Current concepts. The structure of cell membranes.
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Cell Membrane↗
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[Catalytic characteristics of 5'-nucleotidase in the structure of cell membrane rafts in smooth muscles].
5'-nucleotidase (EN 3.1.3.5) is widely distributed enzyme occurring in vertebrate, bacterial and plant cells. The main physiological function of 5'-nucleotidase is hydrolysis of 5'-AMP to adenosine and Pi. It was found that the detergent-insoluble membrane domains (rafts) are enriched by proteins possessing high 5'-AMPase activity. This study is aimed to investigate some physical and chemical properties of 5'-nucleotidase, which is present in detergent insoluble membrane domains isolated from pig stomach and lung. It was shown for the first time that catalytic properties of the raft-associated 5'-nucleotidase and of the pure enzyme described in literature differ. Our results demonstrate that the greatest activity of the raft-associated enzyme takes place in the physiological conditions contrary to the pure enzyme. Our data suggest that such changes of 5'-nucleotidase catalytic activity might be due to the disruption of its interaction with membrane rafts.
5'-Nucleotidase↗
[Current views on the structure of cell membranes].
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Cell Membrane↗
[Globular structure of cell membranes].
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Animals↗
[Ability of gangliosides to improve the functional state of the body and normalize the biochemical structure of cell membranes in hypoxia].
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Animals↗
Localization of the ASV src gene product to the plasma membrane of transformed cells by electron microscopic immunocytochemistry.
The cellular location of the src gene product (p60src) of the Schmidt-Ruppin strain of avian sarcoma virus has been determined by electron microscopic immunocytochemistry in Schmidt-Ruppin ASV-transformed NRK cells, and the amount of the protein in different regions of the cell has been quantified. The protein is concentrated on the inner surface of the plasma membrane, particularly under ruffles, and it is highly concentrated on the inner surface of the membrane near junctions connecting adjacent cells. Small amounts of p60src were detected in the cytoplasm and in the perinuclear Golgi region of the cell. No significant localization was detected in control NRK cells or in NRK cells transformed by the Kirsten strain of murine sarcoma virus. The presence of p60src on the inner surface of the plasma membrane indicates that the changes in cell growth, cell shape and cell membrane structure noted in ASV-transformed cells are due to an initial action of p60src at the cell membrane.
Alpharetrovirus↗
Foamy cells associated with phagocytosis of glutaraldehyde-treated red blood cells and red cell membranes.
In order to clarify the mechanism for the formation of foamy cells (macrophages with foamy appearance) associated with increased erythrophagocytosis, we tried to reproduce these cells in mice by subcutaneous injection of intact red blood cells (RBCs), OsO4-treated RBCs (Os-RBCs), glutaraldehyde-treated RBCs (G-RBCs), or isolated red cell membranes, and time-course observation was done by light and electron microscopy. Foamy cells were induced by the latter two methods. Within the macrophages, G-RBCs were fragmented into spherules by newly formed small vacuoles, and with time these spherules lost their hemoglobin content transforming into small vacuoles with translucent matrix. In most of these vacuoles, red cell membrane structure was discernible adjacent to the phagocytic vacuole. Such macrophages containing abundant small vacuoles appear foamy in light microscopy. Foamy cells induced by injection of red blood cell membranes were positive for lipid stains and contained abundant laminated membrane structures in electron microscopy. These results suggest that the foamy cells related with increased erythrophagocytosis are heterogeneous with respect to their pathogenesis and cellular inclusions, and proteinaceous constituents resistant to intracellular digestion are also responsible for the occurrence of foamy cells.
Animals↗
The effect of chemical modification of Saccharomyces cerevisiae on electrophoretic mobility, cell-wall structure and amphotericin B uptake.
Saccharomyces cerevisiae NCYC 239 suspended in solutions of NaCl showed two distinct plateaus in plots of electrophoretic mobility vs. pH, corresponding to pKa values of approx. 2 and 5. This is in contrast to cells suspended in buffer where only a single pKa (4) can be determined. Modification of cells with KI/I2 or nitrous acid led to altered electrophoretic mobility, indicating the presence of sulphydryl and amino groups, respectively, in the yeast cell surface, whereas uranyl nitrate modification had little effect, suggesting phosphate groups to be absent. Electron micrographs showed visible effects of KI/I2 and nitrous acid modification on cell membrane structure, and in these modified cells amphotericin B uptake was rapid. It is suggested that diffusion through the cell wall is the rate-limiting step for amphotericin B uptake. An activation energy of 20 kJ X mol-1 was determined for uptake of amphotericin B by unmodified cells.
