| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Epidermal steroid sulfatase and cholesterol sulfotransferase are regulated during late gestation in the fetal rat Hanley, K., Y. Jiang, et al. (1997), J Invest Dermatol 108(6): 871-5. Abstract: Lipids in the stratum corneum (SC) are organized into lamellar membrane unit structures that provide the permeability barrier. Cholesterol sulfate, a SC membrane lipid, is synthesized by cholesterol sulfotransferase (CSTase) in the lower epidermis and hydrolyzed to cholesterol by steroid sulfatase (SSase) in the SC. To determine whether these enzymes are induced during barrier ontogenesis, we examined their activity in epidermis of fetal rats before (gestational day 17), during (day 19), and after (day 21) barrier formation. CSTase activity increased approximately 10-fold between day 17 and day 19, then declined between day 19 and day 21. In contrast, SSase activity reached its peak activity on day 21, increasing >5-fold. Fetal rat skin explants develop a SC and barrier over the same time course in vitro as in utero. Likewise, CSTase and SSase activities during in vitro ontogenesis precisely mirrored those obtained in utero. Moreover, hormones that accelerate barrier ontogenesis (e.g. glucocorticoids, thyroid hormone, and estrogen) accelerated the increase in CSTase and SSase activities during in vitro ontogenesis. mRNA levels of SSase increased in parallel with enzymatic activity, suggesting that these developmental changes are regulated at the genomic level. Finally, addition of exogenous cholesterol sulfate to explants in vitro did not accelerate either SC development or barrier formation. These studies suggest that induction of the cholesterol sulfate cycle enzymes during SC ontogenesis is a component of the fetal epidermal differentiation program and that the synthetic and degradative enzymes of this pathway are differentially regulated. |
| Epidermoid cyst (cholesteatoma) and cholesterol granuloma of the temporal bone and epidermoid cysts affecting the brain Mafee, M. F., A. Kumar, et al. (1994), Neuroimaging Clin N Am 4(3): 561-78. Abstract: Five cases of petrous apex epidermoid cysts, six cases of petrous apex cholesterol granuloma cysts, and seven cases of intradural cerebellopontine angle (CPA) or intracranial epidermoid cysts are reviewed. Petrous epidermoid cysts (cholesteatomas) and cholesterol granuloma cysts cannot be differentiated definitely from each other on CT scans. On MR imaging, epidermoid cysts exhibit long T1 and long T2 characteristics and can be differentiated from cholesterol granuloma cysts, which exhibit short T1 and long T2 characteristics. Intradural epidermoid cysts involving the CPA or other portions of the brain, also demonstrate long T1 and long T2 characteristics on MR scans. Intradural epidermoid cysts exhibit curvilinear areas of higher intensity on T1-weighted images, which were best evaluated on T1-weighted MR images obtained with more averages (6 to 8). |
| Epidermoid cyst and cholesterol granuloma of the orbit Fukuta, K. and I. T. Jackson (1990), Br J Plast Surg 43(5): 521-7. Abstract: Epidermoid cyst and cholesterol granuloma have been confused, but these are different lesions. A case of recurrent orbital epidermoid cyst and another case of orbital cholesterol granuloma are presented in order to describe their distinct pathological, clinical and imaging characteristics and their surgical management. Advanced investigation using our custom-designed three-dimensional imaging allowed a better appreciation of the exact location, and optimal planning of the surgical treatment. The same surgical approach was used for both lesions: total resection via a coronal incision and immediate reconstruction of residual defects using skull bone grafts. |
