括兴奋性毒性、Ca(2+)超载和线粒体功能障碍，都促成了氧化应激介导的神经退行性变。不出所料，许多抗氧化剂，如植物化学物质和维生素，已知可降低氧化毒性。此外，越来越多的证据表明，神经营养因子，如脑源性神经营养因子（BDNF）和雌激素，可显著预防氧化应激引起的神经元损伤。在此，我们回顾并讨论了近期关于该系统中神经营养因子和雌激素保护机制的研究。