Amphotericin B↗
Visualization of plasma membrane compartmentalization with patterned lipid bilayers.
Micrometer-size patterned lipid bilayers containing liganded lipids are used to control the location and size of receptor clusters and enable direct visualization of structural reorganization of cellular components. Subsequent to concentration of Fcepsilon receptor I, the mast cell receptor for IgE, and colocalized tyrosine phosphorylation activity, Lyn kinase and other proteins anchored to the inner leaflet of the plasma membrane redistribute selectively with the receptor clusters in a process that depends on actin polymerization. Surprisingly, outer leaflet components characteristically associated with lipid rafts do not detectably coredistribute with these inner leaflet components. Cell activation using patterned surfaces provides unique insights into cell membrane structural organization, revealing dynamic, large-scale uncoupling of inner and outer leaflet components of lipid rafts.
Actins↗
Lipid microdomains in cell surface membranes.
Lipid microdomains within cell membranes are detected by a variety of experimental techniques, each of which characterizes microdomains on a different time and spatial scale. The sum of the data on lipid microdomains has yet to be integrated into a single model of cell membrane structure. Indeed, one highlight of the past year is a new analysis of experimental results which yields a model of a cell membrane which need not contain any microdomains. Other highlights are an estimate of the number of phospholipid molecules in a membrane microdomain and the detection of domain formation in cell membranes in real time. Some progress has also been made in visualizing lipid microdomains within cell membranes. We still await, however, a new model of membrane structure that integrates all experimental results.
Membrane Lipids↗
Brain cell membrane function during hypoxia in hyperglycemic newborn piglets.
To test the hypothesis that acute hyperglycemia reduces changes in cell membrane structure and function during cerebral hypoxia in the newborn, brain cell membrane Na+,K(+)-ATPase activity and levels of membrane lipid peroxidation products were measured in four groups of anesthetized, ventilated newborn piglets: normoglycemia/normoxia (control, group 1, n = 12), hyperglycemia/normoxia (group 2, n = 6), untreated hypoxia (group 3, n = 10), and hyperglycemia/hypoxia (group 4, n = 7). Hyperglycemia (blood glucose concentration 20 mmol/L) was induced using the glucose clamp technique. The hyperglycemic glucose clamp was maintained for 90 min before onset of hypoxia and throughout the period of hypoxia. Cerebral tissue hypoxia was induced in groups 3 and 4 by reducing fraction of inspired oxygen for 60 min and was documented by a decrease in the ratio of phosphocreatine to inorganic phosphate as measured using 31P-nuclear magnetic resonance spectroscopy. Blood glucose concentration during hypoxia in hyperglycemic hypoxic animals was 20.7 +/- 1.2 mmol/L, compared with 10.3 +/- 1.7 mmol/L in untreated hypoxic piglets (p < 0.05). Peak blood lactate concentrations were not significantly different between the two hypoxic groups (8.4 +/- 2.8 mmol/L versus 7.8 +/- 1.6 mmol/L). In cerebral cortical membranes prepared from the untreated animals, cerebral tissue hypoxia caused a 25% reduction in Na+,K(+)-ATPase activity compared with normoxic controls and an increase in conjugated dienes and fluorescent compounds, markers of lipid peroxidation. In contrast, Na+,K(+)-ATPase activity and levels of lipid peroxidation products in hyperglycemic hypoxic animals were not significantly different from the values in control normoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
Mechanisms by which elevated intracellular calcium induces S49 cell membranes to become susceptible to the action of secretory phospholipase A2.
