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PubMed2005

The effect of PS content on the ability of natural membranes to fuse with positively charged liposomes and lipoplexes.

Supramolecular aggregates containing cationic lipids have been widely used as transfection mediators due to their ability to interact with negatively charged DNA molecules and biological membranes. First steps of the process leading to transfection are partly electrostatic, partly hydrophobic interactions of liposomes/lipoplexes with cell and/or endosomal membrane. Negatively charged compounds of biological membranes, namely glycolipids, glycoproteins and phosphatidylserine (PS), are responsible for such events as adsorption, hemifusion, fusion, poration and destabilization of natural membranes upon contact with cationic liposomes/lipoplexes. The present communication describes the dependence of interaction of cationic liposomes with natural and artificial membranes on the negative charge of the target membrane, charges which in most cases were generated by charging the PS content or its exposure. The model for the target membranes were liposomes of variable content of PS or PG (phosphatidylglycerol) and erythrocyte membranes in which the PS and other anionic compound content/exposure was modified in several ways. Membranes of increased anionic phospholipid content displayed increased fusion with DOTAP (1,2-dioleoyl-3-trimethylammoniumpropane) liposomes, while erythrocyte membranes partly depleted of glycocalix, its sialic acid, in particular, showed a decreased fusion ability. The role of the anionic component is also supported by the fact that erythrocyte membrane inside-out vesicles fused easily with cationic liposomes. The data obtained on erythrocyte ghosts of normal and disrupted asymmetry, in particular, those obtained in the presence of Ca(2+), indicate the role of lipid flip-flop movement catalyzed by scramblase. The ATP-depletion of erythrocytes also induced an increased sensitivity to hemoglobin leakage upon interactions with DOTAP liposomes. Calcein leakage from anionic liposomes incubated with DOTAP liposomes was also dependent on surface charge of the target membranes. In all experiments with the asymmetric membranes the fusion level markedly increased with an increase of temperature, which supports the role of membrane lipid mobility. The decrease in positive charge by binding of plasmid DNA and the increase in ionic strength decreased the ability of DOTAP liposomes/lipoplexes to fuse with erythrocyte ghosts. Lower pH promotes fusion between erythrocyte ghosts and DOTAP liposomes and lipoplexes. The obtained results indicate that electrostatic interactions together with increased mobility of membrane lipids and susceptibility to form structures of negative curvature play a major role in the fusion of DOTAP liposomes with natural and artificial membranes.

Animals↗
PubMed1985

Dynamic changes of the chicken erythrocyte membranes induced by N-methyl-N-aryl-N-nitrosoureas and their tumorigenicity.

The dynamic changes of chicken erythrocyte membranes induced by a series of N-methyl-N'-aryl-N-nitrosoureas (I X) were investigated in comparison with those of N-methyl-N-nitrosourea (MNU) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) by electron spin resonance spectroscopy. Both I X and MNNG increased the intensity of the less mobile lipid component (h1) during the incubation while MNU decreased it. The more mobile lipid component (h2), however, was not much influenced by these agents. A positive correlation was observed between the degree of the spectral alterations (h2/h1) caused by I-X compounds and their tumorigenic potency on mouse skin with the exception of the chloride derivative (I-C1). The present results suggest that the reactions of ultimate carcinogens with cell membranes may play an important role in the tumor promoting process.

Animals↗
PubMed2004

Tamoxifen does not prevent the mobilization of body lipids elicited by oleoyl-estrone.

Oleoyl-estrone is a powerful, slimming adipose tissue-derived signal that has biological effects widely opposed to those of its estrone moiety. The present experiment was designed to determine whether oleoyl-estrone effects on body energy are mediated by the estrogen receptor, blocked with the antagonist tamoxifen. Male Wistar rats were given daily oral doses of 10 micromol/kg d of oleoyl-estrone in oil containing 0 or 0.40 mg/kg d of tamoxifen. The data were compared with controls receiving only oil or 50 nmol/kg d of free estrone. After 10 days, the rats were killed, and their body composition and plasma metabolites and hormones were analyzed. Rats receiving estrone increased their body energy and lipid content compared with controls. Both groups of oleoyl-estrone-treated rats lost body weight, energy, and lipid; the losses in the rats receiving tamoxifen alone were less marked than in those receiving oleoyl-estrone. No significant changes in plasma glucose or triacylglycerols were observed. The patterns of change of estrone sulphate, estradiol, and oleoyl-estrone were consistent with a noticeable hydrolysis of oleoyl-estrone. The lack of differences in the fat mass in oleoyl-estrone-treated rats irrespective of the presence of tamoxifen suggested that the estrogenic pathway was not responsible for the slimming effects observed. Thus, it can be concluded that oleoyl-estrone effects are not mediated through its conversion to estrone or estradiol acting through the estrogen receptor. Tamoxifen partly mimicked the slimming effects of oleoyl-estrone; this could be speculatively explained by tamoxifen acting through the oleoyl-estrone signalling pathway.

