Predisposition to LDL oxidation in patients with and without angiographically established coronary artery disease

Cominacinia, L.; Garbin, Ulisse; Pastorino, Antonio M.; Davoli, A.; Campagnola, M.; Santis, A. De; Pasini, C.; Faccini, Giovanni; Trevisan, Maria Teresa; Bertozzo, L.; Pasini, Francesco; Cascio, Vincenzo Lo

doi:10.1016/0021-9150(93)90051-u

Cited by 91 publications

(34 citation statements)

References 34 publications

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“…A possible explanation is the greater susceptibility to oxidation of LDL in these subjects. 47,48 In conclusion, the present work confirms the heterogeneous distribution of LDL sialic acid content among individuals and shows that this parameter increases with the extension of atherosclerosis and the occurrence of acute coronary complications.…”

Section: Discussionsupporting

confidence: 84%

Sialic Acid Content of LDL in Coronary Artery Disease: No Evidence of Desialylation in Subjects With Coronary Stenosis and Increased Levels in Subjects With Extensive Atherosclerosis and Acute Myocardial Infarction

Chappey

Beyssen

Foos

et al. 1998

ATVB

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Abstract-We recently showed that sialic acid content of LDL was not a marker of early cardiovascular disease (Arterioscler Thromb Vasc Biol. 1995;15:334 -339). Here, we investigated this parameter in patients with advanced coronary artery disease (CAD). We first examined 100 patients having undergone coronary angiography. The distribution of LDL sialic acid values was very similar in subjects with no coronary stenosis (31.3Ϯ3.7 nmol/mg LDL protein, meanϮSD) and those with Ն75% stenosis in at least one main coronary artery or Ն50% stenosis in at least two main coronary arteries (32.1Ϯ5.5 nmol/mg LDL protein). In contrast, LDL sialic acid content was significantly increased in patients with both coronary stenosis and peripheral arterial atherosclerotic lesions compared with those with either no lesion or only one or the other type of lesion. We then examined LDL sialic acid content in 20 patients with acute myocardial infarction. LDL sialic acid content was significantly higher (35.9Ϯ3.2 nmol/mg LDL protein) than that in the CAD(Ϫ) control group. These data suggest that LDL sialic acid content increases with the extension of atherosclerosis and its progression to acute complications. To explain the discordance with Orekhov and coworkers (Atherosclerosis. 1991;86:153-161), who showed that LDL sialic acid content in patients with advanced CAD was lower than that in healthy subjects, we studied the time courses of sialic acid, TBARS, and vitamin E levels in LDL dialyzed in different experimental conditions. A continuous decrease in both sialic acid and vitamin E levels and an increase in TBARS levels were observed in LDL samples containing less than 1 mmol/L EDTA, the intensity and rapidity of which varied with the EDTA concentration in the buffer. Our data support the idea that desialylation may result from in vitro peroxidation of LDL. (Arterioscler Thromb Vasc Biol. 1998;18:876-883.)

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Section: Discussionsupporting

confidence: 84%

Sialic Acid Content of LDL in Coronary Artery Disease: No Evidence of Desialylation in Subjects With Coronary Stenosis and Increased Levels in Subjects With Extensive Atherosclerosis and Acute Myocardial Infarction

Chappey

Beyssen

Foos

et al. 1998

ATVB

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“…Only a few studies have reported the relation between markers of oxidation and coronary heart disease, and the results of these studies are inconsistent (Van de Vijver et al, 1998;de Rijke et al, 1995;Cominacini et al, 1993;Croft et al, 1992). Thus, none of the oxidation markers have yet been validated as risk factors for atherosclerosis, although it may be that markers more representative of in vivo changes, like oxidised LDL antibodies, may be more sensitive to changes in LDL antioxidant content.…”

Section: Discussionmentioning

confidence: 99%

Effect of phenol-rich extra virgin olive oil on markers of oxidation in healthy volunteers

et al. 2001

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Objective: We studied whether consumption of phenol-rich extra virgin olive oil affects the susceptibility of low density lipoproteins (LDL) to oxidation and other markers of oxidation in humans. Design: Randomized cross-over intervention trial, strati®ed according to sex, age and energy intake. Setting: Division of Human Nutrition and Epidemiology, Wageningen University, The Netherlands. Subjects: Forty-six healthy men and women completed the study. Intervention: Subjects consumed two diets supplying 69 g per day of extra virgin olive oil either rich or poor in phenols for 3 weeks each. The mean difference in phenol intake between the treatments was 18 mg per day. Vitamin E intake was low during the whole study. Fasting blood samples were taken twice at the end of each period. Results: Resistance of LDL and high density lipoprotein (HDL) to oxidation was not affected by treatment. The mean lag time of copper-induced formation of conjugated dienes was 1.6 min shorter in LDL and 0.4 min longer in HDL after the high phenol diet. Other markers of antioxidant capacity in plasma were also not affected: mean lipid hydroperoxides were 0.07 mmolal higher, mean malondialdehydes were 0.001 mmolal higher, mean protein carbonyls were 0.001 nmolamg protein lower, and the mean ferric reducing ability of plasma (FRAP) was 0.006 mmolal higher after the high phenol diet. All 95% con®dence intervals enclosed zero. Serum cholesterol concentrations were not affected by the treatment.

