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PubMed2003

Effect of arsenic on cell growth of the cellular slime mould, Dictyostelium discoideum.

The growing D. discoideum cells were killed in a dose-dependent manner when exposed to 100 and 140 ppm of arsenic (As2O3) at mid-log phase for 20 min. Reduced plaque sizes and changed cell and colony morphologies were observed in the treated cells. Endocytotic functions (both phagocytosis and pinocytosis) were also inhibited in the treated cells. Arsenic treated cell showed a lower DNA and protein synthetic activities. These findings are discussed in relation to known mechanism of action of the heavy metal on growth-related cellular functions.

Animals↗

PubMed1991

Mesangial cell activation by bacterial endotoxin. Induction of rapid cytoskeletal reorganization and gene expression.

Cultured glomerular mesangial cells (MC) respond to low concentrations of bacterial endotoxin (ET) by secreting prostaglandins and interleukin-1. To evaluate further the nature of ET-induced mesangial cell activation, the authors evaluated the effects of this agent on MC morphology and cytoskeletal organization. Bacterial ET, in concentrations as low as I ng/ml, induced reversible membrane ruffling, cellular rounding, and extension of many filopodia and lamellopodia. Augmented fluid-phase pinocytosis occurred in parallel, as determined by transmission electron microscopy and tritiated sucrose uptake. These cellular morphologic and functional changes were associated with an extensive, but reversible, depolymerization of actin microfilaments. Actin gene expression was also modified by ET. At 4 to 6 hours after ET exposure, Northern blot analysis showed a twofold to fourfold increase in actin mRNA levels. In situ hybridizations of ET-stimulated cells at the light and electron microscopic levels demonstrated a markedly asymmetric distribution of actin mRNA, which was localized in the cellular periphery at filopodial and lamellopodial extensions, presumably sites of new actin protein synthesis. It is concluded that ET effects on MC are distinct from the nonspecific lytic or 'toxic' actions described for other cell types. Endotoxin induces a global activation of this cell type associated with major changes in membrane structure, cytoskeletal organization, and gene expression, which resemble in many respects the responses to peptide mitogens.

Actins↗

PubMed1990

Effects of drugs on blood-brain barrier permeability in rats chronically intoxicated by ethanol.

Male Wistar rats were divided in free choice conditions into heavy-drinkers consuming greater than 3.5 g/kg of ethanol daily (HD), and light-drinkers consuming less than 2.0 g/kg/day (LD). Subsequent 30 day intragastric administration of 25% ethanol (8-11 g/kg/day) caused an increase in permeability of the BBB to 14C-tyrosine, 14C-tryptophan and 14C-DOPA at all the stages of alcoholization. At late stages of intoxication (20-30 days) the penetration of horseradish peroxidase (HRP) indicating pinocytosis was present. All the changes were more pronounced in LD than in HD rats. Disulfiram, and to a lesser extent phenazepam and diazepam, when repeatedly injected (for 16-30 days) together with ethanol aggravated its effects. Clonidine and haloperidol antagonized ethanol-induced increase of the BBB permeability to labelled compounds and HRP in the two groups of rats. Picamilon, lithium oxybutyrate, chlorpromazine and alpha-tocopherol had little effect on the penetration of radioactive tracers but effectively antagonized the penetration of HRP. The other drugs were without effects on the BBB regulatory and barrier functions altered by chronic alcoholization. In view of the BBB dysfunction in chronic alcoholics the adequacy of the above-mentioned drugs for their treatment is discussed.

Alcohol Deterrents↗

PubMed1979

Metabolism of low density lipoproteins in human fibroblast culture.

The purpose of the study was to investigate the changes which low density lipoproteins (LDL) underwent during incubation with human culture fibroblasts. The results showed a predominant deposition of lipids, a low level of LDL-protein breakdown products in the cells, the altered structure of lipoproteins, absorbed on the cell surface and of lipoproteins in the incubation medium. The authors suppose intensive metabolic transformations to take place on the cell membrane. The partial lipoprotein degradation seems to realize favourable conditions for the subsequent entry of lipids into the cells and for a pinocytosis of lipoprotein particles transformed on the cell surface. The intensity of these membrane metabolic transformations is influenced by the antigenic properties of LDL, the presence of other proteins in the medium, and by the maturity and the metabolic activity of the cultured cells.

