thiobarbituric-acid and Arteriosclerosis

An increased concentration of end products of lipid peroxidation is the evidence most frequently quoted for the involvement of free radicals in human disease. However, it is likely that increased oxidative damage occurs in most, if not all, human diseases and plays a significant pathological role in only some of them. For example, peroxidation appears to be important in atherosclerosis and in worsening the initial tissue injury caused by ischemic or traumatic brain damage. Oxidative stress can damage many biological molecules; indeed, proteins and DNA are often more significant targets of injury than are lipids, and lipid peroxidation often occurs late in the injury process. Many assays are available to measure lipid peroxidation, but no single assay is an accurate measure of the whole process. Application of simple diene-conjugate and thiobarbituric acid (TBA) assays to human tissues and body fluids can produce artifacts. An HPLC-based TBA test can eliminate some of these artifacts.

Topics: Arteriosclerosis; Disease; Fatty Acids, Unsaturated; Free Radicals; Lipid Peroxidation; Metals; Oxygen; Thiobarbiturates

Topics: Arteriosclerosis; Blood Proteins; Cholesterol Esters; Humans; Lipid Peroxides; Lipoproteins, LDL; Liver; Oxidation-Reduction; Thiobarbiturates

This study was carried out to investigate whether dietary vitamin E and ferulic acid (FA) can exert possible interactions on preventions of hypercholesterolemia and atherogenic lesion formation in C57BL/65 apolipoprotein E-deficient (apo E(-/-)) mice. Four-week-old male apo E(-/-) mice were randomly divided into three groups and given one of three types of Western diets with various amounts of vitamin E (0.02%, 0%, or 0.2%) for 15 weeks. FA was added to vitamin E-free Western diet and vitamin E-rich Western diet at the 0.02% level. The plasma total cholesterol concentration was significantly lowered when FA was added to the vitamin E-free and vitamin E-rich Western diet as compared to the normal vitamin E Western diet (0.02% vitamin E), and this was accompanied with a decreased hepatic acyl-coenzyme A:cholesterol acyltransferase activity. The hepatic and erythrocyte thiobarbituric acid-reactive substances levels were significantly lowered when FA was added to the vitamin E-rich Western diet, which was attributable to increased activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) and paraoxonase. Accordingly, vitamin E and/or FA are beneficial for prevention of hypercholesterolemia and atherogenesis in apo E(-/-) mice. In particular, dietary FA exhibited an anti-atherosclerotic property, and this effect was synergistically enhanced with the vitamin E supplement.

Topics: Acyl Coenzyme A; Animals; Anticholesteremic Agents; Antioxidants; Apolipoproteins E; Arteriosclerosis; Coumaric Acids; Diet; Drug Therapy, Combination; Hypercholesterolemia; Lipids; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Phytotherapy; Plant Extracts; Sterol O-Acyltransferase; Thiobarbiturates; Vitamin E

It was established that viral particles, like low-density lipoproteins (LDLP), when subjected to some modification changes, lost their ability to be internalized by tissue somatic cells and acquired tropism to macrophage cells. The data, obtained by us by using the polymerase chain reaction (PCR) method, made it possible to assert that atherosclerotic plaques, isolated from vessels of patients with ischemic heart disease (IHD) who underwent coronary bypass, contained RNA of the A(HINI) and AH3N3) influenza viruses. Whereas, the vessel portions, undamaged by atherosclerosis, did not contain any genetic substances of influenza viruses. It was for the first time that an experimentally supported understanding was expressed on that the atherosclerotic plaques serve as a "reservoir" for influenza viruses. It is also suggested that the mentioned plaques can be the carriers of influenza viruses for a long time, thus, prolonging the persistent form of influenza infection in the human body.

Topics: Aged; Animals; Arteriosclerosis; Coronary Artery Bypass; Coronary Artery Disease; Coronary Vessels; Humans; Influenza A virus; Influenza, Human; Lipid Peroxidation; Lung; Malondialdehyde; Mice; Middle Aged; Myocardial Ischemia; Polymerase Chain Reaction; RNA, Viral; Spectrophotometry; Thiobarbiturates; Time Factors; Tropism