Animals↗
PubMed1999

Antioxidant activity associated with lipid and phenolic mobilization during seed germination of Pangium edule Reinw.

Seeds of the tropical tree Pangium edule Reinw. are widely eaten in Southeast Asia after some treatment or processing. Fermented seeds are a specialty in Indonesia and have been used as spices. Because the tree is wild and has not been cultivated commercially, the physiology of germinated seeds of this tree for food uses is not known. This study reports some biochemical changes during seed germination associated with antioxidant activity and the mobilization of lipids and phenolics. Lipid content decreased, whereas the dominant fatty acids did not change significantly. The dominant fatty acids were oleic acid (C(18:1(n-9))) and linoleic acid (C(18:2(n-6))). During germination, oleic acid decreased while linoleic acid increased proportionally. The hypocotyl synthesized chlorophyll and the tocol composition also changed substantially. The antioxidant activity of phenolic extract increased in proportion to the total phenolics. Guaiacol peroxidase and glucose-6-phosphate dehydrogenase, selected enzymes association with phenolic metabolism, showed that the increased activities coincided with increased total phenolics and free proline.

Antioxidants↗
PubMed2000

Nongenomic effects of steroids on the nicotinic acetylcholine receptor.

A fast signaling mode of natural and synthetic steroids is exerted on some ion channels and cell-surface receptors. This activity contrasts with their classic mode of action, via intracellular receptors. Early studies from our laboratory demonstrated that spin-labeled androstanol and cholestane interact with the nicotinic acetylcholine receptor (AChR) and that lipid mobility at the lipid belt surrounding the AChR is reduced relative to that of the bulk membrane lipid. The occurrence of discrete and independent sites for phospholipids and sterols, both accessible to fatty acids, was subsequently disclosed in the native membrane. Synthetic and natural glucocorticoids were found to act as noncompetitive inhibitors of AChR function. The influence of different substituent groups in the cyclepentane perhydrophenanthrene ring on the channel-shortening potency of various steroids has also been assayed in muscle-type AChR, and we found a certain selectivity of this effect. Some organochlorine pesticides are xenoestrogens, that is, environmental agents capable of disrupting endocrine system signaling. We determined their effects on the AChR membrane using novel fluorescence techniques.

Animals↗
PubMed1995

Modification of fluid lipid and mobile protein fractions of reticulocyte plasma membranes affects agonist-stimulated adenylate cyclase. Application of the percolation theory.

The technique of fluorescence recovery after photobleaching was used to measure the lateral mobility of membrane integral proteins in reticulocyte plasma membranes which were treated to modify the 'fluid' lipid or immobilized protein fractions, hence increasing the relative prevalence of obstacles to protein lateral motion. This was achieved by either: (1) treating the plasma membranes with phospholipase A2 followed by extraction of the hydrolysis products using fatty-acid-free bovine serum albumin, resulting in a decrease in the membrane 'fluid' lipid portion; or (2) preincubating the plasma membranes with polylysines, resulting in plasma membrane protein aggregation and immobilization. As the prevalence of obstacles to lateral motion increased in plasma membranes through the treatments described above, the mobility of the membrane integral proteins diminished. Experimental results for the dependence of protein mobility on the prevalence of obstacles to lateral motion were compared to theoretical data in order to verify the applicability of the percolation theory to reticulocyte plasma membranes. The influence of a decrease in the 'fluid' lipid and an increase in the immobilized membrane protein fractions upon the hormone-stimulated adenylate cyclase activity has been studied as well. As the 'solid' lipid and immobilized membrane protein fractions decreased, both the hormone-stimulated adenylate cyclase activity and the fraction of beta-adrenergic receptors with high affinity to hormone diminished. It was shown that this correlation can be caused by a decrease in membrane fraction accessible to the movement of the interacting proteins of the adenylate cyclase complex. Hormonal stimulation of adenylate cyclase is discussed in terms of the percolation theory.

