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Biomedical subjects

M Inbar

Publications and source records attributed to M Inbar.

At least 73 records · Page 4Linked to original sources
PubMed1977

Increase in lipid fluidity of cellular membranes induced by adsorption of RNA and DNA virions.

Changes in the dynamic behavior of membrane lipids of mammalian cells induced by adsorption of animal viruses were quantitatively monitored by fluorescence polarization analysis with the aid of the fluorescent probe 1,6-diphenyl 1,3,5-hexatriene embedded in the surface membrane lipid core of intact cells. Adsorption of encephalomyocarditis, West Nile, and polyoma viruses to hamster (baby hamster kidney) and mouse (3T3) cells is accompanied by a rapid and significant increase in the degree of fluidity of membrane lipids of the infected cells. These changes in membrane fluidity, which are virus dose dependent, are inhibited by low temperature and by treatment of the cells before-hand with compounds known to block viral receptors on the cell surface. It is suggested that increase in membrane lipid fluidity, induced by the adsorption of virions, is an early event in the process of cell-virus interactions.

Adsorption↗
PubMed1977

Fluidity of membrane lipids and lateral mobility of concanavalin A receptors in the cell surface of normal lymphocytes and lymphocytes from patients with malignant lymphomas and leukemias.

Lymphocytes isolated from the peripheral blood of patients with nonmalignant and malignant disorders were studied for fluidity of membrane lipids and lateral mobility of concanavalin A (Con A) receptors. The degree of fluidity of the surface membrane lipid core was monitored quantitatively by fluorescence polarization analysis using the probe 1,6-diphenyl-1,3,5-hexatriene embedded in lipid regions of the surface membrane of intact cells. Mobility of Con A surface receptors was determined by the cap-forming ability after binding of fluorescent Con A. The present studies were performed on lymphocytes from 28 patients with malignant lymphomas, 22 patients with leukemia, 28 individuals who either were healthy or had nonmalignant disorders, and 5 patients with carcinoma. The results showed that lymphocytes and mononuclear cells from patients with malignant lymphomas and leukemias have a more fluid lipid layer in their surface membrane than do lymphocytes obtained from healthy individuals or from patients with other malignant and nonmalignant disorders. This increase in membrane fluidity was less pronounced in lymphocytes isolated from leukemic patients in clinical remission and from leukemic patients receiving treatment with steroids. The results also show a marked difference in the cap-forming ability of lymphocytes from patients with malignant lymphomas or leukemia as compared with lymphocytes from patients with non-malignant disorders or carcinoma. Lymphocytes isolated from lymphoma and chronic lymphatic leukemia patients during remission stages of the disease exhibited a higher cap-forming ability. The cap-forming ability of cells from patients with chronic lymphocytic leukemia was unaffected by treatment with steroids. The present results, which are in line with previous observations, have shown that normal lymphocytes can be characterized by a low degree of lipid fluidity but a high degree of mobility of Con A receptors, whereas leukemic lymphocytes are characterized by a high degree of lipid fluidity but a low degree of mobility of Con A receptors. These results confirmed our general hypothesis on the dynamic interrelation between membrane lipids and membrane protein receptors, and they indicate that the widely accepted term "membrane fluidity" requires better consideration for different membrane components.

Carcinoma↗
PubMed1977

Fluidity difference of membrane lipids in human normal and leukemic lymphocytes as controlled by serum components.

Lymphocytes isolated from the peripheral blood of patients with chronic lymphatic leukemia and from normal healthy donors were analyzed for fluidity of membrane lipids. The degree of lipid fluidity in normal and leukemic lymphocytes was quantitatively monitored by a method based on fluorescence polarization analysis of a fluorescent probe that is embedded in lipid regions of cellular membrances. The present studies were performed on lymphocytes isolated from 26 blood samples from 16 patients with chronic lymphatic leukemia and 36 blood samples from 36 normal health donors. A signifcant increase in the degree of fluidity of membrane lipids was found in lymphocytes isolated from leukemic patients as compared to that found for lymphocytes isolated from healthy donors. In vitro incubation of leukemic lymphocytes in normal serum resulted in a decrease in the fluidity of cellular membranes, whereas incubation of normal lymphocytes in leukemic serum resulted in an increase in the fluidity of membrane lipids. These observations suggest that normal and leukemic lymphocytes can be quantitatively characterized by monitoring degree of fluidity of cellular membrane lipids and that the fluidity difference between normal and leukemic lymphocytes is controlled by components in the blood serum.

