| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Cholesterol oxidation using hollow fiber dialyzer immobilized with cholesterol oxidase: preparation and properties Lin, C. C. and M. C. Yang (2003), Biotechnol Prog 19(2): 361-4. Abstract: The surface of polyacrylonitrile hollow fibers were hydrolyzed and covalently bonded with cholesterol oxidase (COD) via glutaraldehyde. The immobilized amount of the COD increased with the concentration of glutaraldehyde. However, COD immobilized with 10% glutaraldehyde had higher activity than with other concentrations. The stabilities of immobilized COD to pH and temperature were higher than those of native enzyme. The immobilized enzyme retained 80% of initial activity after 15 days when stored at 4 degrees C, which was longer than native COD. After being reused six times, the COD-immobilized hollow fiber retained more than 80% of the activity. |
| Cholesterol oxidation, macrophage foam cells and atherosclerosis: importance of antioxidants and paraoxonase Aviram, M. (1999), Harefuah 136(8): 620-6. |
| Cholesterol oxidation: health hazard and the role of antioxidants in prevention Valenzuela, A., J. Sanhueza, et al. (2003), Biol Res 36(3-4): 291-302. Abstract: Cholesterol is a molecule with a double bond in its structure and is therefore susceptible to oxidation leading to the formation of oxysterols. These oxidation products are found in many commonly-consumed foods and are formed during their manufacture and/or processing. Concern about oxysterols consumption arises from the potential cytotoxic, mutagenic, atherogenic, and possibly carcinogenic effects of some oxysterols. Eggs and egg-derived products are the main dietary sources of oxysterols. Thermally-processed milk and milk-derived products are another source of oxysterols in our diet. Foods fried in vegetable/animal oil, such as meats and French-fried potatoes, are major sources of oxysterols in the Western diet. Efforts to prevent or to reduce cholesterol oxidation are directed to the use of antioxidants of either synthetic or natural origin. Antioxidants are not only able to inhibit triglyceride oxidation, some of them can also inhibit cholesterol oxidation. Among synthetic antioxidants 2,6-ditertiarybutyl-4-methylphenol (BHT), and tertiary butylhydroquinone (TBHQ) can efficiently inhibit the thermal-induced oxidation of cholesterol. Some natural antioxidants, such as alpha- and gamma-tocopherol, rosemary oleoresin extract, and the flavonoid quercetin, show strong inhibitory action against cholesterol oxidation. |
| Cholesterol oxides accumulate in human cataracts Girao, H., M. C. Mota, et al. (1998), Exp Eye Res 66(5): 645-52. Abstract: Human lens membranes contain the highest cholesterol content of any known biological membrane. Although cholesterol is prone to oxidation, the presence of its oxidation products in human cataract has not been shown before. This study was designed to investigate the presence of cholesterol oxides in human cataractous lenses. Human clear lenses (n = 48) were obtained from Coimbra University Hospital Eye Bank. Human cataracts (n = 54) were obtained by routine extracapsular surgery. Cholesterol oxides were isolated by solid-phase extraction on a C18 cartridge and quantified as TMS-ether derivatives by gas chromatography. The extraction procedure allows for an efficient recovery of the major cholesterol oxides, while retaining virtually all cholesterol. Exposure of membranes isolated from transparent human lenses to the free radical generator 2,2'-Azobis(2-amidinopropane) dihydrochloride (AAPH) produced 7 alpha-hydroxycholesterol (6%), 7 beta-hydroxycholesterol (19%), 5 alpha, 6 alpha-epoxycholestanol (1%) and 7-ketocholesterol (74%) as major oxidation products. Cataractous lenses contained quantifiable amounts of 7 beta-hydroxycholesterol (7.3 +/- 0.74 mmol mol-1 cholesterol), 7-ketocholesterol (4.2 +/- 0.32 mmol mol-1 cholesterol), 5 alpha, 6 alpha-epoxycholestanol (0.9 +/- 0.16 mmol mol-1 cholesterol), 20 alpha-hydroxycholesterol (0.6 +/- 0.13 mmol mol-1 cholesterol) and 25-hydroxycholesterol (0.1 +/- 0.02 mmol mol-1 cholesterol), whereas clear lenses contained no detectable amounts of cholesterol oxides. We have shown, for the first time, that oxysterols accumulate in human cataracts. Although the total amount of oxidized cholesterol in cataracts is not likely to be high it may account for much of the membrane damage associated with cataract formation. |