Cell Membrane↗

PubMed1987

A nonendocytotic mechanism for the selective uptake of high density lipoprotein-associated cholesterol esters.

We have previously described in rats the selective uptake of HDL-associated cholesterol esters (traced by [3H]cholesteryl oleyl ether) in excess of the uptake of HDL-associated apoA-I. In the present studies we show that the mechanism also exists in cultured cells of human and mouse origin as well. This selective uptake represents a net uptake of cholesterol esters and not an isotope exchange, as shown by mass flux studies in adrenal cells. Inhibitors of receptor recycling, chloroquine, monensin, and colchicine, inhibited uptake of apoA-I from HDL by Hep G-2 human hepatoma cells to about the same extent as a reference protein, asialofetuin, but inhibited uptake of the cholesteryl ether tracer much less. Levels of NaN3 which effectively inhibited sucrose pinocytosis inhibited uptake of apoA-I to about the same extent but did not inhibit uptake of the cholesteryl ether at all. Thus, not only receptor recycling, but endocytosis as well, appears not to be involved in selective uptake. This conclusion was supported by studies in which synthetic HDL particles were made to contain two neutral lipid core tracers; one of them, the [3H]cholesteryl ether previously used, was selectively taken up, whereas the other, [14C]sucrose octaoleate, was excluded from selective uptake. Thus, selective uptake cannot involve endocytosis of the entire lipid core, but may involve other specific transfer mechanisms.

Adrenal Cortex Neoplasms↗

PubMed1988

Incorporation of bacterial lipopolysaccharide by human Leu-11a+ natural killer cells. Ultrastructural and functional correlations.

Lipopolysaccharides (LPS) of gram-negative bacteria are known to augment the ability of macrophages and natural killer (NK) cells to lyse susceptible target cells. In the present studies, we sought correlations between the ultrastructural changes and function of Leu-11a+ cells from the peripheral blood mononuclear cells which occurred as a result of their incorporation of LPS. We also studied the effect of LPS on the NK activity of purified Leu-11a+ cells. LPS samples from E. coli and Pseudomonas aeruginosa were utilized. A double-immunolabeling technique employing immunogold and immunoperoxidase markers was used to identify the Leu-11a+ cells with incorporated LPS. Pinocytosis, phagocytosis, and direct insertion into membrane bilayers appeared to be the routes for incorporation of LPS by Leu-11a+ cells. Subsequent ultrastructural effects included dilation of intracellular membrane compartments, formation of tubuloreticular inclusions and increased acid phosphatase activity. Opsonized Staphylococcus aureus were ingested both by control and LPS-treated Leu-11a+ cells; however, the number of Leu-11a+ cells with bacteria increased significantly as a result of LPS treatment. Autoradiography combined with immunolabeling showed no [3H] thymidine incorporation by either control or LPS-stimulated Leu-11a+ cells. NK cell-mediated cytotoxicity was significantly increased as compared with the control (p less than or equal to 0.02) when isolated Leu-11a+ cells were treated with LPS for 24 hours. This result suggests that LPS may have direct effect on the NK cell activity. Tests of peripheral blood mononuclear cell samples after LPS treatment showed up to a 2-fold increase in NK cytotoxicity and a dose-related increase of in vitro interferon production. This latter finding together with the ultrastructural observations of tubuloreticular inclusions in Leu-11a+ cells suggests that, in addition to any direct effect of LPS, cytotoxic activity could be indirectly augmented as a result of autocrine or paracrine interferon, or lymphokine production.

Acid Phosphatase↗

PubMed1989

Cohort movement of different ligands and receptors in the intracellular endocytic pathway of alveolar macrophages.

