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At least 973 records · Page 54Linked to original sources
PubMed1993

Chronic myeloid leukemia granulocytes have lower amounts of cytoplasmic actin.

Chronic myeloid leukemia (CML) granulocytes had earlier been shown to be defective in microfilament mediated phenomena such as chemotaxis and fluid phase pinocytosis when compared to normal granulocytes. The present studies were carried out to determine whether a quantitative alteration in actin or a change in isoform status could be responsible for some of the defects. Relative proportions of beta and gamma isoforms were found to be unaltered between normal and CML granulocytes. The amount of actin was significantly lower in CML cells. When the actin was expressed as percent of total protein in the granulocytes, it was found to be significantly lower in CML cells. The lower amount of actin may be responsible for some of the defects seen in CML cells.

Actins↗
PubMed1987

Differential uptake of neutral red by macrophages from three species of estuarine fish.

Macrophage endocytosis is part of the immune response to foreign material and includes the processes of phagocytosis, ingestion of particulate material, and pinocytosis, the uptake of liquid droplets. This work reports the development of a quantitative method to measure in vitro uptake of neutral red by fish macrophages, based on the spectrophotometric measurement of ingested neutral red dye. We have used this method to monitor the rates of uptake in three species of fish: spot, Leiostomus xanthurus; hogchoker, Trinectes maculatus; and summer flounder, Paralichthys dentatus. For the species tested, there appeared to be an intrinsic pattern of uptake which was highest in flounder, lowest in hogchoker and intermediate in spot. The excellent reproducibility of this assay should make it useful for detecting toxicological effects in the environment.

Animals↗
PubMed1986

Neurochemical coupled actions of transmitters in the microvasculature of the brain.

The discovery that monoamine nerves end on the central microvessels of the choroid plexus, pia-arachnoid and parenchyma has prompted an intense investigation as to their physiological and neuropathological roles. The source of the monoamine fibers to the pial vessels and choroid plexus was shown to be the superior cervical ganglion. Ganglionic stimulation causes vasoconstriction or vasodilation of pial vessels, an event depending upon the functional ratio of alpha to beta adrenergic receptors. Moreover, stimulation of the superior cervical ganglion evokes an inhibition of cerebrospinal fluid formation in choroid plexus. The locus coeruleus is the site of adrenergic nerve supply to the parenchymal capillaries and stimulation of this nucleus increases capillary permeability to small molecules and water. Neurotransmitter receptors (adrenergic, histamine, adenosine, dopamine, prostacyclin, prostaglandins and specific amino acids or neuropeptides) have been identified on microvessels and in many instances these transmitter actions are coupled to cyclic AMP synthesis. Moreover, cyclic AMP has been shown to increase the rate of capillary endothelial pinocytosis and produce brain edema. In small vessels containing smooth muscle cells cyclic AMP production improves cerebral blood flow via an initiation of vasodilatory processes. The presence of receptors for serotonin and acetylcholine have likewise been demonstrated to occur on cerebral microvessels. Limited information is available as to the receptor coupled actions of these two transmitters, but cholinergic mechanisms may act to restrict catecholamine-induced formation of cyclic AMP. Altered sensitivity of microvessels to neurotransmitters has been demonstrated following conditions of stroke, hypertension, aging, diabetes and X-irradiation.

Acetylcholine↗
PubMed1988

Neuronal and glial gap junctions in the goldfish preoptic area, a thin section and freeze-fracture study.

In freeze-fracture, both large macular gap junctions and long thin gap junctions surrounded by a strand of tight junction were found on neurosecretory cells. Preoptic neurons show large areas of soma-to-soma apposition, but thin section showed no evidence for gap junctions between neuronal somata. Neurosecretory cell neurites formed parallel bundles in neuropil lateral to the nucleus, and gap junctions were found between the neurites. These junctions apparently correspond to macular junctions seen on neurosecretory elements in freeze-fracture. Some large macular gap junctions found in freeze-fracture presumably correspond to junctions seen between glial cells in thin section. However, glial membranes lacked characteristics distinguishing them from neuronal membranes. In one instance, a large apparent glial sheet process formed both macular and long thin gap junctions on different surfaces. The long thin gap junctions that were surrounded by a strand of tight junction were formed with a large neurosecretory cell soma. Extensive pinocytosis was observed at some membranes forming gap junctions.

