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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chemical composition of the gaseous, vapour and particulate phases of the atmosphere has been reported in terms of background, urban and highly polluted levels. Too little is known about the chemical composition of polluted atmospheres and other environments, and the situation will worsen as a result of the steadily increasing production of a wide variety of chemicals. This and other evidence presented in this paper indicates that the human race has not yet felt the full impact of the burgeoning chemical environment in terms of genotoxic effects. Some highly suggestive data from the literature have been presented to indicate that carcinogenesis and mutagenesis in human beings involve not only the attack of a primary genotoxicant, but that genetic factors, cofactors, antifactors and sometimes precursors can play important roles in the process of genotoxicity. Evidence has been presented to indicate that genotoxic effects are much more prevalent among human beings than is commonly believed. Since inherited effects arise from mutation of a germ cell, cancer probably from mutation of a somatic cell, atherosclerosis possibly from some mutagenic effect and the debilitating effects of some aspects of ageing possibly from a somatic mutation of the metabolic type, then mutagenesis in these four postulated types could be the overwhelmingly major cause of death in modern society.
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PMID:Chemical composition and potential 'genotoxic' aspects of polluted atmospheres. 32 57

An integrative theory is proposed in which environmental carcinogenesis is viewed as a process by which the genetic control of cell division and differentiation is altered by carcinogens. In this theory, carcinogens include physical, chemical, and viral "mutagens," as well as chemical and viral gene modulators. Existing explanations of carcinogenesis can be considered either as somatic mutation theories or as epigenetic theories. Evidence seems to support the hypothesis that both mutations and epigenetic processes are components of carcinogenesis. The mutational basis of cancer is supported by the clonal nature of tumors, the mutagenicity of most carcinogens, high mutation frequencies in cells of cancer-prone human fibroblasts lacking DNA repair enzymes, the correlation of in vitro DNA damage and in vitro mutation and transformation frequencies with in vivo tumorigenesis, age-related incidences of various hereditary tumors, and the correlation between photoreactivation of DNA damage and the biological amelioration of UV-induced neoplasms. Since both mutagens and gene modulators can be carcinogenic it may be that carcinogens affect genes which control cell division. An integration of the mutation and epigenetic theories of cancer with the "two-stage" theory and Comings's general theory of carcinogenesis is proposed. This integrative theory postulates that carcinogens can affect regulatory genes which control a series of "transforming genes." A general hypothesis is advanced that involves a common mechanism of somatic mutagenesis via error-prone repair of DNA damage which links carcinogenesis, teratogenesis, atherosclerosis and aging. Various concepts are presented to provide a framework for evaluating the scientific, medical, and social implications of cancer.
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PMID:Environmental carcinogenesis: an integrative model. 36 70

The only limit to the use and application of the autopsy in research is the imagination of the investigator. As pathologists, it would appear that we have really neglected this powerful tool in recent decades and have undersold the potentiality of this method. As we hope to have made evident by the foregoing discussion, the field of research utilizing autopsy tissues is truly as broad as medicine itself, and if developed properly, becomes an indispensable part of the fabric of on-going research in areas of carcinogenesis, environmental disease, atherosclerosis, and aging.
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PMID:The use and application of autopsy in research. 62 65

The antioxidation defenses recognized thus far appear too weak. Needed are inert barriers to encapsulate foci of activated oxygen (FAOs) and contain their spreading. These capsules must: 1. self-assemble nonenzymatically and spontaneously in face of adversity; 2. resist oxidation and dissolution in water; and 3. be moderately fluid and elastic enough to withstand flexing by tissues. Evidence shows activated oxygen: a. is produced by common cholesterolester (CE)-raising agents; b. boosts accumulation of CEs; and c. splits low-density lipoproteins (LDL), thus releasing CE-rich coalescence-prone lipid micelles. I am proposing that CEs, combined with polar lipids, are uniquely suited to form inert-lipid antioxidation barriers (ILABs). Porous ILAB capsules self-assemble from lipid micelles released by oxidatively degraded LDL. The capsules are thermodynamically unstable but elastic, durable and capable of self-repair through oxidation of ambient LDL. All capsules tend to contract into spheres. Enclosed needle-like "foreign bodies", such as asbestos, puncture the contracting capsules. Hence the odd bulbous architecture of asbestos bodies. ILABs protect from--and their failure initiates and promotes--carcinogenesis and atherosclerosis. ILABs may be mediators of membrane biogenesis. The loss of arterial flexibility in atherosclerosis protects ILAB capsules from breakage.
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PMID:Biological autoxidation. II. Cholesterol esters as inert barrier antioxidants. Self-assembly of porous membrane sacs. An hypothesis. 74 27

