Showing papers on "Membrane lipids published in 1989"
TL;DR: The degree of membrane lipid peroxidative damage in erythrocytes was significantly correlated with the level of glycosylated hemoglobin, an index of mean glucose level for the preceding 3–4mo, which suggests that peroxidation of membrane lipids and accumulation of MDA occurs in ERY Throcytes of diabetic patients.
Abstract: Erythrocytes of diabetic patients have abnormal membrane properties. We examined in vivo membrane lipid peroxidation in erythrocytes of diabetic subjects and its possible relationship with hyperglycemia. Lipid peroxidation was assessed in fresh, untreated erythrocytes by quantitating thiobarbituric acid reactivity and an adduct of phospholipids and malonyldialdehyde (MDA), an end product of lipid peroxidation, with thin-layer chromatography of lipid extract of diabetic erythrocytes. There was a significantly increased membrane lipid peroxidation in diabetic erythrocytes compared with nondiabetic erythrocytes. The degree of membrane lipid peroxidative damage in erythrocytes was significantly correlated with the level of glycosylated hemoglobin, an index of mean glucose level for the preceding 3-4 mo. This suggests that peroxidation of membrane lipids and accumulation of MDA occurs in erythrocytes of diabetic patients.
607 citations
09 May 1989
508 citations
TL;DR: These studies suggest that an essential role that cholesterol plays in mammalian cell biology is to enable crucial membrane enzymes to provide function necessary for cell survival.
Abstract: Recent studies of structure-function relationships in biological membranes have revealed fundamental concepts concerning the regulation of cellular membrane function by membrane lipids. Considerable progress has been made in understanding the roles played by two membrane lipids: cholesterol and phosphatidyl-ethanolamine. Cholesterol has been shown to regulate ion pumps, which in some cases show an absolute dependence on cholesterol for activity. These studies suggest that an essential role that cholesterol plays in mammalian cell biology is to enable crucial membrane enzymes to provide function necessary for cell survival. Studies of phosphatidylethanolamine regulation of membrane protein activity and regulation of membrane morphology led to hypotheses concerning the roles for this particular lipid in biological membranes. New information on lipid-protein interactions and on the nature of the lipid head groups has permitted the development of mechanistic hypotheses for the regulation of membrane protein activity by phosphatidyl-ethanolamine. In addition, intermediates in the lamellar-nonlamellar phase transitions of membrane systems containing phosphatidylethanolamine, or other lipids with similar properties, have recently been implicated in facilitating membrane fusion. Finally, studies of transmembrane movement of lipids have provided new insight into the regulation of membrane lipid asymmetry and the biogenesis of cell membranes. These kinds of studies are harbingers of a new generation of progress in the field of cell membranes.
494 citations
TL;DR: Elevated glucose levels can cause the peroxidation of membrane lipids in human RBC, and a significant positive correlation was observed between the extent of glucose-induced membrane lipid per oxidation and the osmotic fragility of treated RBC.
381 citations
TL;DR: A relationship between the total lipid content of the stratum corneum and barrier function is supported and removal of nonpolar species alone appears to cause only a modest level of barrier disruption, while removal of sphingolipids and free sterols leads to a more profoundlevel of barrier perturbation.
343 citations
TL;DR: Binding fluorescent or radioactive reporter molecules to the lipid bilayer of cell membranes allows cell growth and trafficking to be monitored in vivo.
Abstract: Binding fluorescent or radioactive reporter molecules to the lipid bilayer of cell membranes allows cell growth and trafficking to be monitored in vivo.
321 citations
TL;DR: The model predicts a relation between tension and voltage at breakdown and this relation is verified experimentally for the three reconstituted membrane systems studied here.
274 citations
TL;DR: Nanometre-level analyses of the movements of membrane glycoproteins tagged with gold particles demonstrate that diffusing particles are not under the influence of a lipid flow, although a subset of particles which appear attached to the cyto-skeleton are moving rearward.
Abstract: Nanometre-level analyses of the movements of membrane glycoproteins tagged with gold particles demonstrate that diffusing particles are not under the influence of a lipid flow, although a subset of particles which appear attached to the cytoskeleton are moving rearward.
269 citations
TL;DR: It is shown for the first time that myosin-I can bind directly to NaOH-extracted membranes isolated from Acanthamoeba and to vesicles of pure lipids with an affinity sufficient for extensive binding in the cell.