Animals↗
PubMed1986

Further studies on the effect of chloroquine on the uptake, metabolism and intracellular translocation of [35S]cystine in cystinotic fibroblasts.

The present study uses the lysosomotropic drug chloroquine to investigate the mechanisms by which exogenous [35S]cystine is able to label the intracellular (intralysosomal) cystine pool(s) in cystinotic fibroblasts. When cystinotic fibroblasts were labelled for short periods of time (8 h or less), chloroquine (20 microM) inhibited the labelling of the intracellular cystine pool(s). However, when the cells were labelled for longer periods of time (24 h or more) chloroquine stimulated the labelling of the intracellular cystine pool(s). The short-term effect was selectively abolished when the cells were washed free of chloroquine, while the long-term effect was selectively abolished when the medium was depleted of cystine. Two routes of translocation of exogenous cystine to the lysosomes could be defined. One route was fast, had a low capacity, was inhibited by chloroquine and increased with increasing medium pH, while the other route was slow, had a high capacity, was stimulated by chloroquine and was more active at low pH. The former pathway probably consisted of plasma membrane transport of cystine into the cytosol followed by direct or indirect transport into the lysosomes. The latter route possibly consisted of pinocytosis with fusion of the cystine-containing pinosomes with lysosomes.

Biological Transport↗
PubMed1996

Ultrastructural changes in the respiratory lamellae of the catfish, Heteropneustes fossilis after sublethal exposure to malathion.

Transmission electron microscopy study of the gills of Heteropneustes fossilis, exposed to 4 mg/liter of malathion (1/3 of LC50) for 24, 48, 72, and 96 h showed significant changes in its ultrastructures. Exposure to the pesticide after 24 h caused a slightly disarrayed condition in the double layered epithelial structure. Lymphatic spaces became more apparent, and a few chloride cells appeared which protruded toward the peripheral margin of the secondary lamellae. Chloride cells were exposed to the exterior by an apical pit. Pinocytosis was observed with marginal folds (MF) originating from the pillar and epithelial cells. Some vascular constrictions were also seen in the capillaries with erythrocytes. After 48 h exposure, the outer epithelial cells were stretched into a thin boundary wall and lymphatic spaces were engorged with plasma exudate. Chloride cells transversed the whole epithelium of the lamella and came into direct contact with lymphoid space and exterior to epithelial lining. Basement membrane of the capillaries became thicker. After 72 h a distorted lamellar epithelium ruptured in a few places allowing many spheroid bodies and some chloride cells come out. Marginal folds of pillar cells migrated into vascular spaces. Basement membrane of capillaries became thicker and blood channels were constricted causing vascular stasis. No erythrocytes were visible. Blood channels were filled with leukocytes and amoebocytes. After 96 h exposure to malathion narrowing of lymphatic spaces, proliferation of epithelial cells and development of pinocytotic vesicles from marginal folds of pillar cell flanges were observed. Only marginal blood channels maintained normal configuration. Vascular stasis due to thickening of the basal lamina were still evident in centrally located blood channels filled with leukocytes. Vascular stasis would likely cause a decrease in respiratory efficiency. This study has revealed that the gills of H. fossilis were affected by a sublethal dose of malathion. The ultrastructural damages to the gills were observed as early as at 24 h exposure, but the most severe damage occurred at 72 h exposure. However, signs of gill structure regeneration were seen in malathion-exposed fish after 96 h.

Journal Article↗
PubMed1988

On the mechanism of transfer of heavy metals across cell membranes.

In rat jejunal mucosa cells, Cd bound to the outside of the brush border can be distinguished from internalized Cd by its reaction with extracellular chelators; internalized Cd is only released after destruction of the cell. Similar results have been obtained with rabbit erythrocytes and resealed ghost cells. A temperature-dependent process carries Cd from the EDTA-sensitive into the EDTA-insensitive compartment. In enteric cells, only 1/3 of the external binding sites permit subsequent internalization. EDTA does not remove Hg from cell ligands, but internalized Hg can be distinguished from externally bound Hg with the help of dimercaptopropanol; internalization of Hg bound to active membrane sites must be relatively rapid. Internalization of Cd and Hg by ghost cells and by isolated membrane vesicles, as described elsewhere, suggests that the process is independent of pinocytosis. The results therefore support a previously suggested model describing the movements of non-essential and poisonous metals across cell membranes in terms of a non-specific binding step, followed by what may represent the activity of mobile carriers.

