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R Averdunk

Publications and source records attributed to R Averdunk.

At least 37 records · Page 2Linked to original sources
PubMed1979

Zinc metabolism in normal, lectin-stimulated and leukemic lymphocytes.

Gel filtration of the cytoplasmic fraction of homogenate from human peripheral lymphocytes incubated with 65Zn gave five separate peaks with molecular weights of greater than 150,000, 90,000, 65,000, 20,000, and less than 1000 daltons. Peaks I--IV consisted of proteins. The low molecular weight (peak V) may consist of nucleotides, polyamines and amino acids. After gel filtration 75-80% of the 65Zn activity was found in peak V. Lectin-induced stimulation of normal lymphocytes revealed a distribution pattern of 65Zn binding similar to that of unstimulated cells. There was only a slightly enhanced incorporation into the protein peaks I--IV. When peripheral lymphocytes of B lymphocyte origin from patients with chronic lymphocytic leukemia were incubated with 65Zn the same peaks were seen as with supernatants obtained from normal lymphocytes. Lectin-induced stimulation of leukemic lymphocytes had no significant effect on the 65Zn distribution pattern.

Carrier Proteins↗
PubMed1977

Differentiation between various effects of cytotoxic fractions of lymphocyte culture medium.

This paper describes the partial characterization of supernatants derived from mitogen stimulated lymphocytes by ammonium sulfate precipitation, ultrafiltration on Hollow-Fiber beakers and gelchromatography. Fractions from these purification procedures were tested on FL-target cells and the following target cell alterations were measured: RNA- and protein synthesis, 3H-TdR incorporation, cell number and lysis of target cells. Target cell alterations of control fractions from supernatants of non-stimulated lymphocytes, from culture medium and from FCS were compared to the effects of fractions from activated lymphocytes. 3H-TdR incorporation was not only inhibited by the fractions of activated lymphocyte cultures but also by fractions of various controls. Inhibition of 3H-TdR incorporation disappeared when control fractions were serially diluted. Only fractions of supernatant from activated lymphocytes could lyse target cells. It were the same fractions which still inhibited 3H-TdR incorporation of target cells after serial dilution and which showed stimulating effects on RNA synthesis. MW of fractions which were differentiated from control fractions with respect to target cell lysis were: 90,000, 45,000 and lower than 20,000 d.

Cell Line↗
PubMed1976

[Effect of trenimon on single phases of the cell cycle of Yoshida ascites tumor cells (author's transl)].

Yoshida ascites tumor cells were synchronized in suspension cultures with thymidine in excess or with fluordeoxyuridine. Cells were washed after incubation with thymidine or treated with thymidine after incubation with fluordeoxyuridine. 2 h after terminating the S phase blockade 74--80% of the cells are S phase cells, 6 h later 70--80% of the cells had accumulated in the G 2 phase. Cultures enriched with cells of the S phase or the G 2 phase were treated with Trenimon. Increase of cell numbers within the following 48 h was inhibited in both cases in the same order of magnitude. In addition cells in various phases of growth were separated by density gradient zentrifugation and treated with Trenimon. Again cell numbers after 48 h were identical.

Animals↗
PubMed1976

[Studies on the mechanism of activation of lymphocyte membrane ATP-ases by concanavalin A (author's transl)].

The ouabain-sensitive and ouabain-intensitive ATP-ases of intact lymphocytes, and of the lymphocyte microsomal fraction and a purified plasma membrane fraction, are all activated by concanavalin A. The Na+, K+, and Mg+-dependence of the plasma membrane ATP-ases were defined at different substrate concentrations. Enzyme activation was rather greater at lower K+ concentrations. From these studies it appears improbable, but not impossible, that concanavalin A exerts an allosteric effect on the ATP-ases.

Adenosine Triphosphatases↗
PubMed1976

[Concanavalin A induced changes of lymphocyte p-nitrophenylphosphatase (author's transl)].

The effect of K+, Na+, Mg2+ and ATP on the p-nitrophenylphosphatase activity was investigated. As an enzyme preparation a microsomal fraction of sheep lymphocytes was used. Low concentrations of Mg2+, K+ and Na+ increased, whereas high concentrations decreased the enzyme activity. There was an inhibition of activity by ATP without Na+ in the incubation medium and an increase of enzyme activity at low K:Na-ratio. By concanavalin A in a concentration of 15 mug/ml the p-nitrophenylphosphatase activity was increased in intact cells and the microsomal fraction for 30-40%. The activation was not Na+, K+, Mg2+, p-nitrophenylphosphate or ATP dependent.

4-Nitrophenylphosphatase↗
PubMed1976

[Action of the "Ca-ionophore" X-537A on the electrolyte content and metabolism of Yoshida ascites tumour cells: a model for the analysis of Mg deficiency (author's transl)].

X-537A, an ionophore for divalent cations, causes a rapid replacement of extracellular Na+ by intracellular K+ in Yoshida ascites tumour cells. The loss of K+ is prevented by high extracellular concentrations of K+. In incubation solutions containing Ca2+, the Ca2+ content of the tumour cells increases in the presence of X-537A, but the Mg2+ content is not affected. The intracellular level of cyclic AMP is also increased. In all the incubation media used, the presence of X-537A resulted in a decrease in biosynthesis in the order RNA greater than DNA greater than protein, at constant ATP concentration. The observed changes in the content of electrolytes and cyclic AMP, and on the metabolism of DNA, RNA and protein in Yoshida ascites tumour cells in response to X-537A, correspond to those observed during Mg deficiency in these cells. These changes are caused by changes in the intracellular concentrations of Ca2+ and/or K+.

Animals↗
PubMed1975

[The role of cyclic AMP and Ca in the altered permeability of tumour cells grown with a deficiency of Mg].

Yoshida-Ascites tumour cells grown with a deficiency of Mg show an increased passive permeability. This results in an accelerated efflux of Na+. The uptake of aminobutyric acid is decreased, while its release is unchanged. The uptake and release of alpha-methylglucopyranoside are unchanged. In the cells grown with a deficiency of Mg, the concentration of cyclic AMP is slightly increased. The addition of dibutyryl cyclic AMP results in similar but smaller changes in the cellular concentration of cations, to those found in Mg deficiency. It is suggested that the effects of Mg deficiency result from the action of cyclic AMP and/or an increase in the Ca concentration of the cell.

Animals↗