| Epistatic interaction between beta2-adrenergic receptor and neuropeptide Y genes influences LDL-cholesterol in hypertension Tomaszewski, M., F. J. Charchar, et al. (2004), Hypertension 44(5): 689-94. Abstract: Beta2-adrenergic receptor gene and neuropeptide Y gene may potentially influence lipid metabolism and overall energy balance. Therefore, we examined associations of these genes with lipid fractions and obesity-related phenotypes in hypertensive subjects. A total of 638 white individuals from 212 Polish families with clustering of essential hypertension were phenotyped for cardiovascular risk determinants. Each subject was genotyped for functional polymorphisms of beta2-adrenergic receptor gene (Arg16Gly and Gln27Glu) and neuropeptide Y (Leu7Pro). Of 3 common haplotypes of beta2-adrenergic receptor gene, Arg16Gln27 was overtransmitted to offspring with elevated levels of total cholesterol (Z=2.2; P=0.026) and LDL-cholesterol (Z=3.2; P=0.002). Individually, Leu7Pro was not associated with any of the metabolic phenotypes in family-based tests or case-control analyses. However, in the presence of Arg allele of Arg16Gly and Gln allele of Gln27Glu, homozygosity for Leu variant of the Leu7Pro polymorphism was associated with 2.1-increased odds ratio (confidence interval, 1.10 to 3.81; P=0.024) of elevated LDL in hypertensive subjects, independent of age, gender, body mass index, adjusted blood pressures, antihypertensive therapy, and use of nonselective beta-blockers and diuretics. Consistently, there was a significant multilocus association among variants of Arg16Gly, Gln27Glu, and Leu7Pro in hypertensive probands with elevated LDL (cases; P=0.028) but not in hypertensive subjects with normal LDL (controls). This study revealed an association of LDL-cholesterol with beta2-adrenergic receptor gene haplotype and provided evidence for epistatic interaction between beta2-adrenergic receptor gene and neuropeptide Y gene in determination of LDL-cholesterol in patients with essential hypertension. |
| Epitope mapping of cytochrome P450 cholesterol side-chain cleavage enzyme by sera from patients with autoimmune polyglandular syndrome type 1 Liiv, I., K. Teesalu, et al. (2002), Eur J Endocrinol 146(1): 113-9. Abstract: OBJECTIVE: Autoimmune polyglandular syndrome type 1 (APS-1) is a disease associated with defects of the autoimmune regulator gene and is characterized by autoimmune lesions of several tissues, predominantly endocrine glands, with multiple autoantibodies. In this study we describe autoantigenic epitopes on cholesterol side-chain cleavage enzyme (P450scc) using sera from Finnish and Sardinian patients with APS-1, and analyze the epitope reactivities during disease follow-up. METHODS: A series of P450scc cDNA fragments were expressed in E. coli and tested by immunoblotting assay using the patients' sera. RESULTS: Epitope regions were found over the whole P450scc molecule except the last N- (amino acids (aa) 1-40) and C-termini (aa 456-521). The strongest reactivity with patients' sera was found with central and C-terminal regions of the P450scc protein. All studied patients had IgG1 subclass antibodies. CONCLUSIONS: The results show that Finnish and Sardinian patients with APS-1 have similar, polyclonal immune reactions against P450scc, and that epitope reactivities did not change during the disease course. These results support the opinion that autoantibodies against P450scc and their epitope reactivity pattern are formed at an early stage of steroidogenic autoimmunity. |
| Epoxidation and reduction of cholesterol, 1,4,6-cholestatrien-3-one and 4,6-cholestadien-3beta-ol Ma, E., H. Kim, et al. (2005), Steroids 70(4): 245-50. Abstract: Many naturally occurring polyhydroxylated sterols and oxysterols exhibit potent biologic activities. This paper describes reagent and position selectivity of epoxidation and reduction of cholesterol derivatives. Cholesterol was reacted with m-chloroperoxybenzoic acid (m-CPBA) to form 5alpha,6alpha-epoxycholestan-3beta-ol, but in reaction with 30% H(2)O(2), it did not reacted. 1,4,6-cholestatrien-3-one was obtained from cholesterol and 2,3-dichloro-5,6-dicyano-1,4-benzoquinone in dioxane. 1,4,6-cholestatrien-3-one was reacted with 30% H(2)O(2) and 5% NaOH in methanol to give 1alpha,2alpha-epoxy-4,6-cholestadien-3-one, which was stereoselectively reduced with NaBH(4) to form 1alpha,2alpha-epoxy-4,6-cholestadien-3beta-ol and reduced with Li metal in absolute ethanol to give 2-ethoxy-1,4,6-cholestatrien-3-one. And 1,4,6-cholestatrien-3-one was epoxidized with m-CPBA in dichloromethane to afford 6alpha,7alpha-epoxy-1,4-cholestadien-3-one, which was reacted with NaBH(4) to synthesize 6alpha-hydroxy-4-cholesten-3-one and reduced Li metal in absolute ethanol to form 2-ethoxy-1,4,6-cholestatrien-3-one, respectively. 1,4,6-cholestatrien-3-one was reduced with NaBH(4) in absolute ethanol to form 4,6-cholestadien-3beta-ol, which was reacted with 30% H(2)O(2) to leave original compound, but was reacted with m-CPBA to give 4beta,5beta-epoxy-6-cholesten-3beta-ol as the major product and 4beta,5beta-epoxy-6alpha,7alpha-epoxycholestan-3beta-ol as the minor product. |