Animals↗
PubMed1989

Methyl phosphonate as a 31P-NMR probe for intracellular pH measurements in Dictyostelium amoebae.

Methyl phosphonate at concentrations up to 20 mM was found to be non toxic towards the growth of Dictyostelium amoebae and the starvation-induced differentiation program. In contrast, phenyl phosphonate at the same concentrations was found to inhibit growth. Methyl phosphonate possessed good 31P-NMR characteristics for use as a pH probe in Dictyostelium. The entry of methyl phosphonate into the cytoplasm required about 150 min of incubation before an equilibrium was reached with added extracellular methyl phosphonate. A semilogarithmic plot of the efflux of methyl phosphonate out of the amoebae was linear as a function of time, and the kinetic first-order constant was k = 0.016 min-1. The kinetic parameters were consistent with an uptake of methyl phosphonate by fluid-phase pinocytosis. The pH calculated from the chemical shift of the internalized methyl phosphonate signal was found to be pH 7.4 in aerobic Dictyostelium amoebae. The intracellular methyl phosphonate environment turned more acidic in response to anaerobiosis (delta pH = 0.8) or in the presence of a weak acid such as propionate. These pH determinations were in agreement with the values of cytosolic pH derived from the chemical shift of Pi. Methyl phosphonate should be a useful probe for pH measurements in 31P-NMR studies of Dictyostelium in situations where the signal of Pi cannot be attributed with certainty.

Dictyostelium↗
PubMed1989

The low uptake of an abrin A-chain immunotoxin by rat hepatic cells in vivo and in vitro.

The therapeutic value of antibody-ricin A-chain conjugates (immunotoxins) as antineoplastic agents is limited by their rapid removal from the circulation, primarily by cells of the liver which take up the immunotoxin through receptor mediated recognition of mannose-containing oligosaccharides in the toxin A-chain. We have therefore examined the uptake by rat hepatic cells of a monoclonal antibody (LICR-LOND Fib 75) conjugate assembled with the ricin related, but carbohydrate free, A-chain of the plant toxin abrin. The abrin A-chain immunotoxin was very poorly taken up in vivo and in vitro by both hepatic parenchymal and non parenchymal cells whereas a comparable conjugate assembled with ricin A-chain was actively accumulated by liver cells particularly the hepatic non-parenchymal cells. Furthermore, the abrin A-chain immunotoxin uptake by non-parenchymal cells in vitro was unaffected by mannose and the immunotoxin bound less readily to liver cells than did the ricin A-chain conjugate, consistent with a proposal that its accumulation by hepatic cells is brought about by endocytosis following non-specific binding or by fluid phase pinocytosis. These results suggest abrin A-chain immunotoxins might be further explored as anti-cancer agents since in some cases they could have an improved therapeutic efficacy over immunotoxins constructed with ricin A-chains.

Abrin↗
PubMed1995

Regulation of glutamine and glucose metabolism by cell volume in lymphocytes and macrophages.

The effects of osmotically and sucrose-induced cell volume changes on glutamine and glucose metabolism were investigated in rat lymphocytes and macrophages incubated for 10-60 min at 37 degrees C in Krebs-Henseleit bicarbonate buffer (pH 7.4). Decreasing extracellular osmolarity from 336 to 286 mOsmol by decreasing medium NaCl from 119 to 94 mM increased cell volume and the rates of glutamine metabolism and glycolysis in both cell types. Conversely, increasing extracellular osmolarity from 286 to 386 mOsmol by the addition of 50 and 100 mM D-mannitol progressively decreased both cell volume and the rates of glutamine and glucose metabolism in lymphocytes and macrophages. At the same medium osmolarity of 336 mOsmol, the rates of glutamine metabolism and glycolysis were greater with the addition of 50 mM sucrose than with that of 25 mM NaCl. The sucrose-induced increase in cell volume, which is due to the uptake of sucrose by lymphocytes and macrophages via pinocytosis, is associated with enhanced rates of glutamine metabolism and glycolysis. Our findings suggest that cell volume change may be a hitherto unrecognized mechanism for regulating metabolism in lymphocytes and macrophages. The enhanced glutamine and glucose metabolism in these cells in response to mitogenic stimulation or immunological activation may result, at least in part, from the concomitant increase in cell volume.