Abstract: The single-headed myosins called myosin-I were first isolated from the protozoan Acanthamoeba and subsequently identified in other cells. We previously reported evidence that myosin-I is responsible for the movement of membranes, extracted from Acanthamoeba, along actin filaments in vitro. Here we show for the first time that myosin-I can bind directly to NaOH-extracted membranes isolated from Acanthamoeba and to vesicles of pure lipids with an affinity sufficient for extensive binding in the cell. Membrane-bound myosin-I may provide a mechanism for many cellular movements previously thought to involve filamentous myosin-II.
265 citations
TL;DR: A frequency distribution of amino acids bracketing approximately 400 transmembrane peptide sequences showed Cys to be the least frequently occurring amino acid at this putative interfacial membrane region, indicating Cys at the interface of cells may stabilize protein-lipid interactions.
264 citations
TL;DR: Low concentrations of tert-butyl hydroperoxide (less than 1.0 mM) lethally injure cultured hepatocytes by a mechanism that depends on the peroxidation of cellular lipids, and DPPD and catechol do not detoxify a radical species that kills the cells and initiates lipid per oxidation as an epiphenomenon.
TL;DR: Application of different types of free radical scavengers, such as ascorbic acid, reduced glutathione, α-tocopherol-acetate and bovine serum albumin, delayed the development of the HR and are consistent with the hypothesis that membrane deterioration during bacterially induced HR is caused by various forms of activated oxygen.
TL;DR: C6-NBD-SM endocytosis was not inhibited when the microtubules were disrupted with nocodazole; rather, the fluorescent lipid was distributed in vesicles throughout the cell periphery instead of being internalized to the perinuclear region of the cell.
Abstract: We examined the metabolism and intracellular transport of the D-erythro and L-threo stereoisomers of a fluorescent analogue of sphingomyelin, N-(N-[6-[(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino] caproyl])-sphingosylphosphorylcholine (C6-NBD-SM), in Chinese hamster ovary (CHO-K1) fibroblast monolayers. C6-NBD-SM was integrated into the plasma membrane bilayer by transfer of C6-NBD-SM monomers from liposomes to cells at 7 degrees C. The cells were washed, and within 10-15 min of being warmed to 37 degrees C, C6-NBD-SM was internalized from the plasma membrane to a perinuclear location that colocalized with the centriole and was distinct from the lysosomes and the Golgi apparatus. This perinuclear region was also labeled by internalized rhodamine-conjugated transferrin. C6-NBD-SM endocytosis was not inhibited when the microtubules were disrupted with nocodazole; rather, the fluorescent lipid was distributed in vesicles throughout the cell periphery instead of being internalized to the perinuclear region of the cell. The metabolism of C6-NBD-SM to other fluorescent sphingolipids at 37 degrees C and its effect on C6-NBD-SM transport was also examined. To study plasma membrane lipid recycling, C6-NBD-SM was first inserted into the plasma membrane of CHO-K1 cells and then allowed to be internalized by the cells at 37 degrees C. Any C6-NBD-SM remaining at the plasma membrane was then removed by incubation with nonfluorescent liposomes at 7 degrees C, leaving cells containing only internalized fluorescent lipid. The return of C6-NBD-SM to the plasma membrane from intracellular compartments upon further 37 degrees C incubation was then observed. The half-time for a complete round C6-NBD-SM recycling between the plasma membrane and intracellular compartments was approximately 40 min. Pretreatment of cells with either monensin or nocodazole did not inhibit C6-NBD-SM recycling.
TL;DR: It is proposed that the hydroxyl radical may not be involved in the peroxidation of membrane lipids, but instead lipid peroxidated requires both Fe2+ and Fe3+.
TL;DR: Cold acclimation dramatically alters the behavior of the plasma membrane during a freeze/thaw cycle—increasing the tolerance to osmotic excursions and decreasing the propensity for dehydration-induced lamellar to hexagonal-II phase transitions.
Abstract: Disruption of the plasma membrane is a primary cause of freezing injury. In this review, the mechanisms of injury resulting from freeze-induced cell dehydration are presented, including destabilization of the plasma membrane resulting from (a) freeze/thaw-induced osmotic excursions and (b) lyotropic phase transitions in the plasma membrane lipids. Cold acclimation dramatically alters the behavior of the plasma membrane during a freeze/thaw cycle--increasing the tolerance to osmotic excursions and decreasing the propensity for dehydration-induced lamellar to hexagonal-II phase transitions. Evidence for a casual relationship between the increased cryostability of the plasma membrane and alterations in the lipid composition is reviewed.