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“…There is growing evidence of a relationship between susceptibility of LDL to in vitro oxidation and atherosclerotic risk [13,16,17]. A novel strategy in the prevention of atherosclerosis could therefore be to prevent the deleterious effect of oxidized LDL by reducing the oxidation rate.…”

Section: Discussionmentioning

confidence: 99%

“…This enhanced susceptibility has been observed in patients with familial hypercholesterolaemia [14,15], coronary artery disease [16,17], renal failure [18,19], hypertension [20] and diabetes mellitus [21].…”

mentioning

confidence: 99%

Effects of troglitazone on in vitro oxidation of LDL and HDL induced by copper ions and endothelial cells

Cominacini

Garbin

Pastorino³

et al. 1997

Diabetologia

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Low density lipoprotein (LDL) oxidation is believed to play an important role in the development of atherosclerotic plaques [1][2][3][4][5]. This view is supported by LDL with characteristics similar to those of oxidatively modified LDL being present in atheromatous lesions [6]. Studies in cultured cells have demonstrated that oxidized LDL is chemotactic for monocytes and stimulates monocyte endothelial cell interaction [7,8]. It can also cause initial endothelial cell damage and increase uptake by scavenger receptors on macrophages, leading to cholesterol accumulation and foam cell formation [7,9].Oxidative modification of LDL is not likely to occur in circulation [3]. In view of the difficulties in identifying oxidized lipoprotein in plasma, many workers have attempted to analyse the oxidation susceptibility of isolated LDL particles in vitro [10,11]. If LDL can penetrate macrophages only after its modification [3], the ability of LDL to resist oxidation could be an Diabetologia (1997) Summary Troglitazone is a new oral antidiabetic agent able to reduce lipid peroxidation. In this study we evaluated its effect on the susceptibility of LDL and HDL to in vitro oxidation induced by copper ions and endothelial cells. In Cu ++ -induced LDL modification, different amounts of troglitazone were added to aliquots of the same pool of plasma with subsequent ultracentrifuge separation of LDL and HDL. Differences in LDL and HDL susceptibility to in vitro oxidation with Cu ++ were studied by measuring the changes in fluorescence intensity (expressed as lag phase). LDL derived from plasma incubated with different amounts of troglitazone were also incubated with umbilical vein endothelial cells (HU-VEC), the modification being monitored by LDL relative electrophoretic mobility and fluorescence. During Cu ++ -and HUVEC-induced LDL oxidation, the decay rate of vitamin E, and the potency of troglitazone as a radical scavenger in comparison with vitamin E were also studied. Troglitazone determined a significant, dose-dependent decrease in Cu ++ -induced LDL and HDL oxidation. Incubation with HUVEC was also followed by a progressive, significant decrease of LDL relative electrophoretic mobility and fluorescence intensity. During Cu ++ -and HU-VEC-induced-LDL modification, troglitazone significantly reduced the rate of vitamin E decay. In this study we also demonstrated that under the same oxidative stress, troglitazone was much more potent as a radical scavenger than vitamin E. In conclusion, the results demonstrate that troglitazone can reduce LDL and HDL in vitro oxidation and that, during this process, it can protect vitamin E. In addition to ensuring blood glucose control, the drug may therefore be useful in inhibiting lipoprotein peroxidation. [Diabetologia (1997)

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Predisposition to LDL oxidation in patients with and without angiographically established coronary artery disease

Cited by 91 publications

References 34 publications

Sialic Acid Content of LDL in Coronary Artery Disease: No Evidence of Desialylation in Subjects With Coronary Stenosis and Increased Levels in Subjects With Extensive Atherosclerosis and Acute Myocardial Infarction

Sialic Acid Content of LDL in Coronary Artery Disease: No Evidence of Desialylation in Subjects With Coronary Stenosis and Increased Levels in Subjects With Extensive Atherosclerosis and Acute Myocardial Infarction

Effect of phenol-rich extra virgin olive oil on markers of oxidation in healthy volunteers

Effects of troglitazone on in vitro oxidation of LDL and HDL induced by copper ions and endothelial cells

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