| Cholesterol oxides and carcinogenesis Morin, R. J., B. Hu, et al. (1991), J Clin Lab Anal 5(3): 219-25. Abstract: Experimental evidence indicates a relationship between cholesterol alpha-epoxide and skin cancer, and exposure of skin fibroblasts to ultraviolet radiation enduces formation of significant levels of this oxide. Colon cancer is also etiologically linked to cholesterol oxidation products. Higher than normal levels of cholestanetriol have been found in patients with colon cancer and also in those with precancerous disorders such as adenomatous polyps and ulcerative colitis. Higher than normal levels of cholesterol alpha-epoxide have been found in breast fluid aspirates of women with benign breast disease, with or without atypical hyperplasia of the epithelium, and this may be a factor in the increased incidence of breast cancer associated with hyperplasia. Similarly, the observed increased levels of cholesterol alpha and beta-epoxides in prostatic fluid of men with benign prostatic hypertrophy may be associated with subsequent development of prostate cancer. Cholesterol alpha-epoxide has been found to be mutagenic to fibroblasts in culture and to induce morphological transformation in hamster embryo cells and in mouse C3H cells. 25-Hydroxycholesterol and 20 alpha-hydroxycholesterol are potent suppressors of generation and proliferation of tumor-specific cytotoxic T lymphocytes. Although investigations into the role of cholesterol oxidation products in cancer are still in the early stages, evidence to date indicates a potentially significant role in the induction of some types of cancer. |
| Cholesterol oxides and natural autoantibodies Hwee Ming, C. and S. Kalyana (1998), Atherosclerosis 141(2): 347-8. |
| Cholesterol oxides in plasma and lipoproteins of magnesium-deficient rabbits and effects of their lipoproteins on endothelial barrier function Mahfouz, M. M., Q. Zhou, et al. (1994), Magnes Res 7(3-4): 207-22. Abstract: The cholesterol oxide (ChO) levels in the plasma and low density lipoproteins (LDL and VLDL) in four groups of rabbits fed for seven weeks either normal (NC) or high cholesterol (HC) with low or normal magnesium (Mg) diets were determined and compared with the NC group fed a standard rabbit diet. The plasma from the NC group contained low levels of different cholesterol oxides. These cholesterol oxides were significantly elevated in the plasma of rabbits fed a HC-normal magnesium or a HC-low magnesium diet. In the NC-low Mg group, 7 alpha-hydroxycholesterol, 7 beta-hydroxycholesterol and 7-ketocholesterol were elevated while the other cholesterol oxides remained within the normal range of the NC group. When the cholesterol oxides were assayed in the LDL and VLDL fractions as micrograms/mg protein, the fractions obtained from the groups fed NC-low Mg, HC-normal Mg or HC-low Mg diets showed higher levels of cholesterol oxides than the fractions obtained from the NC group. When LDL and VLDL fractions from the different groups were incubated at equal protein concentration with confluent endothelial cell monolayers, transendothelial albumin transfer was significantly increased by the lipoproteins from the experimental groups as compared to the control group. These results suggest that elevation of cholesterol oxides in magnesium deficiency or hypercholesterolaemia may be related to their atherogenic effects through decreasing the endothelial barrier function which could enhance the deposition of cholesterol rich lipoproteins into the arterial wall. |
