Distribution and Valence State of Radiochromium in Intracellularly Labeled Ehrlich Mouse Ascites Carcinoma Cells.

Rajam, P. C.; Jackson, Anne-Louise

doi:10.3181/00379727-99-24298

Cited by 24 publications

(9 citation statements)

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“…It had been assumed that chromium is complexed to macromolecular protein (Henney, 1973;Ferluga & Allison, 1974;Martz, Burakoff & Benacerraf, 1974;Steinitz & Weiss, 1975), but there was no clear data supporting this view, and at least two earlier reports that the chromium occurred as a small molecule (Ronai, 1969;Rajam & Jackson, 1958). It had been assumed that chromium is complexed to macromolecular protein (Henney, 1973;Ferluga & Allison, 1974;Martz, Burakoff & Benacerraf, 1974;Steinitz & Weiss, 1975), but there was no clear data supporting this view, and at least two earlier reports that the chromium occurred as a small molecule (Ronai, 1969;Rajam & Jackson, 1958).…”

Section: Assay Of Cell Death By Release Of Isotope Markers ( I ) Genementioning

confidence: 99%

The Mechanism of Lymphocyte‐mediated Cytotoxicity

Sanderson

1981

Biological Reviews

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Summary 1. Three classes of cytotoxic lymphocyte are discussed: thymus‐derived T cells, antibody‐dependent K cells and NK (natural killer) cells. Each of these cytotoxic lymphocytes has receptors allowing the formation of adhesions (contact) with a target cell (the cell to be killed). The type of receptor and the corresponding ligand on the target cell is different in each class. Cytotoxic T cells (and probably NK cells) react with a target cell antigen, in a manner rather like antibody‐antigen reactions (although not involving classical serum antibody). K cells have a receptor for the Fc part of immunoglobulin (IgG) and hence can make contact with antibody‐coated target cells. 2. It seems likely that all three classes of cytotoxic lymphocyte have a similar basic mechanism of killing, which is different from the membrane leakage occurring in complement‐mediated lysis. Much more information is available on cytotoxic T cells than on the other types of cell. 3. Cytotoxic T cell killing can be divided into two phases. A reversible phase in which the T cell is in contact with the target cell, but causes no apparent damage. This phase can vary from a few minutes up to several hours, when a single T cell interacts with a single target cell. If the T cell detaches or is inactivated the target cell survives. The second phase is irreversible, once the lethal event has occurred, and the target cell will progress to eventual lysis in the absence of the Tc cells. 4. The lethal event initiates a period of zeiosis (membrane blebbing) in the target cell, which is accompanied by increased effiux of 86rubidium. Cell lysis occurs at a variable time after the initiation of zeiosis, when the soluble contents of the cytoplasm burst out of the target cell. The fact that both these phases are of variable length leads to the accumulation of cytoplasmic markers (such as 51chromium) in the medium in an approximately linear fashion. 5. The nature of the lethal event is unknown, but it is suggested that it involves changes inside the target cell rather than at the target cell membrane. Remarkable long projections from the T cell (and also seen from K cells and NK cells), apparently arising as a result of the receptor‐ligand interaction, may be involved in the delivery of the lethal event.

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Section: Assay Of Cell Death By Release Of Isotope Markers ( I ) Genementioning

confidence: 99%

The Mechanism of Lymphocyte‐mediated Cytotoxicity

Sanderson

1981

Biological Reviews

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“…Most intracellular chromium in erythrocytes incubated with 51-chromate is protein bound, largely to the P-chain of the globin moiety of hemoglobin (8). There is evidence that hexavalent chromate (Cr VI) is reduced to the trivalent state (Cr III) before, or during the binding to hemoglobin (9), and after uptake into Ehrlich ascites cells (10) and leukocytes (11). Cr III does not exist in biological systems in a simple cationic form but rather as coordination compounds with substituent groups of low molecular weight compounds, such as glutathione, or larger molecules, such as proteins (6,12).…”

Section: Methodsmentioning

confidence: 99%

Chromate transport in human leukocytes

Lilien¹,

Spivak²,

Goldman³

1970

J. Clin. Invest.

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A B S T R A C T Chromium is a trace metal of importance in human physiology and, in addition, as 51-chromate, has been extensively used as a label in the study of blood cell pool sizes and intravascular kinetics. The transport characteristics of 51-chromate were investigated in normal human leukocytes. Chromate uptake is unidirectional over a 1 hr incubation with extracellular chromate concentrations up to 200 omoles/liter. Under these conditions, intracellular 51-chromium is in a form in which it is nonexchangeable. Influx is temperature sensitive with a Qio of approximately 2 and may be energy dependent since a variety of metabolic poisons strongly inhibit uptake. The unidirectional influx of chromate follows Michaelis-Menten kinetics; the maximum velocity is 52 m/moles/g dry weight of cells per min and the chromate concentration at which influx velocity is half maximal is 87 /Lmoles/liter. This transport mechanism is highly specific for chromate; other divalent tetrahedral anions only slightly inhibit influx at concentrations up to 10 times that of chromate. Metavanadate, however, competitively inhibits chromate influx at equimolar concentrations. Exposure of cells to unlabeled chromate leads to inhibition of subsequent influx of 51-chromate. It is suggested that this is due to a primary inhibitory effect of chromate on cellular energy metabolism.

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“…Uptake of 51Cr, released by labeled host tissues into the me dium, by the HeLa cells is improbable. Most of the soluble chromium released from cells is trivalent [11], hence does not penetrate the intact plasma membrane. Organotypical co cultivation of HeLa cells and labeled host tissues with inter position of a piece of vitelline membrane, where invasion does not occur and where the 51Cr-activity of HeLa and host tissue can be measured separately, showed that the HeLa cells take up less than 0.5 % of the total 51Cr (unpublished results).…”

Section: Discussionmentioning

confidence: 99%

Invasion of Malignant Cells into <sup>51</sup>Cr-Labeled Host Tissues in Organotypical Culture

Mareel¹,

Bruyne²,

Ridder³

1977

Oncology

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We have attempted to quantitate malignant invasion in vitro. Therefore we adapted the 51Cr-release cytotoxicity test to organotypical culture systems, that proved useful for morphological analysis of invasion. We counted ⁵¹Cr-release from labeled fragments of embryonic chick heart and mesonephros, cultured either on semisolid or in fluid medium, during their invasion by HeLa cells. Although demonstrated morphologically, malignant invasion did not bring about significant changes of ⁵¹Cr-release as compared to control cultures without HeLa cells. The failure of the ⁵¹Cr-release test in our experimental device might shed some light on the mechanisms of malignant invasion.

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Distribution and Valence State of Radiochromium in Intracellularly Labeled Ehrlich Mouse Ascites Carcinoma Cells.

Cited by 24 publications

References 0 publications

The Mechanism of Lymphocyte‐mediated Cytotoxicity

The Mechanism of Lymphocyte‐mediated Cytotoxicity

Chromate transport in human leukocytes

Invasion of Malignant Cells into <sup>51</sup>Cr-Labeled Host Tissues in Organotypical Culture

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