TL;DR: Data indicate that during ischemia proximal tubule tight junctions open, which in turn leads to the lateral intramembranous diffusion of membrane components into the alternate surface membrane domain.
Abstract: In proximal tubular cells ischemia is known to result in the redistribution of apical and basolateral domain-specific lipids and proteins into the alternate surface membrane domain. Since tight junctions are required for the maintenance of surface membrane polarity, the effect of ischemia on tight junction functional integrity was investigated. In vivo microperfusion of early loops of proximal tubules with ruthenium red (0.2%) in glutaraldehyde (2%) was used to gain selective access to and outline the apical surface membrane. Under control situations ruthenium red penetrated less than 10% of the tight junctions. After 5, 15, and 30 min of ischemia, however, there was a successive stepwise increase in tight junction penetration by ruthenium red to 29, 50, and 62%, respectively. This was associated with the rapid duration-dependent redistribution of basolateral membrane domain-specific lipids and NaK-ATPase into the apical membrane domain. Taken together, these data indicate that during ischemia proximal tubule tight junctions open, which in turn leads to the lateral intramembranous diffusion of membrane components into the alternate surface membrane domain.
TL;DR: Apparently, lindane does not perturb the fluid phase of representative native membranes, namely, mitochondria, sarcoplasmic reticulum, myelin, brain microsomes and erythrocytes in agreement with the results obtained in fluid phospholipid bilayers, despite the reasonable incorporation of the insecticide in these membranes, as previously reported.
TL;DR: Transport of newly synthesized PE to the plasma membrane was found to be a rapid process similar to that previously reported for interphase cells, and alternative mechanisms for delivery of the newly synthesised lipids to the outer leaflet of the plasma membranes bilayer are discussed.
TL;DR: It is remarkable that membrane phospholipid asymmetry can be (partly) restored when activated platelets are treated with reducing agents, and the disappearance of phosphatidylserine from the outer leaflet where it was previously exposed during cell activation is discussed.
Abstract: Membrane phospholipid asymmetry is considered to be a general property of biological membranes. Detailed information is presently available on the non-random orientation of phospholipids in red cell- and platelet membranes. The outer leaflet of the lipid bilayer membrane is rich in choline-phospholipids, whereas amino-phospholipids are abundant in the inner leaflet. Studies with blood platelets have shown that these asymmetries are not maintained when the cells are activated in various ways. Undoing the normal asymmetry of membrane phospholipids in activated blood cells is presumably mediated by increased transbilayer movement of phospholipids. This process, which leads to increased exposure of negatively charged phosphatidylserine at the outer surface, plays an important physiological role in local blood clotting reactions. A similar phenomenon occurs in sickled red cells. Phospholipid vesicles breaking off from reversibly sickled cells contribute similarly to intravascular clotting in the crisis phase of sickle cell disease. The loss of membrane phospholipid asymmetry in activated platelets seems to be strictly correlated with degradation of cytoskeletal proteins by endogenous calpain. It is remarkable that membrane phospholipid asymmetry can be (partly) restored when activated platelets are treated with reducing agents. This leads to disappearance of phosphatidylserine from the outer leaflet where it was previously exposed during cell activation. These observations will be discussed in relation to two mechanisms which have been recognized to play a role in the regulation of membrane phospholipid asymmetry; i.e. the interaction of aminophospholipids to cytoskeletal proteins, and the involvement of a phospholipid-translocase catalyzing outward-inward transbilayer movement of amino-phospholipids.
TL;DR: The pathway was correlated with known long‐chain alkylsulfatases and alcohol dehydrogenases in this isolate and indicated that hydrophobic metabolites of the alkyl chain of surfactants can be incorporated into cellular components such as membrane lipids without prior degradation by beta‐oxidation.
Abstract: Metabolism of sodium dodecyl sulfate (SDS) by the detergent-degrading bacterium Pseudomonas C12B has been studied using a 14C radiotracer in combination with radio-respirometry, radio-TLC, and GLC. Metabolism was extensive with 70% of the radiolabel released as 14CO2 at completion. The remainder of the radiolabel was incorporated almost totally into cells. Ether extraction of cells indicated that 14C-labeled cellular material appearing early in the uptake process was predominantly ether-extractable (mainly 1-dodecanol) and was subsequently converted to more polar metabolites. Analysis of the extractable lipids established the sequential production from [1-14C]SDS of 1-dodecanol, dodecanal, and dodecanoic acid. At this point the pathway diverged leading either to formation of 14CO2 via beta-oxidation or to elongation to C14, C16, and C18 fatty acyl residues with rapid incorporation into lipid fractions such as phospholipids. The pathway was correlated with known long-chain alkylsulfatases and alcohol dehydrogenases in this isolate and indicated that hydrophobic metabolites of the alkyl chain of surfactants can be incorporated into cellular components such as membrane lipids without prior degradation by beta-oxidation.