Adenylyl Cyclases↗
PubMedDate not supplied

Catabolic factors in cancer cachexia.

A lipid mobilizing factor has been purified from a cachexia-inducing mouse colon adenocarcinoma (MAC16) using a combination of ion exchange (Mono Q), exclusion (Superose) and reverse phase hydrophobic chromatography. The purification process led to a 3,500-fold increase in the specific activity. Serum from mice bearing the MAC16 tumour contained antibodies reactive with fractions containing lipid mobilizing activity and detectable as a 24 kDa immunoreactive band on Western blotting. Serum from mice transplanted with a related tumour, MAC13, not producing cachexia, did not contain antibodies. A similar immunoreactive band was detectable in the urine of patients with cancer cachexia, but was absent from the urine of normal subjects. A monoclonal antibody produced by fusion of splenocytes from mice bearing the MAC16 tumour with mouse Balb/c myeloma cells attenuated the development of cachexia in mice transplanted with the MAC16 tumour and inhibited tumour growth. These results suggest that the M(r) 24 kDa antigen may be important in tumour growth and cachexia.

Adenocarcinoma↗
PubMed1999

1H-MRS lipid signal modulation and morphological and ultrastructural changes related to tumor cell proliferation.

Changes in signal intensity of (1)H-MRS mobile lipids, mostly triglycerides, have been observed in cultured HeLa cells during exponential growth. Signals were intense in the first days after seeding and almost disappeared after a few days in culture. Choline-based metabolites were not affected by growth. Treatment with the antitumor drug lonidamine, which blocks cell proliferation and cell progression through cycle, increased lipid signal intensity. Morphological changes in the organization of the cell surface were detected by scanning electron microscopy during exponential growth, and were confirmed by freeze fracture analysis. The observed metabolic and structural modifications during cell growth were correlated to cell cycle progression of HeLa cells, as high-intensity lipid signals were typical of cells with a high percentage of S- and( )G(2) + M-phases, while cells with a high frequency in G(1)-phase were characterized by mobile lipid signals of very low intensity. Magn Reson Med 42:248-257, 1999.

Antineoplastic Agents↗
PubMed2002

Differential sensitivity of oleosins to proteolysis during oil body mobilization in sunflower seedlings.

Until now, there has been no conclusive demonstration of any in vivo oleosin degradation at the early stages of oil body mobilization. The present work on sunflower (Helianthus annuus L.) has demonstrated limited oleosin degradation during seed germination. Seedling cotyledon homogenization in Tris-urea buffer, followed by SDS-PAGE, revealed three oleosins (16, 17.5 and 20 kDa). Incubation of oil bodies with total soluble protein from 4-day-old seedlings resulted in oleosin degradation. In vitro and in vivo degradation of the 17.5-kDa oleosin was faster than the other two, indicating its greater susceptibility to proteolysis. Oleosin degradation by the total soluble protein resulted in a transient 14.5-kDa polypeptide, followed by an 11-kDa protease-protected fragment, which appeared post-germinatively and accumulated corresponding to increased rate of lipid mobilization. A 65-kDa protease, active at pH 7.5-9.5, was zymographically detected in the total soluble protein. Its activity increased along with in vivo accumulation of the protease-protected fragment during seed germination and accompanying lipid mobilization. Protease-treated oil bodies were more susceptible to maize lipase action. Differential proteolytic sensitivity of different oleosins in the oil body membranes could be a determinant of oil body longevity during seed germination.

Darkness↗
PubMed2006

Lipid lateral mobility and membrane phase structure modulation by protein binding.

Using a combination of fluorescence correlation and infrared absorption spectroscopies, we characterize lipid lateral diffusion and membrane phase structure as a function of protein binding to the membrane surface. In a supported membrane configuration, cholera toxin binding to the pentasaccharaide headgroup of membrane-incorporated GM1 lipid alters the long-range lateral diffusion of fluorescently labeled probe lipids, which are not involved in the binding interaction. This effect is prominently amplified near the gel-fluid transition temperature, Tm, of the majority lipid component. At temperatures near Tm, large changes in probe lipid diffusion are measured at average protein coverage densities as low as 0.02 area fraction. Spectral shifts of the methylene symmetric and asymmetric stretching modes in the lipid acyl chain confirm that protein binding alters the fraction of lipid in the gel phase.