| Cholesterol oxides induce programmed cell death in microglial cells Chang, J. Y., J. A. Chavis, et al. (1998), Biochem Biophys Res Commun 249(3): 817-21. Abstract: N9 microglial cells were used as a model to examine the effect of cholesterol oxides on central nervous system microglia. Results indicated that 25-OH-cholesterol was the most cytotoxic agent among the cholesterol oxides tested. During the process of cell death, this agent caused prominent nuclei condensation and significant DNA fragmentation, a phenomenon association with programmed cell death. Cholesterol oxides were able to potentiate the bacterial lipopolysaccharide (LPS)-induced nitric oxide production to various degrees. Consistent with this finding, Northern blot analysis indicated that 25-OH-cholesterol potentiated the LPS-induced nitric oxide synthase RNA levels. The cytotoxicity of 25-OH-cholesterol could be prevented by methyl-beta-cyclodextrin, a glucose polymer known to cause cholesterol oxide efflux from cells. While much attention has been focused on the cytotoxicity of cholesterol oxides on immune cells within the blood, including lymphocytes and macrophages, the results from this study indicated for the first time that these agents are toxic to microglial cells derived from the central nervous system. |
| Cholesterol oxides mediated changes in cytoskeletal organisation involves Rho GTPases small star, filled Girao, H., P. Pereira, et al. (2003), Exp Cell Res 291(2): 502-13. Abstract: The small GTPases Rho, Rac, and Cdc42 regulate the actin cytoskeleton in all eukaryotic cells. In this study we have evaluated the effect of cholesterol oxides (7-ketocholesterol and 25-hydroxycholesterol) on cell migration, cell adhesion, and cytoskeletal organisation of lens epithelial cells (LEC). Effects of cholesterol oxides on cytoskeleton were evaluated by immunofluorescence confocal microscopy. The 7-ketocholesterol induced cell arborisation, with bundling of vimentin and tubulin in the cell processes and formation of filopodia and stress fibres. Cells treated with 25-hydroxycholesterol showed a collapse of vimentin filaments towards the nucleus and formation of lamellipodia. In addition, cells treated with 7-ketocholesterol or 25-hydroxycholesterol showed decreased migration. The effects of cholesterol oxides on cytoskeletal proteins involve the activation of the small GTPases Rho, Rac, and Cdc42. Indeed, formation of both filopodia and stress fibres induced by 7-ketocholesterol is inhibited by overexpressing dominant negatives forms of Cdc42 and RhoA, respectively. Similarly, the collapse of vimentin intermediate filament network and the formation of lamellipodia, induced by 25-hydroxycholesterol, is inhibited by overexpressing dominant negatives forms of Rac1. The effects of cholesterol oxides described in this study for LEC are also observed for at least two other cell lines (H36CE and U373), suggesting that this may represent a general mechanism whereby cholesterol oxides induces cytoskeletal disorganisation. |
| Cholesterol oxides, cholesterol, total lipid, and fatty acid composition in turkey meat Baggio, S. R., E. Vicente, et al. (2002), J Agric Food Chem 50(21): 5981-6. Abstract: The contents of cholesterol oxides, cholesterol, and total lipid, and the fatty acid composition were determined in frozen turkey meat. The 7-ketocholesterol content varied from 33 microg/100 g in the breast to 765 microg/100 g in the skin, and the levels of 7 beta-hydroxycholesterol varied from not detected in the leg, breast, and skin to 370 microg/100 g in the skin. The values for total lipid (g/100 g) in the wings, legs, breast, and skin were 0.9 +/- 0.4, 1.1 +/- 0.2, 0.5 +/- 0.1, and 12 +/- 3, respectively. The contents for cholesterol (mg/100 g) were 46 +/- 5, 35 +/- 2, 27 +/- 3, and 81 +/- 6 in the wing, legs, breast, and skin, respectively. The main fatty acids identified in all cuts were C18:2n6, C18:1n9, C16:0, C18:0, and C20:4n6. |
| Cholesterol oxides: their occurrence and methods to prevent their generation in foods Savage, G. P., P. C. Dutta, et al. (2002), Asia Pac J Clin Nutr 11(1): 72-8. Abstract: Eight cholesterol oxides are commonly found in foods with high cholesterol content, such as meat, egg yolk and full fat dairy products. Factors known to increase the production of cholesterol oxides in foods are heat, light, radiation, oxygen, moisture, low pH, certain pro-oxidising agents and the storage of food at room temperature. Processes, such as pre-cooking, freeze-drying, dehydration and irradiation, have all been reported to result in increased production of cholesterol oxides in meats. As prepared consumer foods are becoming increasingly popular, the consumption of higher levels of cholesterol oxides in foods is inevitable. An understanding of the mechanisms involved in the generation of cholesterol oxides may assist in their reduction in foods and possibly reduce the impact of these compounds on human health. |