TL;DR: It is suggested that lipid-protein interactions contribute to targeting the precursor toward mitochondria and are important for its translocation across the outer mitochondrial membrane and the final localization of cytochrome c toward the outside of the inner mitochondrial membrane.
TL;DR: The altered lipid composition in white matter in AD and VD suggests that the myelin sheath is the primary lesion site, and that the white matter involvement is not caused by alteration of theMyelin structure.
Abstract: The lipid composition of white matter and myelin from the semioval centre was studied in autopsy material from cases with Alzheimer's disease (AD) (n = 11), vascular dementia (VD) (n = 7), and age-matched controls (n = 11). In AD and VD the white matter content of phospholipids and cholesterol was reduced to 72-76% of the control values (P less than 0.01), the diminution of cerebrosides and sulphatides was more pronounced (55-69%) (P less than 0.001) while the concentration of gangliosides did not change significantly (87-90%). The myelin composition was the same in the 3 groups, suggesting that the white matter involvement is not caused by alteration of the myelin structure. The altered lipid composition in white matter in AD and VD suggests that the myelin sheath is the primary lesion site.
TL;DR: This chapter discusses the purification and reconstitution of glucose transporter from human erythrocytes, and the identification has been achieved either through immunoblotting with polyclonal or monoclonal antibodies raised against the purified ERYthrocyte transporter or through photoaffinity labeling with the 3 H-labeled ligand cytochalasin B.
Abstract: Publisher Summary This chapter discusses the purification and reconstitution of glucose transporter from human erythrocytes. Purification and reconstitution of the erythrocyte transporter are achieved by the following steps: preparation of erythrocyte membranes by the osmotic lysis of erythrocytes; removal of the peripheral (cytoskeletal) proteins from the membranes by treatment with dilute base; partial solubilization of the protein-depleted membranes with the detergent octylglucoside; separation of the transporter and some membrane lipids from this detergent extract by chromatography on Diethylaminoethyl (DEAE)-cellulose; and reconstitution of the transporter into a membrane of these lipids through the removal of the detergent by dialysis. Protein is assayed by a modification of the Lowry procedure used for membrane proteins, with bovine serum albumin as the standard. The lack of success with these lipids in the octylglucoside dialysis method led to the testing of erythrocyte lipids, which allow the assay of the transport function. The identification has been achieved either through immunoblotting with polyclonal or monoclonal antibodies raised against the purified erythrocyte transporter or through photoaffinity labeling with the 3 H-labeled ligand cytochalasin B.
TL;DR: The principles underlying the phase-mixing behavior of model membrane systems can be used to provide useful information about the factors that determine the stability of biomembranes under physiological and non-physiological conditions.
Abstract: Biological membranes consist of a complex assortment of lipids and proteins. The arrangement of the components, particularly in regard to their lateral disposition in the plane of the membrane under physiological conditions, is dependent on the phase behavior of the different membrane lipids and the way that this behavior is modified by interaction with other membrane components and electrolytes in the aqueous medium. Irreversible phase separation of components within the membrane may result from exposure to extreme environmental conditions including temperature, pressure, or electrolyte concentration. The principles underlying the phase-mixing behavior of model membrane systems can be used to provide useful information about the factors that determine the stability of biomembranes under physiological and non-physiological conditions. These data are reviewed and used to predict events that take place when membranes are exposed to environmental stress.
TL;DR: The salt resistance of Protador relative to LGH (salt-sensitive) appears to be related to higher K+ fluxes and cytoplasmic concentrations, and lower Na+ and Cl fluxes, when grown in NaCl.
Abstract: Cytoplasmic concentrations, fluxes of K+, Na+ and Cl and microsomal membrane lipids were investigated in a salt-sensitive and salt-resistant variety of Zea mays. The salt resistance of Protador relative to LGH (salt-sensitive) appears to be related to higher K+ fluxes and cytoplasmic concentrations, and lower Na+ and Cl fluxes and cytoplasmic concentrations, when grown in NaCl. There were no apparent differences in the simple chemical composition of root microsomal membrane lipids between the two varicties, neither were these affected by salt.
