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PubMed1995

Effects of an azasterol inhibitor of sterol 24-transmethylation on sterol biosynthesis and growth of Leishmania donovani promastigotes.

Leishmania donovani promastigotes were cultured in the presence of an azasterol (20-piperidin-2-yl-5 alpha-pregnane-3 beta,20-diol) to determine the effects on sterol biosynthesis and cell proliferation. Inhibition of growth increased gradually with azasterol concentrations up to 5 micrograms/ml; concentrations of azasterol exceeding 5 micrograms/ml were lethal. Sterol biosynthesis was affected by the azasterol when administered at concentrations as low as 100 pg/ml. The primary site of action was the alkylation at C-24 of a delta 24-sterol precursor. The 24-alkylated sterols [ergosta-5,7,24(24(1))-trien-3 beta-ol and ergosta-5,7,22-trien-3 beta-ol] of the protozoan were replaced by delta 24-cholesta-type sterols which then accumulated in the cells. Administration of the azasterol together with a bis-triazole inhibitor of the 14 alpha-methylsterol 14-demethylase reaction, which operates in sterol biosynthesis, resulted in depletion of 24-alkylsterols and their replacement with predominantly 14 alpha-methylsterols lacking a 24-alkyl group. Continuous subculture of promastigotes in the presence of the azasterol resulted in gradual depletion of 24-alkylsterols and their complete replacement by delta 24-cholesta-type sterols. Transfer of the azasterol-treated cells to medium lacking azasterol resulted in a gradual restoration, after several subcultures, of the normal 24-alkylsterol pattern. The results indicate that, although 24-alkylsterols are normally produced by the protozoan, it can nevertheless survive with sterols possessing only the cholestane skeleton. Thus there is no absolute requirement for 24-alkylsterols to fulfil some essential 'sparking' role associated with cell growth in promastigotes.

Animals↗
PubMedDate not supplied

Evidence for the presence of "metabolic sterols" in Pneumocystis: identification and initial characterization of Pneumocystis carinii sterols.

Mixed life cycle stages of rat-derived Pneumocystis carinii were isolated from host lungs and their sterols were compared with those present in lungs from normal and immunosuppressed uninfected rats. Gas-liquid chromatography consistently detected, resolved, and quantified 9, 10, and 20 sterol components in the total nonsaponifiable neutral lipid fraction of lungs from normal rats, lungs from immunosuppressed uninfected rats, and P. carinii preparations, respectively. In all samples, cholesterol was the most abundant sterol present, comprising 97%, 93%, and 78% of total sterols in lungs from normal rats, lungs from immunosuppressed uninfected rats, and P. carinii, respectively. Tentative identifications of several rat lung and P. carinii minor sterols were made based on gas-liquid chromatogram retention times and fragmentation patterns from mass spectral analyses. Campesterol (ergost-5-en-3-ol), cholest-5-en-3-one, and beta-sitosterol (stigmast-5-en-3-ol) were among the minor components present in both types of lung controls, and were also components of P. carinii sterols. In contrast to lung controls, the sterols of P. carinii were enriched in C28 and C29 sterols with one or two double bonds, and a hydroxyl group at C-3 (ergost-5-en-3-ol, ergost-7-en-3-ol, ergosta-dien-3-ol, stigmast-5-en-3-ol, stigmast-7-en-3-ol and stigmasta-dien-3-ol). Steryl esters of P. carinii, probably stored in cytoplasmic lipid droplets, were dominated by those present in the host lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Long-term effects of sterol depletion in C. elegans: sterol content of synchronized wild-type and mutant populations.

Three major long-term effects of sterol deprivation in Caenorhabditis elegans are described. 1) The life expectancy of sterol-deprived wild-type animals is decreased by more than 40%. Similar decreases are found in animals carrying mutations in the daf-9, daf-12, daf-16, and clk-1 genes, suggesting that previously described aging pathways involving these genes are not involved in the life-extending effects of sterols. 2) There is a premature loss of motility, measured by response to mild touch. 3) There is a rapid postreproductive onset of sarcopenia (muscle wasting) as measured by total body fluorescence in a myo3::GFP-expressing strain. We also report that five sterols (the desmethylsterols cholesterol, 7-dehydrocholesterol, and lathosterol and the 4alpha-methyl sterols lophenol and 4alpha-methyl-cholesta-Delta8(14)-en-3beta-ol) are found in significant amounts at all stages of development and aging in cholesterol-fed animals. Supplying any one of these as the sole sterol confers similar protection from the long-term effects of sterol deprivation. These findings suggest that sterols are required continuously throughout the animal's life.

