Plasma Cholesterol Oxidation Products (Oxysterols) in Human Subjects Fed a Meal Rich in Oxysterols

Abstract

There is no evidence whether humans absorb cholesterol oxidation products (COPS) from food sources. Therefore, (after-meal) absorption of COPS in humans was studied following consumption of a powdered egg meal containing 30-90 ppm each of four different COPS. Both total plasma and plasma chylomicron COPS concentrations increased. By contrast, subjects consuming fresh eggs containing very low levels of the same four COPS (O-2 ppm) demonstrated no significant rise in plasma COPS. We concluded that the human subjects studied had the capacity to absorb COPS from food sources. The brief residence time of COPS observed in both chylomicrons and plasma suggested rapid transfer of COPS among lipoprotein fractions and/or clearance from plasma.

7‐Ketocholesterol favors lipid accumulation and colocalizes with Nile Red positive cytoplasmic structures formed during 7‐ketocholesterol–induced apoptosis: Analysis by flow cytometry, FRET biphoton spectral imaging microscopy, and subcellular fractionation

“…Moreover, because an increased cellular content of 7KC can disturb numerous signaling pathways (12), the interaction between 7KC and cellular lipids was investigated by FRET. Under these conditions, when U937 cells are treated with 7KC at a concentration of 20 g/ml, i.e., the level measured in plasma after a meal rich in fat (45) and in cholesterol-fed rich rabbits (46), we demonstrate that 7KC favors the intracellular accumulation of lipids (including free cholesterol) and colocalizes with myelin figures enriched in cholesterol, phospholipids, and sphingomyelin.…”

Involvement of a calcium-dependent dephosphorylation of BAD associated with the localization of Trpc-1 within lipid rafts in 7-ketocholesterol-induced THP-1 cell apoptosis

“…This oxysterol, whose concentration used in this study is in the range of levels measured in the plasma of subjects after a meal rich in fat 26 and in rabbits that are fed a cholesterol-rich diet, 27 induces a form of cell death with apoptotic features such as mitochondrial depolarization, cytochrome c release into the cytosol, caspase-9 and -3 activation, PARP degradation, and condensation/fragmentation of the nuclei. 7,8 However, the mechanisms prior to the involvement of mitochondria are not well known.…”

7-Ketocholesterol Induces Protein Ubiquitination, Myelin Figure Formation, and Light Chain 3 Processing in Vascular Smooth Muscle Cells

“…We used a concentration of 100 mol/L 7-KC, which is Ϸ1000-fold higher than the 7-KC levels in human plasma 20 and Ϸ25-fold higher than the plasma 7-KC levels after a fat-rich meal. 21 Autophagy is a general manifestation of injury that involves the sequestration of intracellular components and their subsequent degradation in secondary lysosomes. 16,22 This process occurs in at least 2 steps: first, organelles or portions of cytosol are sequestrated by an enveloping membrane, resulting in the formation of an autophagosome.…”