Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, CHS 23-120, Box 951735, Los Angeles, CA 90095-1735, USA.
J Bioenerg Biomembr. 2009 Dec;41(6):487-91. doi: 10.1007/s10863-009-9254-2.
It has been long thought that neuronal loss in Parkinson's disease (PD) is related to reactive oxygen species from mitochondrial dysfunction. However, there have been few investigations surveying both transcriptome and proteome in PD. This review focuses on recent work using microarrays and mass spectrometry to examine neurotoxicological models of PD in the mouse. Molecular pathways involved in oxidative phosphorylation, oxidative stress, apoptosis/cell death, signal transduction and neurotransmission were highlighted. Analysis of tyrosine nitration suggested that this important post-translational modification, due to conjugation of reactive oxygen species with nitric oxide, may play an important role in signal transduction as well as the molecular pathology of PD. Thus, the combined investigations highlight known pathways in PD but also point to new directions for research, implicating particularly the role of relatively understudied classes of post-translational modifications in normal cell signaling and neurological disorders.
长期以来，人们一直认为帕金森病 (PD) 中的神经元丧失与线粒体功能障碍产生的活性氧有关。然而，针对帕金森病的转录组和蛋白质组进行调查的研究却很少。本综述重点介绍了使用微阵列和质谱法研究 PD 小鼠神经毒理学模型的最新工作。重点介绍了涉及氧化磷酸化、氧化应激、细胞凋亡/死亡、信号转导和神经递质传递的分子途径。酪氨酸硝化分析表明，这种由于活性氧与一氧化氮结合而导致的重要的翻译后修饰可能在信号转导以及 PD 的分子病理学中发挥重要作用。因此，综合研究不仅突出了 PD 中的已知途径，还为研究指明了新的方向，特别涉及相对研究较少的翻译后修饰类别在正常细胞信号和神经紊乱中的作用。
