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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Peroxidation of unsaturated phospholipids, glycolipids, and cholesterol in biological membranes under oxidative stress conditions can underlie a Waterproof Coveralls 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 prostate-stimulator 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.