Roles of Lipid Peroxidation in Modulation of Cellular Signaling Pathways, Cell Dysfunction, and Death in the Nervous System
Roles of Lipid Peroxidation in Modulation of Cellular Signaling Pathways, Cell Dysfunction, and Death in the Nervous System
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脂质过氧化在神经系统细胞信号通路、细胞功能障碍和死亡调节中的作用
DOI：
10.1515/revneuro.1998.9.2.105
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发表时间：
1998
影响因子：
4.1
通讯作者：
M. Mattson
中科院分区：
文献类型：
--
作者：
Jeffery N. Keller;M. Mattson
众所周知，自由基是生理条件下的天然副产物，与阿尔茨海默病(AD)、肌萎缩侧索硬化症(ALS)、帕金森病(PD)和缺血等多种神经病理条件下观察到的神经元丢失有关。氧自由基诱导的细胞毒性是由于活性氧物种的慢性和急性增加引起随后的脂质过氧化(LP)。通过与不同细胞膜中的多不饱和脂肪酸反应，氧自由基，如羟基(OH.)和过氧亚硝酸盐(ONOO)产生多种脂质过氧化产物(LPP)，包括4-羟基壬烯醛(HNE)和丙二醛(MD)。一旦形成，这些过氧化代谢产物已被证明在细胞内具有相对较长的半衰期(几分钟到几小时)，允许与细胞成分进行多次相互作用。新的数据表明，LP和LPP可能是在许多神经退行性疾病中观察到的神经元变化和神经毒性的基础。支持这种参与的数据包括在包括AD、ALS、PD和缺血在内的各种神经病理条件下检测到LP和LPP的形成。其次，无论是在体内还是在体外，LPP的直接应用都被证明是细胞毒性的，并模拟了在神经病理条件下观察到的神经元变化。此外，在各种神经退行性变的范例中，防止LP和随后的LPP的形成已被证明具有神经保护作用。此外，Lp和LPP参与了中枢神经系统内一系列活动的调节，包括长时程增强、轴突生长和增殖。了解LP参与这些过程的机制(S)和参与这些过程将极大地提高对神经生理和神经病理条件下氧自由基和离子动态平衡的理解。这篇综述的重点是描述脂质过氧化发生的过程，并建立其参与中枢神经系统的框架。
Free radicals are known to occur as natural by-products under physiological conditions and have been implicated in the neuronal loss observed in a variety of neuropathological conditions including Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and ischemia. Oxyradical-induced cytotoxicity arises from both chronic and acute increases in reactive oxygen species which give rise to subsequent lipid peroxidation (LP). By reacting with polyunsaturated fatty acids in the the various cellular membranes, oxyradicals such as hydroxyl (OH.) and peroxynitrite (ONOO) give rise to a variety of lipid peroxidation products (LPP), including 4-hydroxynonenal (HNE) and malondialdehyde (MD). Once formed, these peroxidation metabolites have been demonstrated to have relatively long half-lives within cells (minutes to hours), allowing for multiple interactions with cellular components. Emerging data suggest that LP and LPP may underlie the neuronal alterations and neurotoxicity observed in numerous neurodegenerative conditions. Data supporting this involvement include the detection of LP and formation of LPP in a variety of neuropathological conditions including AD, ALS, PD, and ischemia. Secondly, direct application of LPP, either in vivo or in vitro, has been shown to be cytotoxic and mimic neuronal alterations observed in neuropathological conditions. Furthermore, prevention of LP and subsequent LPP formation have been demonstrated to be neuroprotective in a variety of neurodegenerative paradigms. Additionally, LP and LPP have been implicated in the modulation of a wide array of activities within the central nervous system including long term potentiation, neurite outgrowth, and proliferation. Understanding the mechanism(s) and involvement of LP in these processes will greatly enhance the understanding of oxyradical and ion homeostasis in neurophysiological and neuropathological conditions. The focus of this review is to describe the process by which lipid peroxidation occurs and establish a framework for its involvement in the central nervous system.
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大脑中的应激基因反应。
DOI：
--
发表时间：
1996
期刊：
Cerebrovascular and brain metabolism reviews.
影响因子：
--
作者：
Massa,SM;Swanson,RA;Sharp,FR
通讯作者：
Sharp,FR
DOI：
10.1016/0005-2760(90)90118-h
发表时间：
1990-03
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
F. V. Kuijk;L. Holte;E. Dratz
通讯作者：
F. V. Kuijk;L. Holte;E. Dratz
DOI：
10.1073/pnas.93.18.9893
发表时间：
1996-09-03
影响因子：
11.1
作者：
Murphy, AN;Bredesen, DE;Fiskum, G
通讯作者：
Fiskum, G
影响因子：
7.4
作者：
D. Spitz;S. Sullivan;Robert R. Malcolm;R. Roberts
通讯作者：
D. Spitz;S. Sullivan;Robert R. Malcolm;R. Roberts
最低限度氧化的 LDL 刺激 Gs 并抑制 Gi 蛋白功能。
DOI：
10.1161/01.atv.15.11.2019
发表时间：
1995
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Parhami,F;Fang,ZT;Yang,B;Fogelman,AM;Berliner,JA
通讯作者：
Berliner,JA