Adult↗
PubMed1976

Fluidity difference in the surface membrane lipid core of human lymphoblastoid and lymphoma cell lines.

Twenty-five human hematopoietic cell lines established from patients with malignant and non-malignant diseases have been studied for membrane fluidity. The degree of fluidity in the surface membranes was quantitatively monitored by fluorescence polarization analysis of the fluorescence probe, 1,6-diphenyl 1,3,5-hexatriene, when embedded in the lipid region of the surface membrane of intact cells. The results have shown that cells derived from malignant diseases have a more fluid lipid layer in their surface membrane than cells derived from non-malignant disorders. It is, therefore, suggested that a quantitative analysis of fluidity differences in the cell surface membrane lipid core can be of value to the studies on basic differences between normal and malignant cell lines established from the human hematopoietic system.

Burkitt Lymphoma↗
PubMed1976

Microviscosity parameters and protein mobility in biological membranes.

A fluorescence polarization technique with 1,6-diphenyl 1,3,5-hexatriene as a probe were employed to determine the microviscosity, n, in liposomes and biological membranes of different cholesterol to phospholipid mol ratio. From the temperature profile of n the flow activation energy, deltaE, and the unit flow volume, V, were derived. The increase of cholesterol/phospholipid ratio in liposomes is followed by a marked increase in n and a decrease in both deltaE and V. Liposomes of the same phospholipid composition as human erythrocyte membranes display in the extreme cases of cholesterol/phospholipid ratios 0 and 1.4 the values of n(25 degrees C) = 1.8 and 9.1 P, and deltaE = 15.0 and 6.5 kcal/mol, respectively. For most membranes studied the fluorescence polarization characteristics and the corresponding n values are similar to those obtained with these liposomes when the cholesterol/phospholipid level of the liposomes and the membranes were the same. However, unlike in liposomes deltaE of all membranes is in the narrow range of 6.5-8.5 kcal/mol, regardless of its cholesterol/phospholipid level. It is plausible that this is a general characteristic of biological membranes which originates from the vertical movement of membrane proteins to an equilibrium position which maintains constant deltaE and V values. This type of movement should affect the interrelation between lipid fluidity and protein mobility. Lipid microviscosity and the degree of rotational mobility of concanavalin A receptor sites in cell membranes were therefore determined. The examined cells were normal and malignant fibroblasts, as an example of cells that form solid tumours in vivo, and normal and malignant lymphocytes, as an example of cells that form ascites tumours in vivo. In both cell systems, opposite correlations between the lipid fluidity and the mobility of concanavalin A receptors were observed. In the fibroblasts the malignant cells possess a lower lipid fluidity but a higher receptor mobility, whereas in the lymphocytes the malignant cells possess a higher lipid fluidity but a lower receptor mobility. Thus, in these cell systems the degree of rotational mobility of concanavalin A receptors increases upon decreasing the lipid fluidity and decreases upon increasing the fluidity of the lipid core. This dynamic feature is in line with the above proposal according to which the concanavalin A receptor sites become more exposed to the aqueous surrounding upon increasing the microviscosity of the lipid layer and vice versa.

Animals↗
PubMed1974

Cholesterol as a bioregulator in the development and inhibition of leukemia.

Leukemia in mice and humans is accompanied by a marked deficiency of unesterified cholesterol in the surface membrane of leukemic cells as compared to normal leukocytes. This deficiency induces a significant reduction in their membrane microviscosity. Since cholesterol in the cell surface membrane is exchangeable with cholesterol in the serum lipoproteins, concomitant to the cellular deficiency of cholesterol, the average level of cholesterol in the blood serum of leukemic patients is substantially below the average normal level. Based on these observations and the effect of membrane microviscosity on biological functions, a working hypothesis that describes the role of cholesterol in the development and inhibition of leukemia is suggested. This hypothesis can also account for the effect of cholesterol and membrane microviscosity on various other cellular activities of leukocytes.