The rate of movement of different receptors and ligands through the intracellular endocytic apparatus was studied in alveolar macrophages. Cells were exposed to iodinated alpha-macroglobulin-protease complexes, mannose terminal glycoproteins, diferric transferrin, and maleylated proteins. By use of the diaminobenzidine density shift procedure, we demonstrated that these ligands were internalized into the same endocytic vesicle. We then compared the rates of transfer to the lysosome or recycling to the cell surface of different ligands/receptors contained in the same endosome. We found that although the rate constant for degradation was ligand specific, the lag time prior to the initiation of degradation was the same for all three ligands. We also found that molecules taken up nonspecifically by fluid-phase pinocytosis had the same lag time prior to degradation as ligands internalized via receptor-mediated endocytosis. These data suggest that different molecules within the same endocytic compartment are transferred to the lysosome (or degradative compartment) at the same rate. We measured the rate of return of receptors to the cell surface by either inactivating surface receptors by protease treatment at 0 degrees C, or by incubating cells with saturating amounts of nonradioactive ligand at 37 degrees C. We then measured the rate of appearance of "new" receptors on the cell surface. Using these approaches, we found that three different receptors were transferred from internal pools to the cell surface at the same rate. The rate of transfer was independent of whether receptors were initially occupied or unoccupied. Our observations indicate that receptor/ligands, once inside alveolar macrophages, are transported by vesicles which transfer their contents as a cohort from one compartment to another. The rate of movement of these receptors is determined by the movement of vesicles and is independent of their content.

3,3'-Diaminobenzidine↗

PubMed1988

Limitations of transmembrane transport in drug delivery.

The plasma membrane of all living cells controls the flow of substances, energy as well as information, between the internal cell order and surrounding cell disorder. There are three general routes along which substances may cross this barrier; free diffusion, passive and active transport, and endocytic processes. The subject of polymer drugs where biologically inert polymers bear therapeutically active low molecular weight drugs and targeting moiety became a popular issue in last decade. This review is devoted to the question of the interaction of drugs with the plasma membrane and their transport across it. As the polymer-drug conjugates are macromolecular substances, the main emphasis is focused on the problems of phagocytosis and pinocytosis.

Biological Transport↗

PubMed1988

Novel receptor-mediated internalization of interleukin 2 in B cells.

Novel IL-2-binding molecules (p70 and p75) mediating internalization and degradation of IL-2 were examined by employing a human B lymphoblastoid line, SKW6-4 cells. High concentrations of IL-2 induced IgM secretion in these cells through a receptor distinct from Tac antigen. The acid-wash technique revealed that more than 60% of 125I-labeled IL-2 bound to the cells became acid-unremovable in the first 30 min of incubation at 37 degrees C and degradation products of 125I-IL-2 increased after 30 min of incubation. Treatment of the cells with NaN3 buffer inhibited the appearance of acid-unremovable 125I-IL-2, suggesting that acid-unremovable 125I-IL-2 was not due to fluid-phase pinocytosis but due to internalization. Loss of labeled bands by incubation of cells with 125I-IL-2 at 37 degrees C before affinity cross-linking demonstrated that 125I-IL-2 was internalized via novel IL-2-binding molecules. These results suggest that novel IL-2-binding molecules are responsible for internalization and may mediate signal transduction in B cells in the absence of Tac antigen.

Azides↗

PubMed1988

Potentiation of lymphokine-induced macrophage activation by tumor necrosis factor-alpha.