Although age is a strong risk factor for atherosclerosis, it is unclear whether age may directly influence the process of atherogenesis. We, therefore, performed several studies in young (2-4 months old), mature (10-14 months old), and old (20-22 months old) mice to determine if the rate of aortic lesion formation increases with age, and whether this is related to increases in oxidative stress or vascular cell adhesion molecule (VCAM-1) expression in the aortic wall. In chow-fed low-density lipoprotein receptor-deficient (LDLR-/-) mice, plasma total cholesterol levels increased with age (250 +/- 52 mg/dl in young, 276 +/- 58 in mature, and 314 +/- 101 mg/dl in old mice). In contrast, the extent of atherosclerosis rose more rapidly, increasing from 3.6 +/- 2.7% of the aortic surface in mature mice to 18.2 +/- 8% in old mice. Plasma and tissue levels of antioxidant enzymes and molecules, as well as plasma thiobarbituric acid reactive substances and low-density lipoprotein susceptibility to oxidation, did not change with age. In a second study, VCAM-1 expression in the aortic arch and the extent of atherosclerosis in the aortic origin were significantly greater in old LDLR-/- mice than in young LDLR-/- mice. Additionally, after 1 month of a high-fat diet, which induced equally elevated plasma cholesterol levels in both young and old LDLR-/- mice, VCAM-1 expression and aortic lesion formation were still greater in old mice. The extent of atherosclerosis correlated well (r = .65,p <.01) with the expression of VCAM-1 in the aortic origin. In a final study, we measured VCAM-1 expression and atherosclerosis in young, mature, and old C57BL/6 mice, which have low plasma cholesterol levels (< or =100 mg/dl) when fed a standard chow diet. Although plasma cholesterol levels did not increase with age, old C57BL/6 mice had significantly more VCAM-1 expression in the aortic arch than did young mice. However, no lesions were observed in the aortic origin in either group. These data demonstrate that plasma cholesterol levels and VCAM-1 expression increase with age and suggest that this may contribute to the increased rate of atherosclerotic lesion formation in LDLR-/- mice. Importantly, the age-dependent increase in VCAM-1 expression does not appear to be related to plasma cholesterol levels. This study also suggests that in the absence of elevated plasma cholesterol, an increased expression of VCAM-1 alone is not sufficient for lesion formation.

Topics: Aging; Analysis of Variance; Animals; Aorta; Aortic Diseases; Arteriosclerosis; Catalase; Cholesterol; Dietary Fats; Disease Models, Animal; Gene Expression Regulation; Glutathione Peroxidase; Lipoproteins, LDL; Male; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Oxidation-Reduction; Oxidative Stress; Receptors, LDL; Risk Factors; Superoxide Dismutase; Thiobarbiturates; Vascular Cell Adhesion Molecule-1

The susceptibility to oxidation of freshly isolated LDL from healthy normolipidemic individuals in three age groups was estimated by exposure of LDL to ionizing radiation followed by analyses of vitamin E, TBARS, conjugated dienes, and fluorescent products. The results clearly showed that LDL from elderly subjects was the most susceptible to oxidative damage in vitro. In particular, the greater susceptibility of LDL from elderly subjects in comparison to that from young subjects may be attributed to the much lower (4-fold) concentration of LDL vitamin E in the elderly subjects. The present study reinforces the notion that the susceptibility of LDL to oxidation increases with age.

Topics: Adult; Aged; Aged, 80 and over; Aging; Arteriosclerosis; Cobalt; Gamma Rays; Humans; Lipoproteins, LDL; Male; Middle Aged; Oxidation-Reduction; Radiation Tolerance; Thiobarbiturates; Vitamin E

Atherosclerosis and its complications are prevalent worldwide with a high prevalence in western societies. The disease may sometimes be explained by a defect of low density lipoprotein (LDL) specific receptors. However, the prevalence of receptor defect is rather rare and a large body of evidence supports the possibility that an alternative pathway, the so-called "scavenger pathway", constitutes the gate through which cholesterol enters into the parietal wall and gives origin to the "foam cell". Experimental work has clearly demonstrated that LDL may be modified under the action of chemical and biological offenders, all of which make the LDL an "alien". Some papers suggest that the modifications of LDL may occur also "in vivo" in the microenvironment of the vascular vall. In 1988 we were able to record two LDL subfractions in human plasma; the more electronegative minor subfraction shares many of the peculiar traits of LDLs modified "in vitro". The present article stresses all the points which support the hypothesis that the small more electronegative LDL circulating modified LDL, may represent a certain amount of possibly oxidative in origin.

Topics: Animals; Arteriosclerosis; Artifacts; Chromatography, High Pressure Liquid; Chromatography, Ion Exchange; Humans; Hyperlipidemias; Lipoproteins, LDL; Probucol; Thiobarbiturates

The concentration of thiobarbituric acid reactive substances (TBARS) formed as a result of lipid peroxidation and prostanoid metabolism was measured in the plasma of patients with coronary or peripheric atherosclerosis. From the results conclusions were deduced to the function of reactive O2-species in the atherogenesis. We found in plasma of patients with coronary as well as with peripheric atherosclerosis increased TBARS concentrations dependent on the dimension of atherosclerosis as an index of activation of reactive O2-species formation. The TBARS concentration correlated with the cholesterol and LDL-cholesterol concentration in plasma.