| Cholesterol ozonation products as biomarkers for ozone exposure in rats Pryor, W. A., K. Wang, et al. (1992), Biochem Biophys Res Commun 188(2): 618-23. Abstract: Cholesterol, 1, which is present in both the lung lining fluid and cell membranes of lung tissue, reacts with ozone in aqueous systems to give 3 beta-hydroxy-5-oxo-5,6-secocholestan-6-al (2) as the major product. Reaction of 2 with 2,4-dinitrophenyl hydrazine (DNPH) in aqueous solutions, liposomes or lung extracts affords the anti and syn DNPH derivatives of 2 (3b and 3c) and of the rearrangement product 3,5-dihydroxy-B-norcholestane-6-carboxaldehyde (3a). These derivatives also are detected in lung tissue extracts from rats exposed to 1.3 ppm ozone for 12 hr. |
| Cholesterol packing, crystallization and exchange properties in phosphatidylcholine vesicle systems Phillips, M. C. (1990), Hepatology 12(3 Pt 2): 75S-80S; discussion 80S-82S. Abstract: The properties of phosphatidylcholine/cholesterol vesicles have been studied extensively because of their relevance to the behavior of these components in cell membranes. At equilibrium, phosphatidylcholine bilayers are saturated when equimolar levels of cholesterol are incorporated; the cholesterol molecules interfere with the cooperative lateral interactions of the phosphatidylcholine acyl chains and restrict the fluidity relative to pure liquid-crystal phosphatidylcholine bilayers. Mixed cholesterol/phosphatidylcholine bilayers containing more than equimolar cholesterol are metastable; on storage excess cholesterol is released from the vesicles and forms cholesterol monohydrate crystals. This process models the formation of cholesterol gallstones in bile and the growth of the crystals probably involves, at least in part, diffusion of cholesterol molecules from the vesicle bilayer to the crystal surface. The cholesterol-phosphatidylcholine interaction energy in the lipid-water interface of the donor vesicle has a critical effect on the rate of this transfer process. |
| Cholesterol palmitate in amniotic fluid: confirmation of a simple, rapid, inexpensive, and reliable indicator of fetal pulmonary maturity Jendryczko, A., M. Drozdz, et al. (1992), Zentralbl Gynakol 114(2): 78-80. Abstract: The cholesterol test was previously described and preliminary experience suggested it might be a rapid, inexpensive, and reliable indicator of fetal lung maturity. In this expanded series of 1342 patients delivered of infants within 72 hours of amniotic fluid analysis, the predictive value for mature test was 98.6%. Predictive value for immature test was 55.4%. For the phospholipid profile the predictive value was 97.0% for a mature test result, 31.2% for an immature result. These observations, coupled with its methodologic simplicity, make the cholesterol palmitate test a good first step in a cascade scheme of tests for fetal lung maturity and a valuable test in a facility where the phospholipid profile is not available 24 hours a day. |
| Cholesterol paradox in patients with paroxysmal atrial fibrillation Annoura, M., M. Ogawa, et al. (1999), Cardiology 92(1): 21-7. Abstract: Hypercholesterolemia is a major risk factor for coronary heart disease (CHD), but the associations among lipids, lipoproteins and paroxysmal atrial fibrillation (PAF) have not yet been reported. The associations among lipids, lipoproteins and PAF were examined in a case-control study, in which cases and controls were defined as those with/without definite ECG-detectable PAF, respectively. CHD patients were excluded from the study. The mean values of serum total cholesterol (TC), triglyceride (TG) and high density lipoprotein-cholesterol (HDL-C), after adjusting for age and gender, in patients with PAF were lower than those in patients without PAF (175 +/- 4 mg/dl vs. 190 +/- 3 mg/dl, 104 +/- 7 mg/dl vs. 123 +/- 6 mg/dl, 46.0 +/- 1.7 mg/dl vs. 51.8 +/- 1.4 mg/dl, respectively), as assessed by an analysis of covariance. After controlling for age and gender, TC, TG and HDL-C (all in quartiles) were inversely and linearly (p < 0.05) associated with the percentage of patients with PAF, as assessed by a multiple logistic regression analysis. The associations between TC or TG and PAF varied with the HDL-C level: significant when HDL-C was low (p < 0.05), but not when HDL-C was high. The odds ratio (relative risk of PAF) for patients with both low TC or TG and low HDL-C was 4.08 (95% CI: 1.81-9.57) times or 9. 