Aging↗
PubMed1989

Inhibitors of sterol synthesis. Chromatography of acetate derivatives of oxygenated sterols.

The separation of the acetate derivatives of a number of oxygenated sterols was achieved by medium pressure liquid chromatography on silica gel columns and by normal and reversed phase high performance liquid chromatography. We have explored the application of these chromatographic systems for the analysis of oxygenated sterols of plasma samples from two normal human subjects. The addition of highly purified [14C]cholesterol to plasma permitted the detection and quantitation of oxygenated sterols formed by autoxidation of cholesterol during processing of the samples. Special attempts to suppress autoxidation of cholesterol included the use of an all-glass closed system for saponification and extraction under argon followed by rapid removal of cholesterol from the polar sterols by reversed phase medium pressure liquid chromatography. Chromatographic analyses of the [3H]acetate derivatives of the polar sterols provided a sensitive approach for the detection and quantitation of the individual oxygenated sterols. Oxygenated sterols detected in plasma included cholest-5-ene-3 beta,26-diol, (24S)-cholest-5-ene-3 beta,24-diol, and cholest-5-ene-3 beta,7 alpha-diol. After correction for their formation by autoxidation of cholesterol during processing of the samples, very little or none of the following sterols were observed: cholest-5-ene-3 beta,7 beta-diol, 5 alpha,6 alpha-epoxy-cholestan-3 beta-ol, 5 beta,6 beta-epoxy-cholestan-3 beta-ol, and cholestane- 3 beta, 5 alpha,6 beta-triol, and the 25-hydroxy, 22R-hydroxy, 21-hydroxy, 20 alpha-hydroxy, and 19-hydroxy derivatives of cholesterol.

Acetic Anhydrides↗
PubMed1985

Rates of amphotericin B and filipin association with sterols. A study of changes in sterol structure and phospholipid composition of vesicles.

The influence of structural modifications in sterols and phospholipids on the rate of polyene antibiotic-sterol interaction was studied. For filipin and amphotericin B association with sterols in vesicles, a preferential interaction was found with sterols whose side chain length is close to that of cholesterol. Introduction of trans double bonds into the sterol side chain did not alter the rate of interaction in vesicles. The delta 7-bond of the sterol appears to be of critical importance in amphotericin B-sterol interaction, whereas the delta 5-bond is not essential. These observations are relevant to the well-known effects of amphotericin B on cell membranes containing ergosterol compared with those containing cholesterol. The dependence of the rates of sterol-polyene antibiotic interaction on the phospholipid composition of the vesicles indicates that phospholipid vesicles may be an inadequate model for reaching a comprehensive understanding of the effects exerted on biological membranes by these agents.

Amphotericin B↗
PubMed1979

Selective effects of membrane sterol depletion on surface function thymidine and 3-O-methyl-D-glucose transport in a sterol auxotroph.

Using a sterol-specific auxotroph of LM cells (mouse fibroblasts), we obtained cells with progressively lower sterol contents. 3-O-Methylglucose and thymidine were shown to enter the cells by saturable as well as by nonsaturable processes and it was possible to measure these processes separately at various stages of sterol depletion. Sterol depletion inhibited the saturable as well as the nonsaturable components for both 3-O-methylglucose and thymidine uptake. The extent of inhibition of the saturable process was much more than that of the nonsaturable component at any stage of the sterol depletion. Furthermore, in the course of progressive sterol depletion the saturable component of 3-O-methylglucose or thymidine uptake was inhibited well before the nonsaturable process. Sterol depletion produced reductions in the Vmax values but no change in the Km values for the saturable uptake of these two substrates. The depletion of cellular sterol to 75% resulted in 70% and 90% reduction of the saturable uptake of 3-O-methylglucose and thymidine, respectively, and 30% and 50% reduction of the nonsaturable uptake of 3-O-methylglucose and thymidine, respectively. DNA and protein synthesis, however, were not affected at all when the saturable component of thymidine uptake was inhibited by 50% demonstrating that the observed decrease of transport activity was selective and not a reflection of a gross alteration in cellular physiology.