Cell Membrane↗
PubMed1974

Increase of cholesterol level in the surface membrane of lymphoma cells and its inhibitory effect on ascites tumor development.

An ascites form of malignant transformed lymphoma cells were treated in vitro with liposomes of 1:1 lecithin-cholesterol in order to increase the cholesterol level of the cell-surface membranes and thereby to increase the rigidity of the lipid layer. This treatment was found to inhibit the rate of killing by ascites tumor after intraperitoneal inoculation into adult mice of 10(4) and 10(5) treated cells per animal. With 10(3) treated cells per animal, full survival was observed up to 90 days after inoculation, whereas with the same number of untreated cells all infected mice died within 30 days after inoculation. An analogous treatment of the malignant lymphoma cells with liposomes of pure lecithin did not result in any appreciable inhibitory effect on the ascites tumor development in vivo, as initiated by inoculation of 10(5), 10(4), or 10(3) cells per animal.

Animals↗
PubMed1973

Membrane changes and adenosine triphosphate content in normal and malignant transformed cells.

Transformed fibroblasts had a low content of ATP when grown at a high cell density and a high content of ATP when grown at a low cell density. Concanavalin A agglutinated transformed cells with a low, but not those with a high, ATP content. Transformed cells with a high ATP content gained agglutinability after ATP depletion by inhibitors of the energy-generating systems, and those with a low ATP content lost their agglutinability after restoration of a high ATP content by glucose. Fixation of the surface membrane by formaldehyde, glutaraldehyde, or LaCl(3), inhibited agglutination of cells with an ATP content that allows agglutination. Normal fibroblasts grown at a high or a low cell density were not agglutinated by concanavalin A. Depletion of the cellular ATP content of normal cells induced agglutination only in cells grown at a high, but not at a low, cell density. A similar number of concanavalin A molecules was bound to the surface membrane of agglutinating and nonagglutinating fibroblasts. It is suggested that a high content of ATP inhibits the movement of concanavalin A binding sites, and that a low content of ATP allows, in transformed cells, a new distribution of binding sites to form the clusters required for cell agglutination. Agglutinability of transformed cells is determined by ATP content, and in normal cells changes in the content of ATP are by themselves not sufficient to induce agglutination. Transformed cells, therefore, do not have a control, presumably for membrane stability, that exists in normal cells.

Adenosine Triphosphate↗
PubMed1973

Mobility of carbohydrate-containing structures on the surface membrane and the normal differentiation of myeloid leukemic cells to macrophages and granulocytes.

Clones (D(+)) of a cultured line of myeloid leukemic cells can be induced to undergo normal differentiation to mature macrophages and granulocytes. There are also clones derived from the same cell line (D(-)) that could not be induced to differentiate. The carbohydrate-binding protein concanavalin A was used as a probe to study the mobility of carbohydrate-containing sites on the surface membrane of these cells. Changes in the distribution of concanavalin A binding sites on the surface membrane can be induced by concanavalin A. With the appropriate site mobility, this induction of a new distribution resulted in a concentration of concanavalin A-membrane site complexes on one pole of the cell to form a cap. D(+) and D(-) clones showed 50 and 5% of cells with caps, respectively, although both types of cells bound a similar number of concanavalin A molecules. Treatment of cells with trypsin increased cap formation from 5 to 40% in D(-) cells, but did not change the percentage of cells with caps in D(+) cells. The results show a difference in the mobility of concanavalin A binding sites in these two types of cells and suggest a difference in the fluid state of these carbohydrate-containing structures on the surface membrane. It is suggested that a gain of the ability of myeloid leukemic cells to undergo normal differentiation is associated with an increase in the fluidity of structures on the surface membrane where the concanavalin A sites are located. Differences in fluidity of specific membrane sites may also explain differences in the response of cells to other differentiation-inducing stimuli.

Agglutination↗