Effect of Environmental Tobacco Smoke on LDL Accumulation in the Artery Wall

Roberts, Kim A.; Rezai, Allen A.; Pinkerton, Kent E.; Rutledge, John C.

doi:10.1161/01.cir.94.9.2248

Cited by 41 publications

(30 citation statements)

References 21 publications

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“…This effect appears to be related to modification of LDL by the products of environmental tobacco smoke, a process that may occur in blood. 30 We saw a tendency for MM-LDL to accumulate in the artery wall to a greater extent than did OX-LDL. This could result from a number of possible mechanisms, including induction of substances that increase endothelial layer permeability, such as cytokines (eg, tumor necrosis factor-␣).…”

Section: Discussionmentioning

confidence: 77%

“…6,30 Rats were anesthetized by intraperitoneal injection of sodium pentobarbital (35 mg/kg). After the rat was anesthetized, a midline incision was made in the neck, and both carotid arteries were dissected free from connective tissue.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…If the perfusate concentration of the fluorescently labeled molecules and perfusate flow remain constant, then If 0 determined at the asymptotic value estimated the lumen volume. 30 As the artery continued to be perfused with fluorescent solution, some of the labeled molecules became bound to the endothelium and/or crossed into the artery wall. After washout with the nonfluorescent solution, labeled molecules that remained on the luminal surface or in the artery wall were termed If accumulation.…”

Section: Measurement Of Ldl Accumulation and Lumen Volumementioning

confidence: 99%

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Modified LDL–Mediated Increases in Endothelial Layer Permeability Are Attenuated With 17β-Estradiol

Gardner

Banka

Roberts

et al. 1999

ATVB

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Abstract-Current research suggests that estrogen may have primary effects on the artery wall. To investigate the mechanisms of female sex hormone actions in the artery wall, we used an isolated, perfused, rat carotid artery model to examine the effects of estradiol on the rates of accumulation of normal (N-LDL) and minimally modified (MM-LDL) low density lipoprotein in ovariectomized rats. N-LDL, MM-LDL, and oxidized LDL (OX-LDL) were fluorescently labeled and perfused into individual arteries. The rate of LDL accumulation was measured by quantitative fluorescence microscopy before and after treatment with estradiol (1 nmol/L, 272 pg/mL). Estradiol had no effect on the rate of Key Words: artery Ⅲ arteriosclerosis Ⅲ LDL Ⅲ estrogen Ⅲ oxidized LDL Ⅲ endothelium Ⅲ permeability A cardinal characteristic of the development of atherosclerosis is the accumulation of LDL within the arterial wall. 1-3 Sites of relative increase in LDL permeability have been identified in normal arteries 4 and can be induced by injury to the endothelium. 5-9 Alternatively, others have reported increased binding and decreased efflux of LDL from the vascular wall, even under conditions where LDL influx was not affected. 10,11 Therefore, LDL accumulation in the artery wall potentially occurs by several mechanisms, perhaps depending on the stage of atheroma formation.A large body of evidence indicates that modification of LDL in the artery wall promotes atherosclerosis. 12 Recent studies demonstrate evidence of modification of LDL in the blood. [13][14][15][16][17] Furthermore, a previous study showed increased accumulation and degradation of oxidized LDL (OX-LDL) in the artery wall in vivo. 18 These studies suggest that the reason there is increased accumulation and degradation of OX-LDL is because arterial permeability to undegraded, OX-LDL is greater than arterial permeability to native LDL (N-LDL). However, the precise mechanism(s) by which modified LDL (MM-LDL) affects LDL flux in the artery wall, such as increases in permeability to LDL, remains incompletely understood.Modification of LDL (eg, oxidation), either in the circulation or the artery wall, could promote atherosclerosis by increasing LDL accumulation in the artery. Also, alteration of constituents of the artery wall, such as proteoglycans, could influence LDL binding to the artery wall. Furthermore, oxidant-mediated injury of endothelial cell membranes could compromise the endothelial layer barrier to macromolecules in arteries. 5 To counteract oxidant stress effects on LDL and/or the artery wall, a number of potential antioxidants have been examined. In particular, some estrogens (eg, 17␤-estradiol) are known to reduce LDL accumulation in the artery wall 19,20 and to be potent antioxidants. [21][22][23] In addition, estrogens may protect endothelial cells from oxidative damage. 21,22 This action would be expected to prevent increased LDL permeation into the artery wall. Furthermore, estradiol has been shown to inhibit LDL oxidation in vivo at supraphysiological 24 and physiolo...

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Section: Discussionmentioning

confidence: 77%

Section: Experimental Protocolmentioning

confidence: 99%

Section: Measurement Of Ldl Accumulation and Lumen Volumementioning

confidence: 99%

See 1 more Smart Citation

Modified LDL–Mediated Increases in Endothelial Layer Permeability Are Attenuated With 17β-Estradiol

Gardner

Banka

Roberts

et al. 1999

ATVB

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“…In accordance, 2 to 4 hours of exposure of rats to environmental tobacco smoke has recently been shown to increase LDL accumulation in perfused arteries. 26 An increasing number of reports has documented the harmful effects of environmental tobacco smoke. [27][28][29] We found that a short period of passive smoking changed LDL metabolism, favoring the progression of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

1998

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Background-According to the American Heart Association, passive smoking is an important risk factor for coronary heart disease (CHD), but the mechanisms underlying this association are not fully understood. We studied the acute effect of passive smoking on the factors that influence the development of CHD: the antioxidant defense of human serum, the extent of lipid peroxidation, and the accumulation of LDL cholesterol in cultured human macrophages, the precursors of foam cells in atherosclerotic lesions. Methods and Results-Blood samples were collected during 2 ordinary working days from healthy, nonsmoking subjects (nϭ10) before and after (up to 5.5 hours) spending half an hour in a smoke-free area (day 1) or in a room for smokers (day 2). Passive smoking caused an acute decrease (1.5 hours after exposure) in serum ascorbic acid (PϽ.001) and in serum antioxidant defense (PϽ.001), a decreased capacity of LDL to resist oxidation (PϽ.01), and the appearance of increased amounts of lipid peroxidation end products in serum (PϽ.01). Finally, LDL isolated from subjects after passive smoking was taken up by cultured macrophages at an increased rate (PϽ.05). Conclusions-Exposure of nonsmoking subjects to secondhand smoke breaks down the serum antioxidant defense, leading to accelerated lipid peroxidation, LDL modification, and accumulation of LDL cholesterol in human macrophages. These data provide the pathophysiological background for the recent epidemiological evidence about the increased CHD risk among passive smokers. (Circulation. 1998;97:2012-2016.)

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“…Some papers from the 1990s reported that exposure to environmental tobacco smoke increases the risk of atherosclerosis (16).…”

mentioning

confidence: 99%

Perinatal and infant early atherosclerotic coronary lesions

Milei

Ottaviani

Lavezzi

et al. 2008

Canadian Journal of Cardiology

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Effect of Environmental Tobacco Smoke on LDL Accumulation in the Artery Wall

Abstract: Exposure to ETS acutely increased LDL accumulation in perfused arteries. Repeated exposure to ETS may represent important early events in atherogenesis.

Cited by 41 publications

References 21 publications

Modified LDL–Mediated Increases in Endothelial Layer Permeability Are Attenuated With 17β-Estradiol

Modified LDL–Mediated Increases in Endothelial Layer Permeability Are Attenuated With 17β-Estradiol

Passive Smoking Induces Atherogenic Changes in Low-Density Lipoprotein

Perinatal and infant early atherosclerotic coronary lesions

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