In this study, we examined the possible role of TNF-alpha and lymphotoxin (TNF-beta) as cofactors of macrophage activation. The results demonstrate that both TNF were capable of enhancing the cytostatic and cytolytic activity of murine peritoneal macrophages against Eb lymphoma cells. The potentiation of tumor cytotoxicity became apparent when macrophages from DBA/2 mice were suboptimally activated by either a T cell clone-derived macrophage-activating factor or by IFN-gamma plus LPS. Neither TNF-alpha nor TNF-beta could induce tumor cytotoxicity in IFN-gamma-primed macrophages, indicating that TNF cannot replace LPS as a triggering signal of activation. In LPS-resistant C3H/HeJ macrophages, which were unresponsive to IFN-gamma plus LPS, a supplementation with TNF fully restored activation to tumor cytotoxicity. Furthermore, TNF-alpha potentiated a variety of other functions in low-level activated macrophages such as a lactate production and release of cytotoxic factors. At the same time, TNF-alpha produced a further down-regulation of pinocytosis, tumor cell binding and RNA synthesis observed in activated macrophages. These data demonstrate new activities for both TNF-alpha and TNF-beta as helper factors that facilitate macrophage activation. In particular, the macrophage product TNF-alpha may serve as an autocrine signal to potentiate those macrophage functions that were insufficiently activated by lymphokines.

Adjuvants, Immunologic↗

PubMed1977

The functional capacity of guinea pig megakaryocytes. II. The uptake of particles and macromolecules and the effect of rabbit antiguinea pig platelet antiserum.

The capacity of megakaryocytes to take up particles and macromolecules was tested by exposing them to homologous erythrocytes, latex particles, Micrococcus lysodeikticus, and horseradish peroxidase. Uptake of particles 1.1 to 7 mum. in size was extensive under the experimental conditions employed. After uptake of each of the three particles the addition of tannic acid and calcium to the fixative produced electron-dense deposits within the vacuole surrounding the particle; therefore, the vacuole was not closed off. This finding indicates that many of the particles could be actually trapped within the preformed elements of the demarcating membrane system. Horseradish peroxidase was concentrated within cytoplasmic vacuoles after 2 hours of exposure to 0.1 mg. per ml. The presence of surface membrane receptors was determined by the sheep cell rosette method. The presence of the C3b receptor for complement was determined by the sheep cell rosette method. The presence of the C3b receptor for complement produced rosette formation. The functional capacity of megakaryocytes to react like platelets was also tested by observing cell lytic changes and determining that there was approximately 40% release of 3H-serotonin produced by specific rabbit antiguinea pig platelet antiserum in the presence of complement. These studies demonstrate several functional capacities of megakaryocytes: the uptake of particles, pinocytosis, and the cell lytic response to specific antibody.

Acid Phosphatase↗

PubMed1977

The migrant cells in allotransplants of heart, kidney and skin. II. Monocyte-macrophage activity.

Within a few hours of transplantation the cells of the mononuclear phagocyte system migrate into the interstitial tissues of the organ. The cells arrive on the vascular endothelium of the allotransplanted organ either as macrophages or as monocytes but on entering the interstitial tissues they begin to enlarge, differentiate and undergo active pinocytosis. Along with the cell migration, which would appear to be their stimulus to migrate, is an extravasation of the protein-rich plasma. Erythrocytes also pass into the interstitium and, if effete, are contracted by monocyte-macrophages and phagocytosed in the classical manner. All through the natural history of an allotransplant new monocyte-macrophage recruits arrive the interstitial tissues of the allotransplant. Some of these cells escape via the lymphatics but the vast majority accumulate in the allotransplant, interdigitate and fuse with one another but make no attempt to damage the tissues into which they have migrated. The reaction to an allotransplanted organ fits into the category of an aseptic inflammatory reaction and the only obvious role played by the mononuclear phagocyte system is the classical role of scavenging interstitial debris.

Animals↗

PubMed1985

Mouse peritoneal cells exposed to sodium aurothiomalate in vivo.

The localization of gold in normal, stimulated and activated mouse peritoneal cells exposed in vivo to sodium aurothiomalate was examined by a new histochemical technique based on physical development. Activated macrophages from mice infected with herpes simplex virus type II showed the greatest amount of gold localized within lysosomes. Mast cells contained gold in their granules. Polymorphonuclear leucocytes and lymphocytes, on the other hand, were devoid of gold. Pinocytosis is discussed as the mechanism by which gold is taken up into the cells.

Animals↗

PubMed1985

The permeability of normal, adenomatous, ulcerative colitic and malignant large bowel epithelial cell membranes to inulin.