Cholera Toxin↗
PubMed2004

Effect of zinc-alpha2-glycoprotein (ZAG) on expression of uncoupling proteins in skeletal muscle and adipose tissue.

The plasma protein zinc-alpha2-glycoprotein (ZAG) has been shown to be identical with a lipid mobilizing factor capable of inducing loss of adipose tissue in cancer cachexia through an increased lipid mobilization and utilization. The ability of ZAG to induce uncoupling protein (UCP) expression has been determined using in vitro models of adipose tissue and skeletal muscle. ZAG induced a concentration-dependent increase in the expression of UCP-1 in primary cultures of brown, but not white, adipose tissue, and this effect was attenuated by the beta3-adrenergic receptor (beta3-AR) antagonist SR59230A. A 6.5-fold increase in UCP-1 expression was found in brown adipose tissue after incubation with 0.58 microM ZAG. ZAG also increased UCP-2 expression 3.5-fold in C2C12 murine myotubes, and this effect was also attenuated by SR59230A and potentiated by isobutylmethylxanthine, suggesting a cyclic AMP-mediated process through interaction with a beta3-AR. ZAG also produced a dose-dependent increase in UCP-3 in murine myotubes with a 2.5-fold increase at 0.58 microM ZAG. This effect was not mediated through the beta3-AR, but instead appeared to require mitogen activated protein kinase. These results confirm the ability of ZAG to directly influence UCP expression, which may play an important role in lipid utilization during cancer cachexia.

Adipocytes↗
PubMed2002

Poisson-Boltzmann theory for membranes with mobile charged lipids and the pH-dependent interaction of a DNA molecule with a membrane.

We consider a planar stiff model membrane consisting of mobile surface groups whose state of charge depends on the pH and the ionic composition of the adjacent electrolyte solution. To calculate the mean-field interaction potential between a charged object and such a model membrane, one needs to solve a Poisson-Boltzmann boundary value problem. We here derive and discuss the boundary condition at the membrane surface, a condition that is generally appropriate for biological membranes where two charge-regulating mechanisms are present at the same time: the pH-dependent chemical charge regulation and a regulation through the in-plane mobility of the surface groups. As an application of this general formalism, we consider the specific example of a single DNA molecule, approximated by a cylinder with smeared-out surface charges, interacting with such a model membrane. We study the effect that the two competing charge-regulating mechanisms have on the DNA/membrane interaction and the distribution of surface ions in the plane of the membrane. We find that, at short DNA-membrane distances, membrane fluidity can have a considerable impact on the DNA adsorption behavior and can lead to such counterintuitive phenomena as the adsorption of a negatively charged DNA onto a (on average) negatively charged membrane.

DNA↗
PubMed1993

Visceral obesity: a "civilization syndrome".

