Lipids and oxidised lipids in human atheroma and normal aorta

Carpenter, Keri L. H.; Taylor, Susan; Ballantine, James A.; Fussell, Brynley; Halliwell, Barry; Mitchinson, M. J.

doi:10.1016/0005-2760(93)90151-x

Cited by 139 publications

(69 citation statements)

References 28 publications

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“…CE-containing polyunsaturated lipids are the primary targets for one-electron mediated oxidation, and oxidized CEs are found in lesions 12,13,26,27 but are essentially absent in plasma LDL. 13 CE hydroperoxides (CE-OOH) were not detected in early lesions, ie, stages I-III (Table 2).…”

Section: Resultsmentioning

confidence: 99%

“…The former are the major lipid oxidation products formed when lipoproteins undergo in vitro oxidation and contribute to the in vitro formation of high-uptake LDL. 7 In addition, CE-O(O)H are the major lipid oxidation products in human lesions 1,12,26,31 and hydroxylated fatty acids are associated with plaque instability. 31 Notably, CE-O(O)H and oxysterols are not found in normal iliac arteries 12,32 or in circulating plasma lipoproteins.…”

Section: Discussionmentioning

confidence: 99%

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Disease Stage-Dependent Accumulation of Lipid and Protein Oxidation Products in Human Atherosclerosis

Upston

Niu

Brown

et al. 2002

The American Journal of Pathology

126

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Oxidative modification of low-density lipoprotein is thought to promote arterial lipid accumulation and atherogenesis. Previous studies reported on the presence of certain lipid or protein oxidation products in lesions, although a systematic investigation measuring several oxidation parameters and the accumulation of nonoxidized lipids and antioxidants at various stages of atherosclerosis has not been performed in the same tissue. Using the intimal lipoprotein-containing fraction of human aortic lesions, we demonstrate here that cholesterol accumulated with lesion development and that this increase was already significant at the fatty streak stage. By comparison, cholesterylesters increased significantly only in fibrofatty and more complex lesions that also contained significantly increased amounts of cholesterylester hydro(pero)xides and 27-hydroxycholesterol. Cholesterylester hydroxides were the major lipid oxidation product detected. Despite accumulation of oxidized lipid, ␣-tocopherol was also present and maintained at a comparable level over the disease process. Of the oxidized protein moieties measured only o,o-dityrosine increased with disease, although chlorotyrosines were present at relatively high levels in all lesions compared to healthy vessels. Our data show that accumulation of nonoxidized lipid precedes that of oxidized lipid in human aortic lesions. The development of atherosclerosis to clinical manifestations is a protracted process that spans several decades. It is well established that lipids, specifically cholesterol, accumulate as the disease progresses 1 and that these lipids are derived from plasma low-density lipoprotein (LDL). Aberrant uptake of LDL and its associated lipids by intimal monocytes that have infiltrated from the blood is believed to generate foam cells and thereby initiate atherosclerosis. 2 Foam cells are the hallmark of the fatty streak/early lesion from which the more advanced and complicated lesions derive. In advanced lesions, a fibrous cap is formed from collagen and a lipid-rich necrotic core. Vessel lumen narrowing because of the enlarged fibrous cap and plaque rupture lead to clinical manifestations.The definitive mechanisms leading to the initiation and development of atherosclerosis are unknown. However, retention of LDL in the vessel wall because of interaction and complex formation with extracellular matrix components is well-documented 3 and is thought to be important. Further, a bulk of evidence suggests that oxidative modifications to LDL contribute to its retention. 4 -6 Both arterial wall retention and oxidative modification of LDL are thought to contribute to foam cell formation.In vitro studies with plasma LDL have shown that oxidative modifications proceed in different stages and involve changes to LDL's antioxidants, lipids, and protein components. The nature and extent of these alterations vary depending on the type of oxidant involved, the oxidant to lipoprotein ratio used, and the extent to which oxidation is allowed to proceed. Originally 4 the pa...

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Disease Stage-Dependent Accumulation of Lipid and Protein Oxidation Products in Human Atherosclerosis

Upston

Niu

Brown

et al. 2002

The American Journal of Pathology

126

View full text Add to dashboard Cite

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“…Oxysterols are commonly found in foods of animal origin (19) and have been demonstrated to exist both in OxLDL (20) and in atherosclerotic plaque (21). The predominant oxysterol present in OxLDL is 7-ketocholesterol (7KC), which accounts for up to 30% of the total sterols in OxLDL (22).…”

mentioning

confidence: 99%

Acyl-coenzyme A:cholesterol acyltransferase promotes oxidized LDL/oxysterol-induced apoptosis in macrophages

Freeman

Rusiñol

Linton

et al. 2005

Journal of Lipid Research

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“…Diets based on fat-rich products are known as risk factors of atherosclerosis [5]. The presence of various lipids and the content of their peroxides were shown to correlate with the progress of the disease in human arteries [6,7]. Proatherosclerotic effect is mostly caused by exogenous cholesterol and the role of its oxidation was emphasized in egg-rich diets [8].…”

Section: Introductionmentioning

confidence: 99%

Chemical Composition of Atherosclerotic Plaques οf apoE/LDLR-Double Knockout Mice by Synchrotron Radiation FTIR Microspectroscopy

et al. 2012

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Atherosclerosis is a multietiological inflammatory disease of large and medium-sized arteries of increasing incidence in westernized countries. The aim of this study was to identify the biochemical changes during the progression of atherosclerosis by synchrotron radiation Fourier transform infrared microspectroscopy in atheromas of apoE/LDLR −/− mice fed egg-rich diet supplemented or not with angiotensin converting enzyme inhibitor perindopril. Synchrotron radiation Fourier transform infrared microspectroscopy technique was used to obtain information at high spatial resolution about the distribution of proteins (C-N, N-H, CO for amide I and amide II bands), lipids (CH 2 , CH 3 bands) as well as mineral deposits (calcium carbonates and phosphates). Total contents of lipids and proteins were found to be significantly lower in animals treated with the diet and perindopril. An increase in saturation level of lipids was observed in animals fed with egg-rich diet when compared to the normal diet and perindopril treatment, which did not inhibit this effect. Moreover, a significant change in the secondary structure of proteins (ratio between absorption bands 1634 cm −1 /1656 cm −1 attributed to β-type and α-type, respectively) was observed in both experimental groups in comparison with the control. Principal component analysis was used to analyse the recorded spectra. It has revealed that higher content of phosphates (wavenumber range 950-1020 cm −1 ) was observed between egg-rich diet fed animals and the control group.

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Lipids and oxidised lipids in human atheroma and normal aorta

Cited by 139 publications

References 28 publications

Disease Stage-Dependent Accumulation of Lipid and Protein Oxidation Products in Human Atherosclerosis

Disease Stage-Dependent Accumulation of Lipid and Protein Oxidation Products in Human Atherosclerosis

Acyl-coenzyme A:cholesterol acyltransferase promotes oxidized LDL/oxysterol-induced apoptosis in macrophages

Chemical Composition of Atherosclerotic Plaques οf apoE/LDLR-Double Knockout Mice by Synchrotron Radiation FTIR Microspectroscopy

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