| Equally potent inhibitors of cholesterol synthesis in human hepatocytes have distinguishable effects on different cytochrome P450 enzymes Cohen, L. H., R. E. van Leeuwen, et al. (2000), Biopharm Drug Dispos 21(9): 353-64. Abstract: Six 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (the present cholesterol-lowering drugs known as statins), lovastatin (L), simvastatin (S), pravastatin (P), fluvastatin (F), atorvastatin (A) and cerivastatin (C) are shown to be potent inhibitors of cholesterol synthesis in human hepatocytes, the target tissue for these drugs in man. All six inhibited in the nM range (IC(50) values: 0.2-8.0 nM). As daily used cholesterol-lowering drugs they are likely coadministered with other drugs. While several cytochrome P450 (CYP) enzymes are involved in drug metabolism in the liver and thus play an important role in drug-drug interaction it was investigated which of these enzymes are influenced by the active forms of the six statins. These enzyme activities were studied in human liver microsomal preparations, and in simian and human hepatocytes in primary culture. The following CYP reactions were used: nifedipine aromatization (CYP3A4), testosterone 6beta-hydroxylation (CYP3A4), tolbutamide methylhydroxylation (CYP2C9), S-mephenytoin 4-hydroxylation (CYP2C19), bufuralol 1'-hydroxylation (CYP2D6), aniline 4-hydroxylation (CYP2E1), coumarin 7-hydroxylation (CYP2A6) and 7-ethoxyresorufin O-dealkylation (CYP1A1/2). In the human liver microsomes the statins (concentrations up to 400 microM) did not influence the CYP1A1/2 activity and hardly the CYP2A6 and CYP2E1 activities. Except P, the other five statins were stronger inhibitors of the CYP2C19 activity with IC(50) values around 200 microM and the same holds for the effect of A, C and F on the CYP2D6 activity. L and S were weaker inhibitors of the latter enzyme activity, whereas P did not influence both activities. About the same was observed for the statin effect on CYP2C9 activity, except that F was a strong inhibitor of this activity (IC(50) value: 4 microM). Using the assay of testosterone 6beta-hydroxylation the CYP3A4 activity was decreased by L, S and F with IC(50) values of about 200 microM and a little more by C and A (IC(50) around 100 microM). P had hardly an effect on this activity. To a somewhat less extent the same trend was seen when CYP3A4 activity was measured using nifedipine as substrate. The inhibitory effects observed in microsomes were verified in suspension culture of freshly isolated hepatocytes from Cynomolgus monkey (as a readily available model) and of human hepatocytes. In general the same trends were seen as in the human microsomes, except that in some cases the inhibition of the CYP activity was less, possibly by the induction of the particular CYP enzyme by incubation of the cells with a particular statin. F remained a strong inhibitor of CYP2C9 activity in human and monkey hepatocytes. A induced the CYP2C9 in monkey hepatocytes but was an inhibitor of the CYP2C9 in human hepatocytes. A, S, L and C were moderate inhibitors in both cellular systems of CYP3A4. P was not affecting any of the CYP activities in the three systems studied. It is concluded that different CYP enzymes interact with different statins and therefore differences in between these drugs are to be expected when drug-drug interaction is considered. |