The controversial question of the relationship between obesity and disease has been considerably clearer after the demonstration in several prospective, epidemiological studies that the subgroup of central, visceral obesity is particularly prone to develop cardiovascular disease, stroke, and non-insulin dependent diabetes mellitus. Visceral obesity is associated with multiple central endocrine aberrations. The hypothalamo-adrenal axis is apparently sensitive to stimuli, sex steroid hormone secretion blunted, and hyperandrogenicity is found in women. In addition, there seem to be signs of central dysfunctions in the regulation of hemodynamic factors after stress, and growth hormone secretion appears to be particularly blunted. Several of these endocrine abnormalities are associated with insulin resistance, particularly glycogen synthesis in muscle. Fiber composition with low type I/type II ratio might be secondary to the prevailing hyperinsulinemia, but low capillary density in muscle may well be of importance. In combination with elevated turn-over of free fatty acids (FFA) this will probably provide powerful mechanisms whereby insulin resistance is created. Portal FFA, from the highly lipolytic visceral depots may, in addition, affect hepatic metabolism to induce increased gluconeogenesis, production of very low density lipoproteins as well as to perhaps inhibit clearance of insulin. By these mechanisms a Metabolic Syndrome Visceral adipocytes seem to have a high density of several steroid hormone receptors, directing steroid hormone effects particularly to these depots. The net effect of cortisol is apparently a stimulation of lipid storage, with opposing effects of sex steroid hormones which also facilitate lipid mobilization, regulations most often found at the gene transcription level. Growth hormone inhibits cortisol effects on lipid accumulation, and amplifies the lipid mobilizing effects of steroid hormones. The combined perturbations of hormonal secretions will therefore probably direct triglycerides toward visceral depots. Circulatory and nervous regulatory mechanisms require, however, more attention. The multiple central endocrine and nervous aberrations of visceral obesity suggest neuroendocrine dysregulations, and have features characteristic of the hypothalamic arousal seen after certain types of stress, alcohol intake, and smoking. Such factors can be traced to subjects with visceral fat accumulation. Standardized stress, eliciting a "defeat reaction" in primates is followed by an apparently identical syndrome. This integrated picture of the multiple symptoms of visceral obesity is based on epidemiological, clinical, experimental, cellular, and molecular evidence. The ingredients of positive energy balance, including physical inactivity, stress, smoking, and alcohol consumption are frequent features of modern, urbanized society. Visceral obesity may therefore be an expression of a "Civilization Syndrome."

Adipose Tissue↗
PubMedDate not supplied

Intratumoral lipids in 1H MRS in vivo in brain tumors: experience of the Siemens cooperative clinical trial.

Fifteen institutions cooperated to examine the ability of 1H MRS to characterize metabolism in vivo in 102 primary brain tumors. Spectra were acquired from single 8 cc voxels in the tumor using a spin-echo method with an echo time of 135 ms. The most intense lipid signal was that of fatty acyl methylene protons at 1.3 ppm. Intratumoral lipid signals were not detected in oligodendrogliomas, ependymomas, or meningiomas and were evident in only 1 of 6 primitive neuroectodermal tumors. Among 75 astrocytic tumors, lipid signals occurred in 16% of low grade astrocytomas (AS), 36% of anaplastic astrocytomas (AA), and 44% of glioblastomas (GB). The amount of lipids, expressed as a ratio of the intensity of the methylene signal to that of choline, increased progressively with histopathological grade (p = 0.05). Greater amounts of mobile lipids in vivo in GB, which usually contain necrosis, is in accord with the recently discovered correlation between the fraction of microscopic necrosis and the intensity of the mobile lipid signal observed ex vivo using 1H MRS. The observation of lipid signals in AA, which do not contain necrosis, suggests that mobile fatty acids may appear at a stage of metabolic insult that precedes microscopic signs of cell death, and raises the possibility of an independent correlation between 1H MRS-detectable lipids and prognosis in patients with astrocytic tumors.

Astrocytoma↗
PubMed1996

The regulation of adipose tissue distribution in humans.