Biological Transport, Active↗
PubMed1994

Inhibitors of sterol synthesis. Submicromolar 14 alpha-ethyl-5 alpha-cholest-7-ene-3 beta, 15 alpha-diol causes a major modification of the sterol composition of CHO-K1 cells and a marked change in cell morphology.

Incubation of Chinese hamster ovary cells (CHO-K1) with 14 alpha-ethyl-5 alpha-cholest-7-ene-3 beta,15 alpha-diol (0.1 microM) in lipid-deficient medium led to a major change in cellular sterol composition, which was characterized by a very marked accumulation of C30 sterols (lanosterol and 24,25-dihydrolanosterol). The accumulation of C30 sterols was associated with a striking change in cell morphology. The change in cell shape (elongation) was similar to that described previously (A. W. Hsie and T. T. Puck, 1971. Proc. Natl. Acad. Sci. USA. 68: 358-361; and confirmed herein) for CHO-K1 cells incubated in the presence of dibutyryl cAMP (1 mM). This change in morphology, induced by dibutyryl cAMP, was not accompanied by a change in cellular sterol composition. The cell elongation and accumulation of C30 sterols, induced by the 14 alpha-ethyl diol, were prevented by the addition of cholesterol (10 microM or 100 microM) and were reversed by removal of the 14 alpha-ethyl diol from the incubation medium. Incubation of the cells with the 14 alpha-ethyl diol had no effect on the levels of cAMP under the conditions studied. Incubation of the cells with miconazole (10 microM) or with lanosterol (10 microM) was also associated with the accumulation of C30 sterols and an elongation of the cells. 24,25-Dihydrolanosterol (10 microM) also induced similar changes in cellular morphology. The results presented herein demonstrate that marked changes in the sterol composition of CHO-K1 cells can be effected by incubation of the cells with 14 alpha-ethyl-5 alpha-cholest-7-ene-3 beta, 15 alpha-diol, miconazole, or lanosterol. In addition, the findings reported herein indicate an important role of sterols in the control of the shape of these cells.

Animals↗
PubMed2005

Effects of a diet high in plant sterols, vegetable proteins, and viscous fibers (dietary portfolio) on circulating sterol levels and red cell fragility in hypercholesterolemic subjects.

Plant sterols, soy proteins, viscous fibers, and nuts are advised for cholesterol reduction, but their combined effect on plant sterol absorption has never been tested. We assessed their combined action on serum sterols in hyperlipidemic subjects who were following low-saturated fat diets before starting the study and who returned to these diets post-test. The 1-mon test (combination) diet was high in plant sterols (1 g/1,000 kcal), soy protein (23 g/1,000 kcal), viscous fiber (9 g/1,000 kcal), and almonds (14 g/1000 kcal). Fasting blood was obtained for serum lipids and sterols, and erythrocytes were obtained for fragility prior to and at 2-wk intervals during the study. The combination diet raised serum campesterol concentrations by 50% and beta-sitosterol by 27%, although these changes were not significant after Bonferroni correction; near-maximal rises were found by the end of the first week, but no change was found in red cell fragility despite a 29% reduction in the LDL cholesterol level. No significant associations were observed between changes in red cell fragility and blood lipids or sterols. We conclude that plant sterols had a minimal impact on serum sterol concentrations or red cell fragility in hyperlipidemic subjects on diets that greatly reduced their serum lipids.

Adult↗
PubMed1995

Sterol carrier protein-2 stimulates intermembrane sterol transfer by direct membrane interaction.