Individually and in combination with other oils, the tropical oils impart into manufactured foods functional properties that appeal to consumers. The use of and/or labeling in the ingredient lists give the impression that these oils are used extensively in commercially processed foods. The estimated daily intake of tropical oils by adult males is slightly more than one fourth of a tablespoon (3.8 g), 75% of which consists of saturated fatty acids. Dietary fats containing saturated fatty acids at the beta-position tend to raise plasma total and LDL-cholesterol, which, of course, contribute to atherosclerosis and coronary heart disease. Health professionals express concern that consumers who choose foods containing tropical oils unknowingly increase their intake of saturated fatty acids. The saturated fatty acid-rich tropical oils, coconut oil, hydrogenated coconut oil, and palm kernel oil, raise cholesterol levels; studies demonstrating this effect are often confounded by a developing essential fatty acid deficiency. Palm oil, an essential fatty acid-sufficient tropical oil, raises plasma cholesterol only when an excess of cholesterol is presented in the diet. The failure of palm oil to elevate blood cholesterol as predicted by the regression equations developed by Keys et al. and Hegsted et al. might be due to the dominant alpha-position location of its constituent saturated fatty acids. If so, the substitution of interesterified artificial fats for palm oil in food formulations, a recommendation of some health professionals, has the potential of raising cholesterol levels. A second rationale addresses prospective roles minor constituents of palm oil might play in health maintenance. This rationale is founded on the following observations. Dietary palm oil does not raise plasma cholesterol. Single fat studies suggests that oils richer in polyunsaturated fatty acid content tend to decrease thrombus formation. Anomalously, palm oil differs from other of the more saturated fats in tending to decrease thrombus formation. Finally, in studies comparing palm oil with other fats and oils, experimental carcinogenesis is enhanced both by vegetable oils richer in linoleic acid content and by more highly saturated animal fats. The carotenoid constituents of red palm oil are potent dietary anticarcinogens. A second group of antioxidants, the tocotrienols, are present in both palm olein and red palm oil. These vitamin E-active constituents are potent suppressors of cholesterol biosynthesis; emerging data point to their anticarcinogenic and antithrombotic activities. This review does not support claims that foods containing palm oil have no place in a prudent diet.
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PMID:Tropical oils: nutritional and scientific issues. 134 19

Oxidant injury has been implicated in the pathogenesis of inflammatory, metabolic and toxic insults, in ischemic-reperfusion injury, and in carcinogenesis, aging and atherosclerosis. Oxidant injury is initiated by free radicals and reactive oxygen molecules which are generated by activated neutrophils, monocytes, and mesangial cells, during normal and abnormal metabolic processes, and from the metabolism of exogenous drugs and toxins. When cells and organs are exposed to oxidant stress, several different antioxidant defense mechanisms operate to prevent or limit oxidant injury. When antioxidant defense mechanisms are decreased, or when the generation of reactive oxygen molecules is increased, oxidant injury results from the shift in the oxidant/antioxidant balance. Oxidant-induced alterations of proteins, membranes, DNA, and basement membranes leads to cell and organ dysfunction. Several renal diseases including glomerulonephritis, vasculitis, toxic nephropathies, pyelonephritis, acute renal failure, and others are likely to be mediated at least in part by oxidant injury. In the future, mechanisms to decrease the generation of reactive oxygen molecules and/or antioxidant therapy may develop into new avenues of therapeutic intervention.
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PMID:Reactive oxygen molecules, oxidant injury and renal disease. 166 82