Animals↗
PubMed1992

Cholesterol and mevalonic acid modulation in cell metabolism and multiplication.

Cholesterol in animals is a major structural component of cell membranes. It may therefore play a functional role in the modulation of cell osmolarity, the process of pinocytosis and the activities of membrane-associated proteins such as ionic pumps, immune responses, etc. A major relationship exists between the cell-growth processes and the cholesterol biosynthetic pathway. The cholesterol needed for new membranes may be derived either from endogenous synthesis or from exogenous sources, principally plasma low-density-lipoproteins (LDL) which enter the cells by receptor-mediated endocytosis. Both these pathways are enhanced in rapidly growing cells. Conversely, if synthesis is inhibited and no exogenous cholesterol is available, cell growth is blocked. The 3-hydroxy-3-methylglutaryl CoA (HMGCoA) reductase (the rate-limiting reaction in cholesterol biosynthesis) is the enzyme which catalyzes the conversion of HMGCoA to mevalonic acid. It has been suggested that mevalonate may play an important role in cell proliferation. All cells need at least two products synthesized from mevalonate in order to proliferate, and the only one yet identified is cholesterol. Other melavonate-derived potential candidates as cell-cycle and cell-survival products include the dolichols ubiquinone side chains, isopentenyladenosine derivatives, etc. Furthermore, it has recently been shown that membrane association appears to be an important function in mevalonate-derive modifications of several important proteins such as cellular membrane G proteins, those coded for by oncogenes (ras proteins) and lamins (nuclear proteins). In recent years the development of cholesterol-synthesis-inhibiting drugs, for lowering plasma cholesterol levels has mainly been centred on the control of HMGCoA reductase activity (vastatins). However, because mevalonic acid is the precursor of numerous metabolites, any reduction of such activity may potentiate pleiotropic effects. Vastatins are now, therefore, receiving increased attention as potential pharmacological tools for the control of abnormal cell growth in pathological situations, i.e. tumours and vascular smooth muscle cell proliferation under atherogenic conditions. In our laboratories, we have demonstrated that simvastatin can prevent arterial myocyte proliferation both in vivo and in vitro. Simvastatin can also inhibit in vitro the rate of human glioma cell growth, since it shows a strong synergistic inhibitory effect on cell proliferation when used in association with anticancer agents such as Carmustine or beta-interferon. Both simvastatin-induced cell growth inhibition and the synergy observed with these drugs can be completely reversed by incubating cells with mevalonate. This shows that the effect of simvastatin of cell proliferation is due to its specific inhibitory activity on intracellular mevalonate synthesis.

Animals↗
PubMed1992

Cellular and humoral mechanisms of immunotoxicological tissue manifestations induced by immunotoxic drugs.

The adverse effects on the immune system resulting from acute and subchronic exposure to immunotoxic compounds can be divided into the following three categories. One is the tissue manifestations induced by either immunosuppressive or immunomodulative compounds through the interactions of the drug or its metabolites with cellular/humoral constituents directly or indirectly. For the detection, the functional tests especially NK activity in short-term administration were found to be valuable in the assessment of immunotoxicity of drugs in comparison with hematological and morphological alterations. The second is manifested as an allergic reaction, consisting of three sequential events: (1) sensitization by the exposure of a drug primarily recognized as an antigen; (2) the interaction of antigen and antibody and/or sensitized mononuclear cell (M), and its sequelae, which initiate the chain of events leading to tissue injury: and (3) tissue injury and inflammation. The third is manifested as autoimmunity. Of these, in the first two reactions, a primary manifestation seems to be cellular injury. In this experiment, the morphological and biochemical changes occurring in the cultured cells were analyzed when the compound was added to cultured cells obtained from (a) normal animals, (b) drug-sensitized animal models prepared by using drug-protein conjugates, and (c) animals administered drugs at the dosage equivalent to therapeutic dose. When a test compound was added to short cultured sensitized M, morphological responses observed were characterized by either diffuse swelling of the cells and decrease of pseudopod movement, or gradual shrinking. No such changes were observed in non-sensitized M. In contrast, when immunosuppressants or immunomodulators were used, increases of pseudopod movement and pinocytosis, and excitation of cytoplasmic movement, were observed in both sensitized and non-sensitized M if compounds were cytotoxic. In both cases, inflammatory cytokines responsible for tissue damage were released from the M. Little release of these factors was observed from the non-stimulated cells. For the third category, an attempt is being made to analyze autoimmune disorders immunotoxicologically by using experimentally induced MDP-arthritis in rodents.

