lasalocid and Magnesium-Deficiency

lasalocid has been researched along with Magnesium-Deficiency* in 1 studies

Other Studies

1 other study(ies) available for lasalocid and Magnesium-Deficiency

Article	Year
[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)]. Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie, 1976, Volume: 14, Issue:7 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+. Topics: Animals; Anti-Bacterial Agents; Biological Transport, Active; Calcium; Energy Metabolism; Lasalocid; Magnesium; Magnesium Deficiency; Mice; Models, Biological; Neoplasm Proteins; Nucleic Acids; Potassium; Sarcoma, Yoshida; Sodium	1976

Article

Year

[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)].

Journal of clinical chemistry and clinical biochemistry. Zeitschrift fur klinische Chemie und klinische Biochemie, 1976, Volume: 14, Issue:7

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+.

Topics: Animals; Anti-Bacterial Agents; Biological Transport, Active; Calcium; Energy Metabolism; Lasalocid; Magnesium; Magnesium Deficiency; Mice; Models, Biological; Neoplasm Proteins; Nucleic Acids; Potassium; Sarcoma, Yoshida; Sodium

1976