| Eritadenine-induced alterations of plasma lipoprotein lipid concentrations and phosphatidylcholine molecular species profile in rats fed cholesterol-free and cholesterol-enriched diets Shimada, Y., T. Morita, et al. (2003), Biosci Biotechnol Biochem 67(5): 996-1006. Abstract: The effects of dietary eritadenine on the concentration of plasma lipoprotein lipids and the molecular species profile of plasma lipoprotein phosphatidylcholine (PC) were investigated in rats fed cholesterol-free and cholesterol-enriched diets to obtain insights into the relationship between the changes in PC molecular species profile and the hypocholesterolemic action of eritadenine. The effect of eritadenine on the secretion rate of very low density lipoprotein (VLDL) from the liver was also estimated. Rats were fed the control or eritadenine-supplemented (50 mg/kg) diets with or without exogenous cholesterol for 14 d. Eritadenine supplementation significantly decreased the cholesterol of major plasma lipoproteins, high density lipoprotein and VLDL, in rats fed cholesterol-free and cholesterol-enriched diets, respectively. The ratio of PC to phosphatidylethanolamine, delta6-desaturase activity, and the ratio of arachidonic acid to linoleic acid in liver microsomes were markedly decreased by eritadenine irrespective of the presence or absence of exogenous cholesterol. Dietary eritadenine increased the proportion of 16:0-18:2 molecular species with a decrease in 18:0-20:4 in plasma lipoprotein PC in both rats fed cholesterol-free and cholesterol-enriched diets. Eritadenine did not depress the secretion rate of VLDL in rats fed a cholesterol-free diet containing a high level of choline. The results indicate that dietary eritadenine elicits its hypocholesterolemic action with modulations of the fatty acid and molecular species profiles of PC irrespective of the presence or absence of exogenous cholesterol. The eritadenine-induced alteration of PC molecular species profile is discussed in relation to the hypocholesterolemic action of eritadenine. |
| ERP spectral analysis of cholesterol rich patients Agar, A., P. Yargicoglu, et al. (1995), Int J Neurosci 83(1-2): 93-101. Abstract: Visual event-related potentials (ERPs) were studied in twenty hypercholesterolemic (HC) patients and twenty age-matched healthy controls. ERPs were recorded in two different experimental conditions that the target stimulus (red light) was counted (Test 1) or uncounted (Test 2). Amplitude spectra of ERPs were computed by transient response-frequency characteristics (TRFC) method. Their maxima were found to occupy the frequency bands of 1-2, 3-4, 5-7, 8-12, 13-20, 20.5-32 Hz. The amplitude mean (decibel) of 1-2 and 3-4 frequency bands were decreased in Test 2 compared to Test 1 in the control group, but no significant amplitude differences were found between Test 1 and Test 2 in the HC group. |
| Erythrocyte and plasma cholesterol ester long-chain polyunsaturated fatty acids of low-birth-weight babies fed preterm formula with and without ribonucleotides: comparison with human milk Woltil, H. A., C. M. van Beusekom, et al. (1995), Am J Clin Nutr 62(5): 943-9. Abstract: We investigated whether a regular formula for premature infants (pre) supplemented with ribonucleotides (pre+RN) raises erythrocyte and plasma cholesterol ester (CE) long-chain polyunsaturated fatty acids (LCPUFAs) of low-birth-weight babies (< or = 2.50 kg) compared with their breast-fed counterparts. From days 11 to 42, 31 babies received the pre formula and 37 received pre+RN. Eleven breast-fed babies served as a reference group. Erythrocytes and CE fatty acids were determined on days 11, 21, and 42. There were no differences in the courses of erythrocytes and CE fatty acids between pre formula-fed and pre+RN-fed babies. On day 42, formula-fed babies had lower erythrocytes and CE n-3 and n-6 LCPUFAs compared with breast-fed babies. Subdivision into gestational age- and body weight-matched subgroups gave similar results. RN supplementation does not augment the erythrocyte and CE LCPUFA status of formula-fed babies. |