40 (3.25-32.0) times higher (p < 0.01) than that for patients with high TC or TG and high HDL-C, respectively. In conclusion, low serum levels of TC and TG were found in PAF patients, while reduced HDL-C may cause PAF. Hypolipoproteinemia including low HDL-C may affect atrial vulnerability and cause atrial fibrillation. |
| Cholesterol paradox: is high total or low HDL cholesterol level a risk for Alzheimer's disease? Michikawa, M. (2003), J Neurosci Res 72(2): 141-6. Abstract: Cholesterol is an essential component of membranes for maintaining their structure and functions. The discovery that possession of apolipoprotein E (apoE), allele epsilon4 is a strong risk factor for Alzheimer's disease (AD) leads us to focus on the role of cholesterol in the pathogenesis of AD. Accumulating epidemiological and biological evidence suggests the link between the serum cholesterol level and the development of AD, and the potential therapeutic effectiveness of statins for AD and mild cognitive impairment (MCI), whereas other lines of evidence show controversial results. Cholesterol is known to interact with amyloid beta-protein (Abeta) in a reciprocal manner: cellular cholesterol levels modulate Abeta generation, whereas Abeta alters cholesterol dynamics in neurons, leading to tauopathy. In this review, the relationship between the cholesterol levels in serum or cerebrospinal fluid (CSF) and the induction of AD is discussed. The mechanism(s), if this is the case, of how cholesterol in the central nervous system (CNS) is involved in the induction of pathologies of AD including Abeta generation and tauopathy, and how statins prevent it are also discussed. |
| Cholesterol pericarditis Ito, T. (1996), Ryoikibetsu Shokogun Shirizu(13): 515-9. |
| Cholesterol pericarditis and cardiac tamponade with congenital hypothyroidism in adulthood Van Buren, P. C. and W. C. Roberts (1990), Am Heart J 119(3 Pt 1): 697-700. |
| Cholesterol pericarditis associated with rheumatoid arthritis Knobel, B. and P. Rosman (2001), Harefuah 140(1): 10-2, 87. Abstract: Cholesterol pericarditis (CP) is a rare and unusual disease characterized by chronic pericardial effusion with high cholesterol concentration. Precipitation of cholesterol crystals may occur and induce inflammation and constrictive pericarditis. CP may be idiopathic, but is usually associated with a systemic disease, such as tuberculosis, myxedema, or as in our case, rheumatoid arthritis (RA). We present a 78-year-old woman with RA, typical deformities of the metacarpo- and metatarso-phalangeal joints and subcutaneous rheumatoid nodules. She was hospitalized with increasing dyspnea and weakness and a 2-dimensional transthoracic echocardiogram showed a large pericardial effusion, without tamponade. Blood cholesterol was 208 mg/dl, triglycerides 169 mg/dl, LDH 37 u/L and rheumatoid factor 2560 u; glucose, kidney, and thyroid function tests were normal and PPD test negative. Pericardiocentesis yielded 800 ml of opaque, cloudy fluid, with glucose 19 mg/dl, cholesterol 264 mg/dl (normal 20-40 mg/dl), triglycerides 169 mg/dl, LDH 5820 u/L and rheumatoid factor 40 u; viral titers and cultures for bacterial, mycobacterial and fungal infections were negative. The pericardial fluid had a distinctive scintillating, gold-paint appearance and many cholesterol crystals were evident microscopically. The patient responded to treatment with methotrexate and steroids. Factors responsible for increase in pericardial fluid cholesterol may be its liberation from injured pericardial cells and rheumatoid nodules, lysis of red cells, or lymphatic obstruction and impairment of the absorptive capacity of the pericardium. |
| Cholesterol pericarditis causing cardiac tamponade Ford, E. J., P. A. Bear, et al. (1991), Am Heart J 122(3 Pt 1): 877-9. |