TL;DR: The influence of plasmalogen deficiency on membrane lipid mobility was determined by measuring fluorescence anisotropy of trimethylammoniumdiphenyl hexatriene and diphenylhexatrienylpropanoylhydrazylstachyose inserted in the plasma membranes of human skin fibroblasts deficient in plAsmalogens.
TL;DR: The immunolocalization of sulfated glycoprotein-1 in the cells and fluid of the male reproductive tract is reported, believed to be involved in degradation of lipids in residual bodies and may also assist in modification of membrane lipids during sperm maturation.
Abstract: Sulfated glycoprotein-1 is one of the major protein secretion products of rat Sertoli cells in culture. This 70,000 Mr protein shares substantial sequence similarity with human prosaposin, the precursor of lysosomal saposins. Saposins are known to enhance the activity of lipid modifying enzymes presumably by solubilizing the lipids. We report here the immunolocalization of sulfated glycoprotein-1 in the cells and fluid of the male reproductive tract. The protein is present in secondary lysosomes of Sertoli cells and also in the luminal fluid of seminiferous tubules and epididymis. The highest concentrations of the protein are in seminiferous tubule fluid and rete testis fluid, while relatively low amounts are found in cauda epididymal fluid and serum. Sulfated glycoprotein-1 is believed to be involved in degradation of lipids in residual bodies and may also assist in modification of membrane lipids during sperm maturation.
TL;DR: Results show that the increased fluidity of the erythrocyte membrane in magnesium deficiency is due to physicochemical exchange with the plasma, mainly mediated indirectly via disturbances in lipid metabolism.
Abstract: The erythrocyte membrane was investigated in weanling male rats pair fed with magnesium-deficient and control diets for 8 days. Fluorescence polarization studies revealed a 15% increase in the fluidity of membranes from deficient rats. A similar increase in the fluidity of liposomes indicated that protein was not involved. The change was associated with decreased osmotic fragility of intact erythrocytes; the cells lost their biconcavity and had a flattened appearance with surface irregularities. Analysis of the membranes showed decreased amounts of magnesium, cholesterol, and sphingomyelin in the deficient group. The reduced ratios of cholesterol to phospholipid and sphingomyelin to phosphatidylcholine were consistent with the increased fluidity. Addition of physiological amounts of magnesium to the medium rigidified membranes incubated in tris(hydroxymethyl)-aminomethane buffer, and this was prevented by the presence of EDTA. Cross-incubation experiments with erythrocyte ghosts and plasma from the two groups of rats showed that magnesium-deficient plasma increased the fluidity of control ghosts and control plasma rigidified ghosts from magnesium-deficient rats. Addition of sufficient magnesium chloride to raise the magnesium content of deficient plasma to normal had no significant effect. These results show that the increased fluidity of the erythrocyte membrane in magnesium deficiency is due to physicochemical exchange with the plasma. Although magnesium can directly influence membrane fluidity, the change during its deficiency in vivo is mainly mediated indirectly via disturbances in lipid metabolism.
TL;DR: It is shown that glycolipids, analogous to a variety of protein receptors, are able to recycle to the plasma membrane after internalization, and C6-NBD-glucosylceramide molecules can be shown to return intact to the Plasma membrane.
Abstract: To examine the (intra)cellular fate of a glycolipid, normally residing at the cell surface, a fluorescent analog of glucosylceramide, 6-[N-(7-nitro-2,1,3-benzoxadiazol-4-yl)amino]hexanoylglucosylsp hingosine (C6-NBD-glucosylceramide), was inserted into the plasma membrane of baby hamster kidney cells at low temperature. Upon warming the cells to 37 degrees C, part of the glycolipid analog was internalized. A comparison with receptor-mediated uptake of transferrin revealed that after 2 min of warming, both C6-NBD-glucosylceramide and the transferrin-transferrin receptor complex are localized in the same intracellular compartment (early endosomes). We conclude that C6-NBD-glucosylceramide is internalized along the pathway of receptor-mediated endocytosis. When, after internalization of part of the membrane-inserted glycolipid analog, the residual pool of plasma membrane C6-NBD-lipid was removed by "back exchange" with a lipid acceptor, C6-NBD-glucosylceramide molecules can be shown to return intact to the plasma membrane. This demonstrates that glycolipids, analogous to a variety of protein receptors, are able to recycle to the plasma membrane after internalization.