Animals↗
PubMed1992

Uptake, distribution and fate of bacterial lipopolysaccharides in monocytes and macrophages: an ultrastructural and functional correlation.

Bacterial lipopolysaccharides (LPS), which are important components of the cell wall of gram-negative bacteria, induce a number of host responses both beneficial and harmful. The present review elucidates the uptake, distribution and functions of LPS in mononuclear phagocytes in an attempt to gain an insight into the mechanisms which control the pathogenesis of LPS mediated septic shock. The unique feature of LPS bilayer structure, the tagged LPS and antibodies to LPS provide means for studying binding, uptake, fate and subcellular distribution of LPS in tissues and cells. LPS bind to monocytes and macrophages by specific interaction via receptors such as scavenger receptors, CD14 and CD18 and by non-specific interactions, and enter the cells via receptor-mediated endocytosis, absorptive pinocytosis, phagocytosis, and diffusion. The ingested LPS are localized in pinocytic vesicles, phagocytic vacuoles, cytoplasm, mitochondria, rough endoplasmic reticulum, Golgi apparatus, and nucleus. The interactions of LPS with monocytes and macrophages trigger a broad spectrum of cellular responses, including production of important bioactive factors or mediators, such as IL-1, TNF, interferons, prostaglandins, and macrophage-derived growth factor, which are implicated in the pathogenesis of septic shock and wound healing. However, there is no conclusive evidence indicating that production of the mediators can only be induced through specific interactions.

Animals↗
PubMed1996

Large vesicle formation within cells induced by treatment with a mixed surfactant.

MDCK cells have been treated with a mixed surfactant at low concentrations to study the induced morphological changes. The most significant change at the light microscope level was the appearance of multiple large vesicles, which increased in size with time, up to approximately 40 microns in diameter. Vesicle formation was shown to be linked with the uptake of the fluid medium, as judged by the presence of FITC-dextran within the vesicles, but was not a result of pinocytosis because cytochalasin D treatment had no effect on their formation. Furthermore, nile red staining demonstrated that the vesicles did not represent fusion of pre-existing lipid droplets. Transmission electron microscopy (TEM) analysis indicated that the vesicles lacked any obvious structure. It is hypothesised that the vesicles are large mixed structures synthesised as a result of interactions between cell membranes and detergent components after saturation with the surfactants. This effect is contrasted with the diffuse uptake of dyes and fluorescently labelled proteins following simple anionic or ionic detergent treatment. The effect of vesicle formation was reversible if the cells were placed in fresh medium lacking detergent. Other effects of mixed detergent included the loss of rounded compact colonies, an increase in mean cell diameter and the almost complete loss of surface microvilli as seen with scanning electron microscopy (SEM). In the TEM the cell ultrastructure was seen to have changed markedly following detergent treatment, with a loss of rough endoplasmic reticulum and an apparent clumping of the cytoplasmic constituents.

Animals↗
PubMed2005

Preparation and characterization of active site protected poly(ethylene glycol)-avidin bioconjugates.

Avidin was modified with poly(ethylene glycol) in the presence of a biotin binding site protective agent synthesised by imminobiotin conjugation to branched 20 kDa PEG. Avidin was incubated with imminobiotin-PEG and reacted with high amounts of 5, 10 or 20 kDa PEG to modify the protein amino groups. Circular dichroism demonstrated that the extensive PEGylation does not alter the protein conformational structure. The affinity of avidin-PEG conjugates for biotin and biotinylated antibodies depended on the PEG size or the use of a protective agent. Avidin-PEG 10 and 20 kDa prepared in the presence of imminobiotin-PEG maintained 100% of the native affinity for biotin. The 5 kDa PEG derivative and the ones obtained without biotin site protection maintained 79-85% of the native affinity. The affinity for biotinylated antibodies decreased to 35% when the conjugation was performed without imminobiotin-PEG, while the conjugates obtained with high-molecular-weight PEGs in the presence of protective agent displayed high residual affinity. All conjugates possessed negligible antigenicity and immunogenicity. PEGylation greatly prolonged the avidin permanence in the circulation, reduced its disposition in the liver and kidneys and promoted accumulation into solid tumors. PEGylation was found to prevent the protein cell uptake, either by phagocytosis or pinocytosis.