It is unclear how the cytosolic sterol carrier protein-2 (SCP-2) binds sterols and enhances sterol transfer between membranes. Therefore, human recombinant SCP-2 was used in conjunction with phase fluorometry, dialysis, and chemical labeling techniques to show if a direct membrane effect accounted for this activity. SCP-2 directly interacted with L-cell fibroblast plasma membrane vesicles as determined by increased fluorescence anisotropy of coumarin-labeled protein (CPM-SCP-2). Furthermore, a new fluorescence lifetime component due to plasma membrane-bound CPM-SCP-2 was observed. Dialysis studies with 3H- cholesterol loaded plasma membranes indicated that SCP-2, added to the donor compartment, stimulated sterol transfer whether or not the dialysis membrane was permeable to SCP-2. Nevertheless, ligand-binding experiments indicated that chemically blocking the SCP-2 sterol binding site inhibited the ability of SCP-2 to enhance sterol transfer between plasma membrane vesicles. SCP-2 did not stimulate plasma membrane fusion. Addition of SCP-2 to plasma membranes increased the anisotropy plasma membrane proteins covalently reacted with CPM, but not that of lipids labeled with the fatty acid analogue octadecyl rhodamine B. In conclusion, the data are consistent with SCP-2 stimulating intermembrane sterol transfer by direct interaction with sterol in the membrane and enhancing its desorption from the membrane.

Animals↗
PubMed1994

Regulation of Sterol Content in Membranes by Subcellular Compartmentation of Steryl-Esters Accumulating in a Sterol-Overproducing Tobacco Mutant.

The study of sterol overproduction in tissues of LAB 1-4 mutant tobacco (Nicotiana tabacum L. cv Xanthi) (P. Maillot-Vernier, H. Schaller, P. Benveniste, G. Belliard [1989] Biochem Biophys Res Commun 165: 125-130) over several generations showed that the overproduction phenotype is stable in calli, with a 10-fold stimulation of sterol content when compared with wild-type calli. However, leaves of LAB 1-4 plants obtained after two steps of self-fertilization were characterized by a mere 3-fold stimulation, whereas calli obtained from these plants retained a typical sterol-overproducing mutant phenotype (i.e. a 10-fold increase of sterol content). These results suggest that the expression of the LAB 1-4 phenotype is dependent on the differentiation state of cells. Most of the sterols accumulating in the mutant tissues were present as steryl-esters, which were minor species in wild-type tissues. Subcellular fractionation showed that in both mutant and wild-type tissues, free sterols were associated mainly with microsomal membranes. In contrast, the bulk of steryl-esters present in mutant tissues was found in the soluble fraction of cells. Numerous lipid droplets were detected in the hyaloplasm of LAB 1-4 cells by cytochemical and cytological techniques. After isolation, these lipid granules were shown to contain steryl-esters. These results show that the overproduced sterols of mutant tissues accumulate as steryl-esters in hyaloplasmic bodies. The esterification process thus allows regulation of the amount of free sterols in membranes by subcellular compartmentation.

Journal Article↗
PubMed1998

Polyunsaturated fatty acids decrease expression of promoters with sterol regulatory elements by decreasing levels of mature sterol regulatory element-binding protein.

Membrane physiology, plasma lipid levels, and intracellular sterol homeostasis are regulated by both fatty acids and cholesterol. Sterols regulate gene expression of key enzymes of cholesterol and fatty acid metabolism through proteolysis of the sterol regulatory element-binding protein (SREBP), which binds to sterol regulatory elements (SRE) contained in promoters of these genes. We investigated the effect of fatty acids on SRE-dependent gene expression and SREBP. Consistent results were obtained in three different cell lines (HepG2, Chinese hamster ovary, and CV-1) transfected with SRE-containing promoters linked to the luciferase expression vector. We show that micromolar concentrations of oleate and other polyunsaturated fatty acids (C18:2-C22:6) dose-dependently (0.075-0.6 mmol) decreased transcription of SRE-regulated genes by 20-75%. Few or no effects were seen with saturated free fatty acids. Fatty acid effects on SRE-dependent gene expression were independent and additive to those of exogenous sterols. Oleate decreased levels of the mature sterol regulatory element-binding proteins SREBP-1 and -2 and HMG-CoA synthase mRNA. Oleate had no effect in sterol regulation defective Chinese hamster ovary cells or in cells transfected with mutant SRE-containing promoters. We hypothesize that unsaturated fatty acids increase intracellular regulatory pools of cholesterol and thus affect mature SREBP levels and expression of SRE-dependent genes.

Animals↗
PubMed1999

Regulation of the rat neutral cytosolic cholesteryl ester hydrolase promoter by hormones and sterols: a role for nuclear factor-Y in the sterol-mediated response.

