Cholesterol Oxidation Products and Atherosclerosis

Sandra,; b, Keri Carpenter; a, Rafael Codony; a, Francesc Guardiola

doi:10.1201/9781439822210.ch13

Cited by 16 publications

(17 citation statements)

References 183 publications

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“…However, the analogue compounds issued from cholesterol were studied: 7β-hydroxycholesterol is considered as a good marker of the risk of cardiovascular disease [18] and cholestanetriol was described as cytotoxic [19] and as involved in atherosclerosis [20,21]. For some oxycholesterols, many studies have demonstrated several in vitro biological effects related to the atherosclerotic process and that the systemic administration of some of these compounds to animals induce the formation of atherosclerotic lesions, which indicates that these compounds may play an important role in the initiation and progression of atherosclerosis [22][23][24]. It would be interesting to know if these phytosterol-derived compounds could present the same effects.…”

Section: Discussionmentioning

confidence: 99%

Incorporation of oxyphytosterols in tissues of hamster

et al. 2004

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-Oxyphytosterols (OPS) were fed to hamsters, at different concentrations, in order to observe their eventual incorporation into plasma, aorta, liver, kidneys and heart. The animals receiving the very high level (2500 ppm) presented 7β-hydroxycampesterol, β-epoxycampesterol, campestanetriol, 7-ketocampesterol, 7β-hydroxysitosterol, β-epoxysitosterol, sitostanetriol and 7-ketositosterol in all tissues. The same compounds were observed in the tissues of animals receiving 500 ppm of OPS in their diet, but with much lower levels. In hamsters fed 100 ppm of OPS, as well as in control animals, in most cases, the only observed OPS was sitostanetriol, which seems to be difficult to eliminate from the animal.oxyphytosterol / sitostanetriol / phytosterol / plasma / aorta / liver / kidneys / heart

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Section: Discussionmentioning

confidence: 99%

Incorporation of oxyphytosterols in tissues of hamster

et al. 2004

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“…Alternatively, COPs oxidize lipoproteins to oxLDL (oxidized low density lipoprotein) that induce changes in cell function. Another major factor is the replacement of cholesterol by COPs molecules in membranes (García-Cruset et al, 2002). Similarly, incorporated COPs can modulate membrane fl uidity and the permeability of membranes to albumin and glucose (Osada, 2002).…”

Section: Introductionmentioning

confidence: 99%

Biochemical and histopathological effects of dietary oxidized cholesterol in rats

Soto-Rodríguez

Campillo-Velázquez

Alexander‐Aguilera

et al. 2009

J of Applied Toxicology

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Cholesterol oxidation products (COPs) have been associated with the genesis of chronic degenerative diseases, such as atherosclerosis. The purpose of this work was to study the histological changes by toxic effects of dietary COPs in liver and kidney. Five-week-old male Wistar albino rats were randomly divided into three groups of 10 rats each. Standard rat chow was supplemented with either 1% (w/w) pure cholesterol or 1% oxidized cholesterol and fed to the rats for 8 weeks. Control animals were fed standard rat chow. At the end of the treatment period, the serum lipid profile was determined. The aorta, liver and kidneys were excised immediately, frozen with liquid nitrogen, and held at -70 degrees C. The histological study was carried out using conventional hematoxylin-eosin staining, and histochemical red oil 'O' was applied. COPs were analyzed by gas chromatography. Intake of dietary COPs altered biochemical parameters involved in lipid metabolism associated with atherogenesis in rats: total cholesterol, triacylglycerols and low density lipoproteins in serum. COPs detected in the liver and kidneys modified the organ original structure, caused an inflammatory process and promoted atherogenesis and atrophy of the tissue.

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“…Oxysterols such as 7-ketocholesterol (7-keto) and 7␤-hydroxycholesterol (7␤-OH) (present at enhanced levels in atherosclerotic plaques [5] and plasma of patients with higher atherogenic risk or with coronary artery disease) [6,7] are known to mediate the various effects of Ox-LDL [4] (when taken in isolation or used in mixture [5,8]). These compounds are capable of inducing a complex mode of cell death, combined with mechanisms of apoptosis [9,10]. Therefore, it has been hypothesized that atheromatous lesions might represent "death zones," containing toxic materials such as oxysterols, in which monocytes/macrophages would become dysfunctional and apoptotic [11].…”

Section: Introductionmentioning

confidence: 99%

Activation of caspase-3-dependent and -independent pathways during 7-ketocholesterol- and 7β-hydroxycholesterol-induced cell death: A morphological and biochemical study

Prunet

Lemaire-Ewing

Ménétrier

et al. 2005

J. Biochem. Mol. Toxicol.

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On treatment with 7-ketocholesterol (7-keto) or 7beta-hydroxycholesterol (7beta-OH), which are major oxysterols in atherosclerotic plaques, the simultaneous identification of oncotic and apoptotic cells suggests that these compounds activate different metabolic pathways leading to various modes of cell death. With U937, MCF-7 (caspase-3 deficient), MCF-7/c3 cells (stably transfected with caspase-3), we demonstrate that caspase-3 is essential for caspase-9, -7, -8 activation, for Bid degradation mediating mitochondrial cytochrome c release, for cleavage of poly(ADP-ribose) polymerase and inhibitor of the caspase-activated deoxyribonuclease, and, at least in part, for internucleosomal DNA fragmentation. The crucial role of caspase-3 was supported by the use of z-VAD-fmk and z-DEVD-fmk, which abolished apoptosis and the associated events. However, inactivation or lack of caspase-3 did not inhibit 7-keto- and 7beta-OH-induced cell death characterized by staining with propidium iodide, loss of mitochondrial potential. The mitochondrial release of apoptosis-inducing factor and endonuclease G was independent of the caspase-3 status, which conversely played major roles in the morphological aspects of dead cells. We conclude that caspase-3 is essential to trigger 7-keto- and 7beta-OH-induced apoptosis, that these oxysterols simultaneously activate caspase-3-dependent and/or -independent modes of cell death.

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Cholesterol Oxidation Products and Atherosclerosis

Cited by 16 publications

References 183 publications

Incorporation of oxyphytosterols in tissues of hamster

Incorporation of oxyphytosterols in tissues of hamster

Biochemical and histopathological effects of dietary oxidized cholesterol in rats

Activation of caspase-3-dependent and -independent pathways during 7-ketocholesterol- and 7β-hydroxycholesterol-induced cell death: A morphological and biochemical study

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