We measured the permeability of normal, adenomatous, colitic and malignant large bowel epithelial cells by immersing fragments of large bowel mucosa in radiolabelled inulin and comparing autoradiograph grain density inside and outside cells after incubation. All the carcinomas studied showed extensive uptake of inulin within 5 min, while normal, adenomatous and colitic epithelial cells completely excluded inulin for 30 min. We found no difference in the proportion of epithelial cells incorporating uridine into RNA in carcinomatous and normal mucosa, and this suggests that the increased inulin permeability of carcinoma cell membranes was not due to leakage into non-viable cells. Experiments with cytochalasin B also showed that increased pinocytosis by carcinoma cells could not account for the difference. The relative impermeability of adenomatous and colitic cells suggests that increased permeability is not caused by increased proliferation. The consistent finding of increased permeability in the plasma membranes of carcinoma cells suggests that this may be more than an epiphenomenon of malignancy. It also suggests that measurement of cell permeability may have a role in distinguishing malignant from benign epithelial neoplasms.

Adenoma↗

PubMedDate not supplied

[Vesicular transport of nutrients in the small intestine during natural feeding].

Ultrastructural aspects of the absorption of nutrients by the rat small bowel under natural feeding and administration of a food mixture homogenate to a small bowel strip were studied. It is shown that as early as 25 min after the onset of feeding, nutrients get into the proximal part of the small bowel, run across the epithelial barrier and enter the stroma of the intestinal villi and the vascular bed. Active absorption of nutrients is also observed in situ under limited intracavitary hydrolysis. The identified nutrients penetrate the apical membrane of enterocytes by pinocytosis, are detectable but inside vesicular structures of the cell, and get into the intercellular space by exocytosis. The concept of the existence of the control systems preventing foreign substances from penetration in the body and eliminating the sequels of such a penetration has been worded.

Animal Nutritional Physiological Phenomena↗

PubMed1978

[Pathobiochemical aspects of lysosomal enzymes with special reference to lysosomal storage diseases (author's transl)].

Lysosomal hydrolases participate substantially in the degradation of all classes of biological macromolecules. They act physiologically within the lysosome. The enzymes are either primarily included within primary lysosomes or are transported to these cell organelles after secretion and subsequent adsorptive pinocytosis. The involvement of these enzymes in a variety of pathological conditions can be understood on the basis of the known functions of lysosomal hydrolases. Inactivity of one or several of the enzymes causes lysosomal storage disorders. Similar metabolic consequences are found when the enzymes are unable to be concentrated within the lysosome. Lysosomal hydrolases participate, furthermore, in the pathogenesis of numerous diseases. A distinction can be made between lysosomal overload, pathologically-increased enzyme secretion into the extracellular space, and a release of lysosomal enzymes into the cytosol.

Acid Phosphatase↗

PubMed1975

[A method for the study of relations between the lung and the reticulo-endothelial system].

The experiments reported in this paper draw attention to three new facts : 1) the reticulo-endothelial system (RES) of normal Rat can be " filled " with a non toxic, polymeric substance, PVNO, which is taken up by macrophages by pinocytosis ; 2) a broncho-pulmonary irritation leads to a discharge of PVNO by the macrophage. The macrophages are poured out into the blood stream, whence they arrive in to the lung ; 3) this discharge of a polymer as PVNO which has been previously taken in the macrophage, can happen even 10-12 months after the filling of the RES by the macromolecule.

Animals↗

PubMedDate not supplied

[Interaction of lambda bacteriophages with mammalian cells. II. Elucidation of the role of interacting components].

The study of 3H-thymidine labelled bacteriophage lambda C185757 uptake by HeLa, RH and Chinese hamster cell revealed the lack of cells or phage specificity in the phage interaction with cells. The phage uptake is shown to be an active process depending on the cell state. The mechanism of "protective" action of calcium chloride is found to be as follows: the calcium phosphate precipitate formed in phosphate-containing media absorbs the phage, thus increasing its concentration on the cell surface, which makes the pinocytosis more effective.

Animals↗