Pathophysiological potential of lipid hydroperoxide intermembrane translocation: Cholesterol hydroperoxide translocation as a special case.
Pathophysiological potential of lipid hydroperoxide intermembrane translocation: Cholesterol hydroperoxide translocation as a special case.
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脂质氢过氧化膜间易位的病理生理学潜力：作为特例的胆固醇氢过氧化氢易位。
DOI：
10.1016/j.redox.2021.102096
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发表时间：
2021-10
期刊：
影响因子：
11.4
通讯作者：
Korytowski W
中科院分区：
文献类型：
--
作者：
Girotti AW;Korytowski W
在氧化应激条件下，生物膜中不饱和磷脂、糖脂和胆固醇的过氧化可成为多种病理条件的基础，包括动脉粥样硬化形成、神经变性和致癌。脂质氢过氧化物（LOOH）是过氧化过程中的关键中间体。新生LOOH可能经历单电子还原以加剧膜损伤/功能障碍，或经历双电子还原以减弱这种情况。另一种可能性是LOOH易位到受体位点，随后是这些竞争性还原中的任一种。胆固醇（Ch）衍生的氢过氧化物（ChOOHs）有几个特殊的功能，将在本次审查中强调。除了容易受到单电子与双电子还原的影响外，ChOOH还可以从起源膜转移到另一个膜，在那里可能会发生这种转换。细胞内星星家族蛋白已被证明不仅将Ch递送至线粒体，而且还将ChOOH递送至线粒体。StAR介导的自由基产生的7-氢过氧胆固醇（7-OOH）转移导致（a）类固醇生成细胞中Ch利用和（B）血管巨噬细胞中抗动脉粥样硬化的反向Ch转运受损。这是第一个已知的过氧化物衍生物如何被天然脂质运输途径识别并产生有害后果的例子。对于上面的每个例子，我们将讨论氧化损伤/功能障碍的潜在机制，以及如何通过抗氧化剂干预来缓解。脂质过氧化是许多与氧化应激相关的病理条件的基础。胆固醇衍生的氢过氧化物7α/β-OOH是关键的过氧化中间体。7α/β-OOH向线粒体的转移被星星蛋白加速。7α/β-OOH转移损伤损害类固醇合成和胆固醇稳态。
Peroxidation of unsaturated phospholipids, glycolipids, and cholesterol in biological membranes under oxidative stress conditions can underlie a variety of pathological conditions, including atherogenesis, neurodegeneration, and carcinogenesis. Lipid hydroperoxides (LOOHs) are key intermediates in the peroxidative process. Nascent LOOHs may either undergo one-electron reduction to exacerbate membrane damage/dysfunction or two-electron reduction to attenuate this. Another possibility is LOOH translocation to an acceptor site, followed by either of these competing reductions. Cholesterol (Ch)-derived hydroperoxides (ChOOHs) have several special features that will be highlighted in this review. In addition to being susceptible to one-electron vs. two-electron reduction, ChOOHs can translocate from a membrane of origin to another membrane, where such turnover may ensue. Intracellular StAR family proteins have been shown to deliver not only Ch to mitochondria, but also ChOOHs. StAR-mediated transfer of free radical-generated 7-hydroperoxycholesterol (7-OOH) results in impairment of (a) Ch utilization in steroidogenic cells, and (b) anti-atherogenic reverse Ch transport in vascular macrophages. This is the first known example of how a peroxide derivative can be recognized by a natural lipid trafficking pathway with deleterious consequences. For each example above, we will discuss the underlying mechanism of oxidative damage/dysfunction, and how this might be mitigated by antioxidant intervention. Lipid peroxidation underlies many pathological conditions associated with oxidative stress. The cholesterol-derived hydroperoxides, 7α/β-OOH, are key peroxidation intermediates. 7α/β-OOH-transfer to mitochondria is accelerated by StAR proteins. Damage from 7α/β-OOH transfer impairs steroid synthesis and cholesterol homeostasis.
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影响因子：
7.5
作者：
Cockcroft S;Raghu P
通讯作者：
Raghu P
影响因子：
7.4
作者：
Graham, Annette
通讯作者：
Graham, Annette
DOI：
10.1016/0378-4347(95)00182-4
发表时间：
1995-08-18
影响因子：
3
作者：
KORYTOWSKI, W;GEIGER, PG;GIROTTI, AW
通讯作者：
GIROTTI, AW
影响因子：
4.8
作者：
KODAMAN, PH;ATEN, RF;BEHRMAN, HR
通讯作者：
BEHRMAN, HR
DOI：
10.1016/j.bbalip.2016.08.012
发表时间：
2017-01-01
影响因子：
4.8
作者：
Elustondo, Pia;Martin, Laura A.;Karten, Barbara
通讯作者：
Karten, Barbara