Expression of the rat liver neutral cytosolic cholesteryl ester hydrolase (CEH) gene is regulated by glucocorticoids, thyroxine, and agents that perturb cholesterol metabolism. The present studies identify the putative hormone response elements in the CEH promoter. They also define the roles of two previously identified sterol regulatory elements (SRE-92 and SRE-160) and a putative nuclear factor-Y (NF-Y) binding site with a consensus ATTGG (inverted CCAAT) motif (Natarajan, R., S. Ghosh, and W. M. Grogan. 1998. Biochem. Biophys. Res. Commun. 243: 349;-355). CEH promoter-reporter gene constructs were transiently transfected into HepG2 cells to evaluate promoter activity. Results indicated that the CEH gene has two complex glucocorticoid response units in distal portions of the promoter corresponding to consensus glucocorticoid regulatory sequences as well as putative thyroid hormone response elements. CEH promoter-reporter constructs with the proximal 189 bp of the wild-type or mutated sequences were also transfected into HepG2 cells. Activity of the wild-type construct increased when incubated in sterol depleted media or when co-expressed with a mature sterol regulatory element binding protein (SREBP-2). These responses were suppressed by mutations in SRE-92, SRE-160, or NF-Y, indicating that these cis elements are sufficient for sterol-mediated regulation of the CEH promoter. Gel mobility shift assays further demonstrated that NF-Y binds to the inverted CCAAT box motif and is required for the sterol-mediated regulation. These results indicate that multiple cis-elements regulate transcription of the cholesteryl ester hydrolase (CEH) gene, consistent with the reported regulation of CEH expression.-Natarajan, R., S. Ghosh, and W. M. Grogan. Regulation of the rat neutral cytosolic cholesteryl ester hydrolase promoter by hormones and sterols: a role for nuclear factor-Y in the sterol-mediated response.

Animals↗
PubMed1988

Sterol composition of a delta 5,7-sterol-rich strain of Saccharomyces cerevisiae during batch growth.

Sterol composition was examined during batch growth on complex media containing ethanol, molasses or glucose as the carbon source. The molasses-grown cells exhibited a balanced sterol composition throughout growth, maintaining the proportion of ergosterol to 24:28-dehydroergosterol equal to 1.4. The negative effect of glucose on sterol synthesis manifested itself by decreasing the accumulation of 24:28-dehydroergosterol and total sterols but not of ergosterol. Using ethanol as the sole carbon source, a large amount of 24:28-dehydroergosterol accumulated, partly at the expense of other sterols. The gradual addition of nitrogen source during growth significantly decreased the accumulation of ergosterol, 24:28-dehydroergosterol and of total sterols. A general scheme of regulation of sterol synthesis in baker's yeast is presented.

Ammonia↗
PubMed1991

Effect of sterol side-chain structure on the feed-back control of sterol biosynthesis in yeast.

We measured the incorporation of radiolabeled methionine and acetate into the sterol component of G204, a Saccharomyces cerevisiae mutant strain which is partially heme competent. By comparing the amount of label incorporated into the sterol pool of a control culture, to which no exogenous sterol was added, with a culture which had various sterols added to the growth medium, we were able to determine the specific structural features of ergosterol which facilitate its ability to restrict the sterol biosynthetic pathway. These experiments demonstrate that sterols which contain both a C22 unsaturation and a C24 methyl group are capable of reducing sterol biosynthesis by approx. 50%, regardless of B-ring structure. We examined the regulatory properties of various oxysterols; 24,25-epoxylanosterol reduced endogenous biosynthesis by 49%, whereas all cholesterol derivatives tested, including 25-hydroxycholesterol, had little effect. A new procedure for the synthesis of ergosterol peroxides is also described.

Genes, Fungal↗
PubMed1975

Gas chromatographic differentiation of 4-desmethyl-, 4-monomethyl- and 4,4-dimethyl-sterols. Part III: differentiation of sterols based on deltaROxo-values on four stationary phases.