| Erythrocyte cholesterol content in polycythemia vera: relation to ischemic heart disease Torkhovskaia, T. I., E. M. Khalilov, et al. (2003), Kardiologiia 43(9): 49-51. Abstract: Relative cholesterol content and its distribution between erythrocytes and plasma were studied in 34 patients with polycythemia vera (PV) both with and without concomitant coronary heart disease (CHD). Deformability of erythrocytes, disturbances of microcirculation (blood flow fragmentation, decrease of capillary density) were also assessed. Erythrocytes cholesterol/phospholipids molar ratios (0.68+/-0.03) in patients was lower than normal value (0.8) in spite of decreased cell deformability. This was associated with some increase of peroxidation products. Blood cholesterol distribution between cell and plasma species had some peculiarities caused by high hematocrit: compared with normal value erythrocytes of patients carried relatively larger portion of total blood cholesterol (23.7+/-0.8% and 27-31%, respectively). However in CHD patients these values were significantly lower with correspondent increase of plasma cholesterol quota. This allowed to suggest possible protective role of blood cholesterol redistribution in polycythemia patients, through erythrocytes trafficking of some part of plasma cholesterol. |
| Erythrocyte membrane cholesterol distribution in patients with untreated essential hypertension: correlation with sodium-lithium countertransport Muriana, F. J., J. Villar, et al. (1996), J Hypertens 14(4): 443-6. Abstract: OBJECTIVE: To determine whether the membrane cholesterol distribution is associated with the increased activity of sodium-lithium countertransport in the erythrocytes of normocholesterolaemic and hypercholesterolaemic patients with untreated essential hypertension. METHODS: Erythrocytes were prepared from venous blood samples obtained from normotensive subjects and hypertensive (normocholesterolaemic and hypercholesterolaemic) patients. The membrane cholesterol distribution between the inner and outer monolayers was measured by means of cholesterol oxidation to cholestenone after continuous cholesterol oxidase treatment. The sodiumlithium countertransport activity was determined by measurements of external sodium (150 mmol/l)-stimulated lithium efflux. The statistical analysis was conducted by analysis of variance with Tukey's correction and correlations were performed by linear regression analysis using Pearson's correlation coefficient. RESULTS: The half-times for cholesterol oxidation were significantly higher in patients with untreated essential hypertension, either with (25.4 +/- 5.6 min) or without (21.7 +/- 2.9 min) concomitant hypercholesterolaemia, than in the controls (15.3 +/- 2.8 min). Sodium-lithium counter-transport activities were also higher in the hypertensive patients (0.410 +/- 0.094 and 0.304 +/- 0.037 mmol/h per litre cell for the hypercholesterolaemic and normocholesterolaemic groups, respectively) than in the controls (0.262 +/- 0.081 mmol/h per litre cell). In single-regression analysis, the half-time for membrane cholesterol oxidation was positively correlated to the erythrocyte cation flux mediated by the sodium-lithium countertransport. CONCLUSION: It is hypothesized that the sodium-lithium countertransport activity might be influenced by membrane structural cholesterol domains. |
| Erythrocyte membrane cholesterol/phospholipid changes and hemorheological modifications in familial hypercholesterolemia treated with lovastatin Martinez, M., A. Vaya, et al. (1996), Thromb Res 83(5): 375-88. Abstract: Fourteen patients with familial hypercholesterolemia treated with lovastatin (40 mg/day) for three months were studied to find out whether the expected changes in plasma lipids are accompanied by modifications in the lipid composition of the erythrocyte membrane and whether these in turn induce changes in the rheological behavior of the red blood cell. Our results demonstrate the efficacy of lovastatin in reducing the plasma concentration of cholesterol and LDL cholesterol. The changes observed in the plasma lipids correlate with a significant decrease in the cholesterol/phospholipid ratio of the red blood cell membrane, from 1.19 +/- 0.19 in a basal situation to 0.92 +/- 0.23 (p < 0.01) at the end of treatment. These changes in the lipid composition of the cell are statistically related to a decrease in erythrocyte aggregability and an improvement in blood filterability, which means beneficial change in the patients' hemorheological situation. |