The regulation of adipose tissue distribution is an important problem in view of the close epidemiological and metabolic associations between centralized fat accumulation and disease. With visceral fat accumulation multiple endocrine perturbations are found, including elevated cortisol and androgens in women, as well as low growth hormone (GH) and, in men, testosterone (T) secretion. These abnormalities probably derive from a hypersensitive hypothalamo-pituitary-adrenal axis, with hyperinsulinemia related to a marked insulin resistance as a consequence. These hormonal changes exert profound effects on adipose tissue metabolism and distribution. At the adipocyte level cortisol and insulin promote lipid accumulation by expressing lipoprotein lipase activity, while T, GH and probably estrogens exert opposite effects. The consequences will most likely be more expressed in visceral than subcutaneous adipose tissues because of a higher cellularity, innervation and blood flow. Furthermore, the density of cortisol and androgen receptors seems to be higher in this than other adipose tissue regions. The endocrine perturbations found in visceral obesity with an abundance of the lipid accumulating hormones cortisol and insulin, and a relatively low secretion of the lipid mobilizing sex steroid hormones and GH would therefore be expected to be followed by visceral fat accumulation. The potential significance of local synthesis of steroid hormones in adipose tissue requires more attention. Although studies in vitro are informative when elucidating detailed mechanisms of hormonal interactions, they might not give a true picture of the regional integrated regulation of adipose tissue lipid storage and mobilization. Such information can be obtained by regional measurements of lipid mobilization by free fatty acid turnover or by microdialysis techniques, both showing lower rates of mobilization in leg than in upper body adipose tissues. More detailed information can be obtained by physiological oral administration of triglycerides, labelled with a small amount of oleic acid, followed by measurements of the regional uptake and turn-over of adipose tissue triglycerides. Such studies show lipid uptake in the order omental = retroperitoneal > subcutaneous abdominal > subcutaneous femoral adipose tissues in men, with a similar rank order for half-life of the triglyceride, indicating also a turn-over of triglycerides in that order. T amplifies these differences in men. In premenopausal women subcutaneous abdominal has a higher turnover than femoral adipose tissue. Results of studies in vitro indicate that this difference is diminished at the menopause, and restored by estrogen substitution, suggesting that the functional effects of estrogens in women are similar to those of T in men. The mechanisms are, however, probably indirect because of the apparent absence of specific estrogen and progesterone receptors in human adipose tissue. This interpretation from the studies referred to above fits well with physiological, and clinical conditions with increased visceral fat mass, where the balance between the lipid accumulating hormone couple (cortisol and insulin) and the hormones which prevent lipid accumulation and instead activate lipid mobilization pathways (sex steroid hormones and GH) is shifted to the advantage of the former. Such conditions include Cushing's syndrome, the polycystic ovary syndrome, menopause, aging, GH-deficiency, depression, smoking and excess alcohol intake. With appropriate interventions against hypercortisolemia and substitution of deficient sex steroids and GH, visceral fat mass is decreasing. Based on this evidence from physiological, clinical, interventional observations and detailed studies of mechanisms at cellular and molecular levels it is suggested that the combined endocrine abnormalities in the syndrome of visceral obesity direct storage fat to visceral adipose depots. Therefore, measurements of visceral fat accumulat

Adipose Tissue↗
PubMed2002

Membrane protein topology probed by (1)H spin diffusion from lipids using solid-state NMR spectroscopy.

We describe a two-dimensional solid-state NMR technique to investigate membrane protein topology under magic-angle spinning conditions. The experiment detects the rate of (1)H spin diffusion from the mobile lipids to the rigid protein. While spin diffusion within the rigid protein is fast, magnetization transfer in the mobile lipids is an inefficient and slow process. Qualitative analysis of (1)H spin-diffusion build-up curves from the lipid chain-end methyl groups to the protein allows the identification of membrane-embedded domains in the protein. Numerical simulations of spin-diffusion build-up curves yield the approximate insertion depth of protein segments in the membrane. The experiment is demonstrated on the selectively (13)C labeled colicin Ia channel domain, known to have a membrane-embedded domain, and on DNA/cationic lipid complexes where the DNA rods are bound to the membrane surface. The experiment is designed for X-nucleus detection, which could be (13)C or (15)N in the protein and (31)P for the DNA. Finally, we show that a qualitative distinction between membrane proteins with and without a membrane-embedded domain can be made even by using an unlabeled protein, by detection of lipid signals. This spin-diffusion experiment is simple to perform and requires no oriented bilayer preparations and only standard NMR hardware.

Carbon Isotopes↗
PubMed2002

Germination and storage reserve mobilization are regulated independently in Arabidopsis.

The phytohormone abscisic acid (ABA) inhibits the germination of many seeds, including Arabidopsis, but the mechanism for this is not known. In cereals, ABA inhibits the expression of genes involved in storage reserve mobilization. We have found that in Arabidopsis ABA decreases transcription from the promoters of marker genes for beta-oxidation and the glyoxylate cycle, essential pathways for the conversion of storage lipid (triacylglycerol) into sucrose. Thirty per cent of stored lipid is broken down over 6 days following imbibition of ABA-treated seed. Sucrose levels in ABA-treated seeds, rather than decreasing as under normal growth conditions, actually double during the 3 days following imbibition. This sucrose is derived from triacylglycerol as demonstrated by two mutants disrupted in the conversion of triacylglycerol into sucrose, kat2 and icl1, which do not accumulate sucrose in the presence of ABA. We conclude that the ABA block on germination is not a consequence of inhibition of storage lipid mobilization. Two independent programmes appear to operate, one that is blocked by ABA, governing developmental growth resulting in germination; and a second that governs storage lipid mobilization which is largely ABA-independent.

Abscisic Acid↗