Exposure of S49 lymphoma cells to exogenous group IIA or V secretory phospholipase A2 (sPLA2) caused an initial release of fatty acid followed by resistance to further hydrolysis by the enzyme. This refractoriness was overcome by exposing cells to palmitoyl lysolecithin. This effect was specific in terms of lysophospholipid structure. Induction of membrane susceptibility by lysolecithin involved an increase in cytosolic calcium and was duplicated by incubating the cells with calcium ionophores such as ionomycin. Lysolecithin also activated cytosolic phospholipase A2 (cPLA2). Inhibition of this enzyme attenuated the ability of lysolecithin (but not ionomycin) to induce susceptibility to sPLA2. Lysolecithin or ionomycin caused concurrent hydrolysis of both phosphatidylethanolamine and phosphatidylcholine implying that transbilayer movement of phosphatidylethanolamine occurred upon exposure to these agents but that susceptibility is not simply due to exposure of a preferred substrate (i.e. phosphatidylethanolamine) to the enzyme. Microvesicles were apparently released from the cells upon addition of lysolecithin or ionomycin. Both these vesicles and the remnant cell membranes were susceptible to sPLA2. Together these data suggest that lysolecithin induces susceptibility through both cPLA2-dependent and -independent pathways. Whereas elevated cytosolic calcium was required for both pathways, it was sufficient only for the cPLA2-independent pathway. This cPLA2-independent pathway involved changes in cell membrane structure associated with transbilayer phospholipid migration and microvesicle release.
Calcium↗
Effect of alpha-phenyl-N-tert-butylnitrone on brain cell membrane function and energy metabolism in experimental Escherichia coli meningitis in the newborn piglet.
We evaluated the efficacy of alpha-phenyl-N-tertbutylnitrone as an adjunctive therapy in experimental bacterial meningitis in the newborn piglet. Meningitis was induced by intracisternal injection of 10(8) colony-forming units of Escherichia coli in 100 microl of saline. Alpha-Phenyl-N-tert-butylnitrone 100 mg/kg was given as a bolus intravenous injection 30 min before induction of meningitis. Although it completely abolished the elevated CSF tumor necrosis factor-a level observed in the meningitis group, alpha-phenyl-N-tert-butylnitrone did not down-modulate parameters of inflammatory responses such as increased intracranial pressure, hypoglycorrhachia, elevated CSF lactate level, and CSF leukocytosis observed in this group. However, alpha-phenyl-N-tert-butylnitrone treatment mitigated alterations in brain cell membrane structure and function during meningitis, evidenced by amelioration of increased brain cell membrane lipid peroxidation products (conjugated dienes) and decreased Na+, K+-ATPase activity. Reduced mean arterial blood pressure, cerebral perfusion pressure, brain glucose concentration, and cerebral energy stores and marginally increased brain lactate level observed in the meningitis group were also ameliorated. These results suggest that although it failed to attenuate the inflammatory responses, alpha-phenyl-N-tert-butylnitrone was effective in ameliorating brain injury in neonatal bacterial meningitis.
Animals↗
Macromolecular structure of the Schwann cell membrane. Perinodal microvilli.
The macromolecular structure of perinodal Schwann cell membrane was examined with freeze-fracture electron microscopy. Perinodal microvillous-like processes of Schwann cells exhibit an asymmetrical partitioning of intramembranous particles (IMPs), with a moderate (approximately 900/microns2) density of particles on P-faces and a lower (approximately 300/microns2) density of IMPs on E-faces. The densities of IMPs observed on the fracture faces of perinodal processes are similar to those within the outer membrane of the Schwann cell proper. On both fracture faces of the perinodal processes and the Schwann cell membrane proper, a high (approximately 45%) percentage of the IMPs displayed a large (greater than or equal to 9.6 nm) diameter. Specialized junctions (i.e., gap junctions, tight junctions) between adjacent perinodal Schwann cell processes or between perinodal processes and nodal axolemmal were not observed.
Animals↗
Biochemical aspects of pressure tolerance in marine mammals.
Some marine mammals can dive to depths approaching 2000 m. At these hydrostatic pressures (200 atm), some fish species show alterations in enzyme structure and function that make them pressure-tolerant. Do marine mammals also possess biochemical adaptations to withstand such pressures? In theory, biochemical alterations might occur at the control of enzymatic pathways, by impacting cell membrane fluidity changes or at a higher level, such as cellular metabolism. Studies of marine mammal tissues show evidence of all of these changes, but the results are not consistent across species or diving depth. This review discusses whether the elevated body temperature of marine mammals imparts pressure tolerance at the biochemical level, whether there are cell membrane structural differences in marine mammals and whether whole, living cells from marine mammals alter their metabolism when pressure stressed. We conclude that temperature alone is probably not protective against pressure and that cell membrane composition data are not conclusive. Whole cell studies suggest that marine mammals either respond positively to pressure or are not impacted by pressure. However, the range of tissue types and enzyme systems that have been studied is extremely limited and needs to be expanded before more general conclusions about how these mammals tolerate elevated pressures on a biochemical level can be drawn.
