期刊
REDOX BIOLOGY
卷 46, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.redox.2021.102096
关键词
Cholesterol hydroperoxide translocation; Mitochondrial membrane; Lipid peroxidation; Steroidogenesis; Atherosclerosis
资金
- NIH [CA72630, HL85677]
- Polish National Science Center [2014/13/B/NZ3/000833, 2017/26/M/NZ3/01232]
This review discusses how peroxidation of unsaturated phospholipids, glycolipids, and cholesterol can lead to various pathological conditions, with a focus on cholesterol-derived hydroperoxides. The study shows that cholesterol hydroperoxides can exacerbate oxidative damage by translocating within cells, impairing key cellular functions.
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.
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