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4-Hydroxy-2-Nonenal, a Reactive Product of Lipid Peroxidation, and Neurodegenerative Diseases: A Toxic Combination Illuminated by Redox Proteomics Studies

机译:4-羟基-2-壬醛,脂质过氧化反应产物和神经退行性疾病:氧化还原蛋白质组学研究的有毒组合。

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摘要

Significance: Among different forms of oxidative stress, lipid peroxidation comprises the interaction of free radicals with polyunsaturated fatty acids, which in turn leads to the formation of highly reactive electrophilic aldehydes. Among these, the most abundant aldehydes are 4-hydroxy-2-nonenal (HNE) and malondialdehyde, while acrolein is the most reactive. HNE is considered a robust marker of oxidative stress and a toxic compound for several cell types. Proteins are particularly susceptible to modification caused by HNE, and adduct formation plays a critical role in multiple cellular processes. Recent Advances: With the outstanding progress of proteomics, the identification of putative biomarkers for neurodegenerative disorders has been the main focus of several studies and will continue to be a difficult task. Critical Issues: The present review focuses on the role of lipid peroxidation, particularly of HNE-induced protein modification, in neurodegenerative diseases. By comparing results obtained in different neurodegenerative diseases, it may be possible to identify both similarities and specific differences in addition to better characterize selective neurodegenerative phenomena associated with protein dysfunction. Results obtained in our laboratory and others support the common deregulation of energy metabolism and mitochondrial function in neurodegeneration. Future Directions: Research towards a better understanding of the molecular mechanisms involved in neurodegeneration together with identification of specific targets of oxidative damage is urgently required. Redox proteomics will contribute to broaden the knowledge in regard to potential biomarkers for disease diagnosis and may also provide insight into damaged metabolic networks and potential targets for modulation of disease progression. Antioxid. Redox Signal. 17, 1590-1609.
机译:启示:在不同形式的氧化应激中,脂质过氧化包括自由基与多不饱和脂肪酸的相互作用,进而导致高反应性亲电子醛的形成。其中,最丰富的醛是4-羟基-2-壬烯醛(HNE)和丙二醛,而丙烯醛的活性最高。 HNE被认为是氧化应激的可靠标志物,并且是几种细胞类型的有毒化合物。蛋白质特别容易受到HNE引起的修饰的影响,加合物的形成在多个细胞过程中起关键作用。最新进展:随着蛋白质组学的显着进步,用于神经退行性疾病的假定生物标志物的鉴定一直是数项研究的主要重点,并将继续是一项艰巨的任务。关键问题:本综述着眼于脂质过氧化,特别是HNE诱导的蛋白质修饰在神经退行性疾病中的作用。通过比较在不同的神经退行性疾病中获得的结果,除了更好地表征与蛋白功能障碍相关的选择性神经退行性现象外,还可以识别相似性和特异性差异。在我们实验室和其他实验室获得的结果支持神经变性中能量代谢和线粒体功能的普遍失调。未来方向:迫切需要进行研究,以更好地了解神经变性所涉及的分子机制,并确定特定的氧化损伤靶标。氧化还原蛋白质组学将有助于拓宽有关疾病诊断的潜在生物标记物的知识,还可以深入了解受损的代谢网络和调节疾病进程的潜在靶标。抗氧化。氧化还原信号。 17,1590-1609。

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