Animals↗
PubMed2004

Induction of dendritic cell maturation by IL-18.

IL-18 is a pluripotent proinflammatory cytokine produced primarily by antigen presenting cells involved in numerous aspects of immune regulation most notably on lymphoid cells. The effect of IL-18 stimulation on cells in the myeloid compartment, however, has been poorly studied. Human monocytes did not respond to IL-18. However, the human myelomonocytic cell line KG-1 and monocyte-derived dendritic cells (generated by GM-CSF+IL-4) showed a marked increase in CD83, HLA-DR, and several costimulatory molecules upon stimulation with IL-18. Furthermore, IL-18 decreased pinocytosis of these cells and increased their ability to stimulate alloreactive T cell proliferation, all characteristics of mature dendritic cells. These results suggest that IL-18 is involved in the maturation of myeloid DCs, but not differentiation of monocytes into DCs. The finding that IL-18 is involved in the maturation of dendritic cells is both novel and unexpected and indicates another important role for IL-18 as a key regulator of immune responses.

Cell Line↗
PubMed2004

Influences of dissolved and colloidal organic carbon on the uptake of Ag, Cd, and Cr by the marine mussel Perna viridis.

The cross-flow ultrafiltration and radiotracer techniques were used to study the influences of natural dissolved organic carbon (DOC) and colloidal organic carbon (COC) on the bioavailability of Ag, Cd, and Cr to the green mussel Perna viridis. We examined the uptake of these metals by the mussels at different concentrations of DOC and COC from different origins (estuarine, coastal, and diatom decomposed). Using the DOC originating from the decomposed diatom (Thalassiosira pseudonana), we demonstrated that Cd and Cr uptake, quantified by the concentration factor (DCF), increased linearly with increasing DOC concentration. There was, however, no consistent influence of natural DOC concentration on the metal uptake when the DOC was obtained from different sources of seawater (coastal and estuarine). The influences of COC on metal bioavailability were metal-specific and dependent on the geochemical properties of colloids and colloid-metal complexation. Cd uptake rate was not influenced by the COC concentrations. Uptake of diatom-decomposed colloidal Cr was enhanced by 3.4x, whereas the uptake of diatom-decomposed colloidal Ag was decreased by 8.2x compared with the uptake of low molecular weight Cr and Ag (<1 kDa). The uptake of diatom-decomposed colloidal Cr and Ag was generally lower than the uptake of metals bound with the same type of colloids for 2 days. Further aging of the colloid-metal binding reduced metal bioavailability to the mussels. In the presence of different sizes of colloidal particles where there was no major binding of colloids with the metals, metal uptake by the mussels was not influenced by different COC concentrations. Overall, our study suggests that although metal dissociation from colloids may be an important step for the uptake of colloidal metals, other mechanisms such as pinocytosis and co-transport may also be involved in the uptake of these metals, especially in aquatic environments with high DOC and COC concentrations.

Animals↗
PubMed2006

On the mechanism of apoptosis-inducing activity of human calprotectin: zinc sequestration, induction of a signaling pathway, or something else?

Calprotectin, a heterodimer present in neutrophil cytoplasm, has antimicrobial and apoptosis-inducing activities. At the moment, there are two general hypotheses about the mechanism of action of calprotectin: (i) exclusion of extracellular zinc by calprotectin, and consequently induction of apoptosis; (ii) binding of calprotectin to a cell membrane receptor, and consequently, activation of a signaling pathway for apoptosis. Here, we introduce another hypothesis, i.e. inhibition or destruction of "target" inside cells. We suggest that calprotectin might become internalized non-specifically, maybe in a process like pinocytosis. This process is probably independent of the zinc concentration. We also demonstrated that the internal target hypothesis successfully predicts cell survival behavior of cultured cells as a function of calprotectin concentration. Additional analyses should be performed to elucidate the real calprotectin "target".

Adenocarcinoma↗