The deltaROxo-values, i.e., ratios of retention data for 3-oxo derivatives to those for the corresponding free sterols have been determined for fourteen 4-desmethylsterols, six 4-monomethylsterols and twenty-one 4,4-dimethylsterols on SE-30, OV-17, QF-1 and HiEFF-8B stationary phases. The QF-1 phase is found superior to the others in affording the values which are the most effective for differentiation between the three sterol groups. Within the same sterol group, the values for individual sterol members on any of the stationary phases differ to some extent due to minor variations in their skeletal structure. 4-Desmethyl-delta-5-sterols have strikingly large deltaROxo-values and are distinguishable definitely from other members of the 4-desmethylsterol group. The relative deltaROxo-values, i.e., ratios of deltaROxo-values of individual sterols to the deltaROxo-values of beta-sitosterol, also have been calculated from the deltaROxo-values of individual sterols.

Cholestanes↗
PubMed2001

Comparative behavior of sterols in phosphatidylcholine-sterol monolayer films.

The ability of sterols other than cholesterol (CHOL) to support membrane functions in membranes that normally contain CHOL as the primary, if not sole, sterol may be due, in part, to how well such sterols can mimic CHOL's behavior and physical properties in membranes. We compared the mixing properties of CHOL, 7-dehydrocholesterol (7DHC), and desmosterol (DES) in egg phosphatidylcholine-sterol monolayer films containing 10, 20, and 30 mol percent sterol, measuring pressure-area isotherms on a Langmuir-Blodgett trough with the aqueous, buffered subphase maintained at 37 degrees C. Under the conditions employed, the pressure-area isotherms for all three sterols were similar, with 7DHC exhibiting slightly larger molecular areas on the water surface at all compositions. These results are discussed in the context of the ability of sterols such as 7DHC and DES to substitute structurally and functionally for CHOL in biological membranes.

Animals↗
PubMed1985

High-performance liquid chromatography of sterols: yeast sterols.

It is evident that the high-pressure liquid chromatograph is an excellent tool for studying sterol metabolism. As noted in the text, the individual effects of unsaturations and alkyl groups on reverse phase elution volumes cannot be extrapolated to predict quantitative effects of multiple functional groups. The mechanism(s) of retention seems more complex than can be explained simply by polarity or hydrophobicity. Since the molecular location of these functional moieties seems critical, retention and separation of sterols may involve specific structural configurations and hence specific interactions with the stationary phase material. The association we have drawn between polarity and HPLC elution may indeed be a secondary effect of another phenomenon. Future studies may unveil the true mechanism(s) of HPLC retention and separation, and allow for the construction of HPLC systems which will separate all isomeric combinations of sterols at the analytical level. The simplicity, rapidity, and reproducibility of these methods make the coupled technique very useful for investigating sterol metabolism. Application of this technique to analyzing putative sterol mutants, purifying sterols for auxotrophic feeding, and analyzing the metabolism of supplemented sterols in auxotrophs provides for significant advances in membrane physiology.

Chromatography, High Pressure Liquid↗
PubMed1981

Effects of sterol structure and exogenous lipids on the transbilayer distribution of sterols in the membrane of Mycoplasma capricolum.

Stopped-flow kinetic measurements of the association of filipin with sterols in intact cells and isolated membranes of Mycoplasma capricolum were used to study the effects of varying the phospholipid in the membrane. The phospholipid composition and content of the membrane were varied by growing cells in an albumin-containing medium with cholesterol, palmitic and oleic acids, and various concentrations of exogenous phospholipids. The exogenous phospholipids (phosphatidylcholine, sphingomyelin, and phosphatidic acid) were incorporated up to levels of approximately 50% of the total membrane phospholipids but had no effect on the distribution of cholesterol between the two halves of the membrane bilayer. The sterol structure was varied by growing the cells with 10/micrograms/mL of either cholesterol, beta-cholestanol, 4,6-cholestadien-3 beta-ol, ergosterol, beta-sitosterol, or stigmasterol. With cholesterol, beta-cholestanol, and 4,6-cholestadien-3 beta-ol, approximately 65% of the sterol was found to be present in the outer half of the lipid bilayer. With ergosterol, beta-sitosterol, and stigmasterol, about 89% of the sterol is localized in the outer half of the membrane bilayer. Thus, the behavior of the alkyl-substituted sterols differs from that of cholesterol. The extent to which a sterol is distributed asymmetrically between the two halves of the bilayer is not related to the extent to which maximum growth is produced. These results suggest that growth-supporting sterols need not be translocated extensively.

Cell Membrane↗