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Biomedical subjects

M Inbar

Publications and source records attributed to M Inbar.

At least 91 records · Page 5Linked to original sources
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↗