Adaptation, Physiological↗
An interpretation of liver cell membrane and junction structure based on observation of freeze-fracture replicas of both sides of the fracture.
A modification of the freeze-fracturing technique to permit observation of replicas of both sides of the fracture is described. It has been used to study mouse liver cell membrane structure. Membranes break to give two faces with three-dimensional complementarity, although there is some small-scale mismatching which is discussed. Since the two distinctive sets of membrane faces are complementary sets, they cannot be the two outside surfaces. In particular, structures (such as particles) seen on these faces are within the membrane. It is not possible from this work to say precisely where the fracture plane goes with respect to a plasma membrane, only that it must be close to the interface between membrane and cytoplasm, or at that interface. Models, consistent with the appearance of the matching replicas, are derived for three regions of the plasma membrane: (a) The nonjunctional plasma membrane, which contains many scattered particles. Except for these particles, the otherwise flat fracture face is not at variance with a bimolecular leaflet structure. (b) Gap junctions. Each of the two membranes comprising a gap junction contains a close-packed array of particles. (c) Tight junctions. Here membranes have ridges within them.
Animals↗
Freeze-fracture study of the pavement cell in the lamprey gill epithelium. Analogy of membrane structure with the granular cell in the amphibian urinary bladder.
Freeze-fracture studies of the lamprey gill epithelium reveal structural differences of the luminal and basolateral plasma membrane of the pavement cells. The luminal membrane is characterized by only a few intramembrane particles on the P face and numerous large (10-13 nm) particles on the E face, whereas the basolateral membrane shows the majority of intramembrane particles (6-8 nm) on the P face. The structural specialization of the luminal membrane and the differences between the luminal and basolateral membranes of the pavement cell are similar to those previously demonstrated for the unstimulated granular cell of the amphibian urinary bladder. Because of this similarity, it is suggested that the 2 cell types are analogous and that the luminal membrane of the pavement cell in the lamprey gill epithelium is functionally characterized by a low water permeability. A possible role of sodium uptake by the pavement cells from freshwater and putative differences of osmoregulatory mechanisms in the gills of lampreys and teleosts in freshwater environments are discussed.
Amphibians↗
Peroxyl radicals: inductors of neurodegenerative and other inflammatory diseases. Their origin and how they transform cholesterol, phospholipids, plasmalogens, polyunsaturated fatty acids, sugars, and proteins into deleterious products.
The most oxygen-sensitive constituents of cells are polyunsaturated fatty acids (PUFAs), which are incorporated in the outermost layer of cells in the form of phospholipids. PUFAs easily suffer oxidation. Identical marker compounds of these lipid peroxidation (LPO) processes are generated in both neurodegenerative and cardiovascular diseases, indicating a close relationship between the inducers of these events. Apparently, any alteration of the cell membrane structure influences the channels crossing the cell wall and causes an influx of Ca2+ ions. Ca2+ ions induce activation of phospholipases, which cleave phospholipids. Thus, the generated free PUFAs serve as substrates of lipoxygenases (LOXs) and cyclooxygenases. LOXs transform PUFAs into lipid hydroperoxides (LOOHs). If an outside impact exceeds a certain limit, the catalyzing bivalent iron ions in LOXs are liberated. They cleave the enzymatically generated LOOH molecules and induce a switch to nonenzymatic LPO reactions that produce peroxyl radicals (LOO*). Although LOO* radicals are also intermediates in enzymatic LPO processes, they are prevented from leaving the enzyme complex before the reaction is completed by generation of LOOH molecules. LOO* radicals are much more reactive than LOOH molecules and attack nearly all types of biological molecules. The generated products seem to serve as ligands for proteins that in turn induce gene activation. Thus, PUFA-phospholipids are apparently the precursor molecules of signal molecules that respond in a dose-related manner to any event that influences the cell structure by inducing an appropriate gene response. In this paper an overview of the deleterious chemical reactions initiated by LOO* radicals is presented. Many of these reactions have not been taken into account in previous research. These include epoxidation of cholesterol-PUFA esters, plasmalogens, and sphingolipids, as well as the release of hydrogen peroxide by the reaction of LOO* radicals with alcohols (sugars) and amines. The oxidation of proteins generating plaque formation involves only the LOO* radical-sensitive functional groups in side chains of the protein backbone and is therefore a rather late event in the development of Alzheimer disease and atherosclerosis.
Carbohydrate Metabolism↗