| Erythrocyte plasma membrane perturbations in rats fed a cholesterol-rich diet: effect of drinking sulphurous mineral water Nasuti, C., R. Gabbianelli, et al. (2005), Ann Nutr Metab 49(1): 9-15. Abstract: AIMS: The purpose of the present study was to evaluate the ability of calcic and magnesic-sulphate-sulphurous spring mineral water (SMW) to reduce total and erythrocyte plasma membrane cholesterol in rats fed a cholesterol-rich diet. METHODS: By using different fluorescent probes, 1,6-diphenyl-1,3,5-hexatriene (DPH), 1-4-(trimethylamino)phenyl-6-phenylhexa-1,3,5-triene (TMA-DPH) and Laurdan, a possible correlation was evaluated between cholesterol content changes of the membranes and membrane fluidity. RESULTS: The results clearly show that hydropinic treatment reduced cholesterol level. No significant change was observed in DPH and TMA-DPH anisotropy values. By using Laurdan, an increase was observed in generalized polarization (GP(340)) in both groups of rats (the one that drank tap water and the one that drank SMW) compared with the controls. The rate of haemolysis was reduced in those erythrocyte suspensions in which cholesterol was increased, even if the enzymatic activity of glutathione peroxidase and catalase decreased. CONCLUSION: Hydropinic treatment with SMW is of interest from the biomedical point of view, because it could represent an alternative approach in interventions aimed at ameliorating biological injury deriving from hypercholesterolaemia. |
| Escape phenomenon of low-density lipoprotein cholesterol during lovastatin treatment Rubinstein, A. and M. Weintraub (1995), Am J Cardiol 76(3): 184-6. Abstract: The main issue is whether briefly stopping treatment of the hypercholesterolemic patient will accelerate the atherosclerotic process. This is possible, but such a strategy is preferable only in a subgroup of patients who cannot bear the economic burden of increasing the dosage of statins. In addition, stopping and restarting the drug at different stages lessens the likelihood of more adverse effects occurring when the dosage is increased. |
| ESR as a valuable tool for the investigation of the dynamics of EPC and EPC/cholesterol liposomes containing a carboranyl-nucleoside intended for BNCT Rossi, S., R. F. Schinazi, et al. (2005), Biochim Biophys Acta 1712(1): 81-91. Abstract: Electron Spin Resonance (ESR) spectroscopy of long-chain nitroxides (5-, 7-, and 16-doxyl stearic acid) has been used to evaluate the perturbations induced by beta-5-o-carboranyl-2'-deoxyuridine (CDU) on the structure and dynamics of egg phosphatidylcholine (EPC) and EPC/cholesterol liposomes. Loaded liposomes are intended for the use in Boron Neutron Capture Therapy (BNCT). From a detailed analysis of the motional and order parameters determining the ESR line shape as a function of temperature and of CDU content in liposomes, an increased order and a hindered motion of the phospholipid membranes resulted in the presence of increasing CDU concentration. This occurred particularly at the liposome surface level. Both higher ordering and increased rigidity of the membrane lipids were the result of the constraints exerted by the embedded carboranyl-nucleoside. |
| ESR studies on the effect of cholesterol on chlorpromazine interaction with saturated and unsaturated liposome membranes Wisniewska, A. and A. Wolnicka-Glubisz (2004), Biophys Chem 111(1): 43-52. Abstract: In this study, the effects of chlorpromazine (CPZ) on lipid order and motion in saturated (DMPC, DMPG) and unsaturated (SOPC) liposome membranes were investigated by electron spin resonance (ESR) spin labeling technique. We have shown that above the main phase transition temperature of membrane lipids (T(M)), CPZ slightly increases lipid order in membranes without cholesterol, whereas below T(M) it has a strong opposite effect. Addition of 30 mol% of cholesterol into DMPC and SOPC membranes changes significantly the CPZ effects both above and below T(M). Additionally, above T(M), the ordering effect of CPZ on pure SOPC membrane is stronger at pH 7.4 than at pH 9.0, whereas below T(M), as well as in the presence of cholesterol, pH does not seem to play a role in CPZ effect on both membranes. Because of the strong influence of membrane composition on CPZ effect on membranes, the use of cholesterol as a marker of CPZ photosensitized reactions has been discussed. |