Topics: Adult; Arteriosclerosis; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Humans; Lipid Peroxidation; Male; Middle Aged; Oxygen; Thiobarbiturates; Triglycerides

Thiobarbituric acid reactive substances (TBARS) in 38 low density lipoprotein (LDL) samples from 21 healthy male non-smokers and 17 smokers (greater than 20 cigarettes per day) were measured before and after oxidation. TBARS in the freshly isolated LDL from non-smokers and smokers were similar, however, oxidized LDL samples from smokers developed nearly twofold more TBARS than non-smoker LDL samples. 16 LDLs from 8 smokers and 8 non-smokers were conditioned in redox-metal containing F-10 medium and subsequently added to P 388 D.1 macrophage cultures. LDL dependent cholesteryl ester increase in the P 388 D.1 cells after an 18 h incubation with non-smoker LDL was significantly lower than in the cells incubated with smoker LDL (P less than 0.01). A higher reacylation rate of cholesterol in P 388 D.1 cells incubated with smoker LDL (P less than 0.05) suggests that LDL-cholesterol uptake is significantly higher in P 388 D.1 cells incubated with smoker-LDL than in P 388 D.1 cultures exposed to non-smoker LDL. This finding indicates that smoking might contribute to increased shunting of LDL into macrophages. The vitamin E content of 6 non-smoker LDL samples was significantly higher than that in 6 smoker-LDL samples (P less than 0.01). We conclude that the vitamin E/LDL ratio may differ significantly in heavy smokers and non-smokers.

Topics: Adult; Arteriosclerosis; Cholesterol Esters; Humans; Lipoproteins, LDL; Macrophages; Male; Risk Factors; Smoking; Thiobarbiturates; Vitamin E

Patients with transient ischemic attacks (TIA) were previously shown to have high plasma values of thiobarbituric acid-reactive substances (TBA-RS). To study whether these changes could be related to platelet activability, TBA-RS was investigated in 24 TIA patients before and 24 h after 1 g aspirin, an inhibitor of platelet cyclooxygenase pathway. Baseline TBA-RS values were significantly higher in TIA than in controls. Conversely, TIA patients had TBA-RS values after aspirin similar to controls, suggesting that the increase of plasma TBA-RS was not attributable to platelet hyperfunction. The evaluation of metabolic profile showed that patients with highest TBA-RS had hypercholesterolemia, hypertriglyceridemia, and/or diabetes mellitus. This study suggests that the increase of plasma TBA-RS in TIA could be an epiphenomenon of altered metabolic pathway.

Topics: Administration, Oral; Aged; Arteriosclerosis; Aspirin; Blood Glucose; Blood Platelets; Coronary Disease; Diabetes Mellitus; Female; Humans; Hypercholesterolemia; Ischemic Attack, Transient; Lipid Peroxides; Male; Middle Aged; Thiobarbiturates

Topics: Animals; Arteriosclerosis; Blood Platelets; Cholesterol, Dietary; Docosahexaenoic Acids; Drug Combinations; Eicosapentaenoic Acid; Fatty Acids, Unsaturated; Fish Oils; Rabbits; Research Design; Thiobarbiturates

The serum concentration of thiobarbituric acid reactive substances (TBARS), which can be used in the characterization of O2-radical metabolism, was analyzed in patients with myocardial infarction in the acute phase, 10-14 days, 1 month, and 6 months after infarction, and compared with the TBARS concentration of a healthy group and a group with atherosclerosis. After myocardial infarction we found increased TBARS concentration at all moments of investigation in comparison with the healthy and atherosclerosis groups. Maximum concentration was found 10-14 days after infarction, afterwards the TBARS concentration decreased, without however attaining the values which we found in the comparison groups. The increased TBARS concentration 6 months after myocardial infarction demonstrates a manifestation of disturbances in the O2-radical metabolism. Such disturbances may be regarded as a high-risk factor to the cardiovascular system.

Topics: Arteriosclerosis; Follow-Up Studies; Free Radicals; Humans; Lipid Peroxides; Male; Middle Aged; Myocardial Infarction; Oxygen; Thiobarbiturates

It has been suggested that lipid peroxidation is an important factor in the pathogenesis of carbon tetrachloride (CCl4) hepatotoxicity. In the present study, experimental liver injury induced by CCl4 could be prevented by levamisole, an antihelminthic agent and immunomodulator. Despite of exposure to CCl4 tissue levels of thiobarbituric acid (TBA) reacting substances in the liver were not increased in rats pretreated with levamisole. On the other hand, when we administered levamisole, 150 mg p. o. daily given on three consecutive days of each week, to six elderly patients with arteriosclerosis. They all showed a significant decrease in serum TBA reactive substances during the 12 weeks of therapy. This provides evidence that levamisole prevents liver damage by CCl4, and indicate the possibility that levamisole might have an antioxidative effect or may prevent the accumulation of TBA reactive substances.

Topics: Aged; Animals; Arteriosclerosis; Carbon Tetrachloride; Female; Humans; Levamisole; Lipid Metabolism; Liver; Oxidation-Reduction; Rats; Thiobarbiturates