Arteriosclerotic plaque

The effect of butadiene exposure on arteriosclerotic plaque development was assessed in white leghorn cockerels exposed for 6 h per day on five days per week for 16 weeks to 20 ppm (44 mg/m ) butadiene. Plaque frequency and size in the abdominal aorta wall were determined for butadiene-exposed animals and controls. Plaques were larger for butadiene-exposed animals than for corresponding air controls and the authors concluded that butadiene exposure markedly accelerated arteriosclerotic plaque development. Since... 

Penn, A. Snyder, C.A. (1996) 1,3-Butadiene, a vapor phase component of environmental tobacco smoke, accelerates arteriosclerotic plaque development. Circulation, 93, 552-557... 

Of 34 Japanese patients with diabetes and chronic hepatitis, 18 were given glycyrrhizin 240-525 mg for over 1 year (447). This resulted in a significant lowering of total testosterone concentrations and increased arteriosclerotic plaque formation. The authors suggested that glycyrrhizin treatment was an independent risk factor for arteriosclerosis. The testosterone lowering effect of liquorice has been confirmed in another trial (448). 

The pathogenic mechanism of ACS is that coronary arteriosclerotic plaques rupture and erode leading to thrombosis. Once injury to the coronary endothelial cells occurs, collagen and von Willebrand factor exposed to subendothelial matrix adhere to platelets. Consequently, these platelets are... 

The cardiovascular toxicity of tobacco is not limited to AMI. For examples, tobacco smoke inhibits neovascularization 21] and promotes arteriosclerotic plaque development. I56 ... 

Penn A, Keller K, Snyder C, et al. The tar fraction of cigarette smoke does not promote arteriosclerotic plaque formation. Environ Health Perspect 1996 104(10) 1108—13. 

Penn A, Snyder C. 1988. Arteriosclerotic plaque development is promoted by polynuclear aromatic hydrocarbons. Carcinogenesis 9(12) 2185-2189. 

It has been postulated that carbon disulfide cardiotoxicity may be mediated by disruption of the energy supply in the heart (Klapperstiick et al 1991). The mechanism for carbon disulfide acceleration of arteriosclerotic plaque formation involves direct injury to the vessel epithelium and changes in lipid metabolism. 

Benditt, E.P. 1977. Implications of the monoclonal character of human arteriosclerotic plaques, Am. J. Pathol, 86, 693. 

PGF are increased following oxidation of LDL by macrophages, endothelial cells, and copper (G6, G7, L5, P2, P4, RIO, W3). PGF have been identified in arteriosclerotic plaques (G4, P4). Increased levels have been identified in persons with hypercholesterolemia and other classical risk factors for CAD (D2, D3, G5, M7, R4) and in persons with peripheral vascular disease (W2). 

HODEs are primarily Cl8 oxidation products of linoleic acid (J9). These have not been as widely studied as isoprostanes, but like isoprostanes, these are specific products of nonenzymatic lipid peroxidation that are associated with arteriosclerotic disease and are found in arteriosclerotic plaques (J9, W2). Likewise, they are measured by specific GC/MS techniques that are generally not available in clinical laboratories (JIO). They have the advantage that they are products of the major PUFA in lipoproteins—linoleic acid— but they have generally been measured only in lipoproteins extracted from plasma. 

Both circulating OxLDL and MDA-LDL have been measured in plasma by ELISA. Most commonly, the capture antibody is a monoclonal antibody against OxLDL or MDA-LDL and the detection antibody, a polyclonal or monoclonal antibody directed against apo B (El, S12, Tl). Usually, the capture antibody is developed against chemically modified MDA-LDL or OxLDL but antibody has been developed against homogenate of human arteriosclerotic plaque. This antibody reacted with oxidized phosphatidylcholines but not native LDL, or MDA-LDL (S12). 

Three specific human monoclonal IgG autoantibodies that recognize oxidized MDA-LDL have been prepared using phage libraries (S6). Such a panel of antibodies may be of value in defining the composition of arteriosclerotic plaques in various stages of development (G2). They may also be directed at cells, lipoproteins, and matrix molecules in a way that can help identify the source of OxLDL in humans. Such human antibodies may also be used in assays. There is still a good deal of research needed to sort out these questions. 

Cholesterol is essential to life. The name originates from the Greek chole (bUe) and stereos (solid) as cholesterol was first isolated in the solid form from gallstones in 1784. More than 200 years later, it is now well established that important biological functions and solubility properties of cholesterol are intimately linked [12]. Indeed its insolubihty in water explains why this molecule is an important component of the hpid membranes of animal cells. It is this very property that makes cholesterol deleterious, if not lethal. Indeed its deposition within the waU of an artery can lead to the formation of arteriosclerotic plaques. Remarkably these are also the imique self-aggregation properties of cholesterol derivatives that were at the heart of the discovery in 1888 of a new state of matter, the Uquid crystal [13]. In many respects, cholesterol is a fascinating molecule a imique molecular building-block that has been widely exploited in supramolecular and materials chemistry [14-17]. 

Tuna, N., andH. K. Mangold In Evolution of the arteriosclerotic plaque, R. J. Jones, Editor, p. 83, Chicago and London The University of Chicago Press (1963). 

The plethora of studies evaluating the possible benefits and risks of dietary vitamin E supplementation on patients who are suffering from or are at risk of cardiovascular disease is based on the hypothesis that lipid oxidation is active in the mechanisms leading to the formation of arteriosclerotic plaques [68]. It is hypothesized that the antioxidant ability of vitamin E could prevent or reduce lipid peroxidation and hence could slow down the formation of plaques. 

Becker, C.G. and Murphy, G.E. Demonstration of contractile protein in endothelium and cells of heart valves, endocardium, intima, arteriosclerotic plaques, and Aschoff bodies of rheumatic heart disease. 

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