| Essential fatty acid preparation reduces cholesterol and fatty acids in rat cortex Yehuda, S., Y. Brandys, et al. (1996), Int J Neurosci 86(3-4): 249-56. Abstract: Previous studies have shown that chronic administration of SR-3 (a 1:4 mixture of alpha-linolenic and linoleic acid) affects spatial learning, thermoregulation, pain threshold, and protection from seizures. The mode of action of SR-3 is unknown. One possible explanation is that SR-3 induces changes in the FA profile and in the cholesterol level in neuronal membranes. This study used 10 independent groups of rats (ni = 12) given 4 weeks of either saline, mineral oil (vehicle), alpha-tocopherol (antioxidant), alpha-linolenic acid, linoleic acid, or one of 5 different ratios of alpha-linolenic acid:linoleic acid (1:3, 1:4, 1:5, 1:6, 1:7) as free fatty acids. FA profile and cholesterol level were examined by GC method in synaptosomes obtained from the frontal cortex of the rats. The mineral oil treated group served as the control group. No difference was found in the FA profile or cholesterol level except for the SR-3 treated group. The ratio of 1:4 was found to have a significant influence on decreasing the cholesterol level and in inducing major changes in the FA profile, such as an increase in EFA. These effects of SR-3 may result in modification of the membrane fluidity, which may, in turn, enhance cognitive and neuropharmacological effects. |
| Essential fatty acids, plasma cholesterol, and fat-soluble vitamins in subjects with age-related maculopathy and matched control subjects Sanders, T. A., A. P. Haines, et al. (1993), Am J Clin Nutr 57(3): 428-33. Abstract: A matched-control study of plasma retinol, alpha-tocopherol, carotenoid, and cholesterol concentrations and the polyunsaturated fatty acid content of plasma and erythrocyte phospholipids was undertaken in 65 elderly patients with age-related maculopathy and 65 control subjects matched for age and sex. Despite the high statistical power of the study and large variations between subjects in the variables under consideration, no significant differences were noted between patients and control subjects. However, several statistically significant differences were noted between male and female subjects independent of their classification with maculopathy or as controls and age: plasma cholesterol, total phospholipids, alpha-tocopherol, and beta-cryptoxanthin concentrations were higher in females than in males. The mean plasma cholesterol concentration for the upper tertile of the whole sample was 7.6 mmol/L. Plasma concentrations of total carotenoids, alpha-carotene, and beta-carotene, but not alpha-tocopherol, were significantly lower in smokers than in non-smokers. The results of this study do not provide any evidence in favor of changing the dietary intake of polyunsaturated fatty acids or fat-soluble vitamins to protect against age-related maculopathy. |
| Essential role for cholesterol in entry of mycobacteria into macrophages Gatfield, J. and J. Pieters (2000), Science 288(5471): 1647-50. Abstract: Mycobacteria are intracellular pathogens that can invade and survive within host macrophages, thereby creating a major health problem worldwide. The molecular mechanisms involved in mycobacterial entry are still poorly characterized. Here we report that cholesterol is essential for uptake of mycobacteria by macrophages. Cholesterol accumulated at the site of mycobacterial entry, and depleting plasma membrane cholesterol specifically inhibited mycobacterial uptake. Cholesterol also mediated the phagosomal association of TACO, a coat protein that prevents degradation of mycobacteria in lysosomes. Thus, by entering host cells at cholesterol-rich domains of the plasma membrane, mycobacteria may ensure their subsequent intracellular survival in TACO-coated phagosomes. |