1. An increasing body of evidence suggests that certain types of fat have beneficial effects on human health. 2. Fish oils in particular have been shown to exert positive effects on atherosclerosis, heart disease and carcinogenesis. 3. These positive effects are thought to be mediated through eicosanoids derived from polyunsaturated fatty acids of the n-3 family which are present in large quantities in fish oils.
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PMID:The metabolic role of n-3 polyunsaturated fatty acids: relationship to human disease. 167 64

A number of active oxygen species are likely implicated in the etiology or manifestation of several pathological conditions, including aging, arthritis, carcinogenesis, atherosclerosis, and muscular dystrophy. Ascorbate plays a key role in protecting cells against oxidative damage. Paradoxically, in the presence of Fe3+ or Cu2+, ascorbate can promote the generation of the same reactive oxygen species (.OH, O2-, H2O2, and ferryl ion) it is known to destroy. This prooxidant activity derives from the ability of ascorbate to reduce Fe3+ or Cu2+ to Fe2+ or Cu+, respectively, and to reduce O2 to O2-. and H2O2. Damage to nucleic acid and proteins results from the binding of either Fe2+ or Cu+ to metal binding sites on these macromolecules followed by reaction of the metal complexes with H2O2; this leads to the production of active oxygen species that attack functional groups at or near the metal binding sites.
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PMID:Ascorbic acid and oxidative inactivation of proteins. 196 58

We reviewed the toxicologic, clinical, and epidemiologic evidence on the health effects of environmental tobacco smoke (ETS). For each type of exposure to environmental tobacco smoke we have sought articles in the English language reporting studies of effects on human health. Formal criteria that stressed study design, quality of execution and generalizability of results were used to select 116 scientifically admissible reports from over 2,900 articles. We concluded that: (a) there is strong evidence of an association between residential exposure to environmental tobacco smoke and both respiratory illness and reduction of lung function, and also between maternal smoking and reduced birth weight; (b) the weight of evidence is compatible with an association between active maternal smoking during pregnancy and increased infant mortality, and also between residential exposure to environmental tobacco smoke (primarily spousal smoking) and the risk of lung cancer; (c) there is evidence consistent with a relationship between exposure to environmental tobacco smoke in the workplace and respiratory symptoms, (d) the evidence is insufficient to implicate residential exposure to environmental tobacco smoke in relation to other forms of malignant disease or congenital malformations; (e) there is no evidence in the literature of an association between nonresidential exposure to environmental tobacco smoke and any form of cancer. Further studies are required to address the effects of exposure to environmental tobacco smoke, especially nonresidential exposure, in carcinogenesis and as a risk factor for atherosclerosis. Further work is also needed to improve measurement of exposure in such studies and to assess the importance of confounding factors.
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PMID:Links between passive smoking and disease: a best-evidence synthesis. A report of the Working Group on Passive Smoking. 174 24

Inhibition by tumor promoting chemicals of intercellular communication via gap junctions may be important in carcinogenesis. In order to investigate the possible role of gap junctional intercellular communication in atherogenesis, we examined the effect of known inhibitors of intercellular communication, 12-O-tetradecanoylphorbol-13-acetate (TPA) and cigarette smoke condensate (CSC), and low density lipoproteins (LDL) and high density lipoproteins (HDL) on cellular communication in smooth muscle cells of human and rat by the microinjection-dye transfer technique. When lucifer yellow CH solution is injected into a cell, the average numbers of human and rat smooth muscle cells that become fluorescent is about 22 and 6, respectively. The tumor promoter (TPA) almost completely blocked gapjunctional communication between smooth muscle cells at 100 ng/ml after 4 h exposure. LDL and CSC were able to inhibit intercellular communication in human and rat cells in a dose-dependent manner up to 60%. LDL-pretreatment of human smooth muscle cells did not affect inhibition of intercellular communication, which suggests that this effect is mainly non-receptor mediated. HDL did not influence junctional communication. The results indicate that inhibition of intercellular communication may also contribute to the pathogenesis of atherosclerotic lesions, such as plaques.
Atherosclerosis 1990 Nov
PMID:Inhibition of intercellular communication in smooth muscle cells of humans and rats by low density lipoprotein, cigarette smoke condensate and TPA. 228 9


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