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Biomedical subjects

T Günther

Publications and source records attributed to T Günther.

At least 145 records · Page 8Linked to original sources
PubMed1986

Protein kinase C in cytosol and cell membranes of concanavalin A-stimulated rat thymocytes.

In concanavalin A-treated thymus cells and phytohemagglutinin-treated spleen cells, the distribution of protein kinase C is changed. Shortly after addition of plant lectins, the activity of protein kinase C increased in the cytosol and decreased in the particulate fraction. 2 h later, the activity of protein kinase C decreased in the cytosol and increased in the particulate fraction. Membrane binding of protein kinase C and tion of DNA synthesis showed the same dependency on concanavalin A concentration. A long-term membrane binding of protein kinase C seems to be essential for lymphocyte stimulation.

Animals↗
PubMed1986

Alteration of prostanoid metabolism in rats with magnesium deficiency.

Plasma and tissue concentrations of prostanoids PGE2, PGF2 alpha. 6-keto-PGF1 alpha (a stable metabolite of prostacyclin) and TXB2 (a stable metabolite of thromboxane A2) were measured in normal and magnesium-deficient rats. The mean values for prostanoids in plasma were significantly higher in magnesium-deficient rats than in normals (515 +/- 43 vs 296 +/- 31 pg/ml for 6-keto-PGF1 alpha, p less than 0.01, 3700 +/- 322 vs 346 +/- 33 pg/ml for TXB2, p less than 0.001 and 1234 +/- 132 vs 434 +/- 51 pg/ml for PGE2, p less than 0.001). Tissue levels of prostanoids were also significantly higher in magnesium-deficient rats as compared to normals. The increased synthesis of prostanoids is apparently linked to enhanced influx and translocation of Ca++ into the cells. If the adenylate cyclase is inhibited in magnesium deficiency, the lowered c-AMP will permit a high cyclooxygenase activity and a drastic increase in TXB2. It is possible that the changes in prostaglandin synthesis in magnesium deficiency are linked to the development of different diseases.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Functional compartmentation of intracellular magnesium.

Due to the distribution of Mg2+-binding ligands, such as DNA, RNA, or Mg2+-binding proteins, e.g. within the intermembranous space of mitochondria, intracellular magnesium is compartmentalized. Furthermore, cytosolic free Mg2+ is enriched at charged surfaces. Thus, the exact concentration of free intracellular Mg2+ can only be ascertained for a small volume element. Compartmentation of intracellular Mg2+ can also be determined by flux measurements with 28Mg2+. In different cell types, cellular Mg2+ is exchanged with different velocities, and, in some cell types, rapidly and slowly or non-exchangeable compartments are detectable. Cells can be Mg2+-depleted gradually by incubation with A23187 and EDTA. In cells which are Mg2+-depleted gradually, the Mg2+-dependent metabolic functions are inhibited in the following sequence: glycolysis, RNA, DNA synthesis, respiration, protein synthesis, protein synthesis appears to be the most sensitive function affected.

Animals↗
PubMed1985

Mg2+ efflux is accomplished by an amiloride-sensitive Na+/Mg2+ antiport.

Mg2+ efflux from Mg2+-preloaded chicken erythrocytes is caused by an electroneutral Na+/Mg2+ antiport. It depends specifically on extracellular Na+, according to Michaelis-Menten kinetics (Km = 25 mM), and is reversibly noncompetitively inhibited by amiloride (Ki = 0.59 mM). In contrast to Na+/H+ antiport, Li+, Ca2+ and N-ethylmaleimide do not interfere with Na+/Mg2+ antiport. The Na+/Mg2+ antiport is driven by the intracellular/extracellular Mg2+ gradient.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1985

Electrolytes and ventricular arrhythmias.

Magnesium concentrations in the blood plasma of patients with ventricular arrhythmias were found to be significantly lower than in controls, whereas the sodium and calcium concentrations of the erythrocytes were significantly higher than in the controls. Intensive magnesium therapy resulted in an increase of the plasma magnesium concentration and in significant changes of Na, K, Ca and Mg in the erythrocytes. By means of long-term ECG recordings, it was shown that the therapy may result in a quantitative decrease of the ventricular arrhythmias.

Aged↗
PubMed1984

Magnesium deficiency and hypertension: correlation between magnesium-deficient diets and microcirculatory changes in situ.

Rats maintained for 12 weeks on diets moderately or more severely deficient in magnesium showed significant elevations in arterial blood pressure compared to control animals. Examination of the mesenteric microcirculation in situ revealed that dietary magnesium deficiency resulted in reduced capillary, postcapillary, and venular blood flow concomitant with reduced terminal arteriolar, precapillary sphincter, and venular lumen sizes. The greater the degree of dietary magnesium deficiency the greater the reductions in microvascular lumen sizes. These findings may provide a rationale for the etiology, as well as treatment, of some forms of hypertensive vascular disease.

Animals↗
PubMed1984

Enzyme histochemistry of malignant T cell lymphoma due to chronic magnesium deficiency in rats.

The lymphocytes of the rat thymus can be grossly differentiated by their cell membrane-bound proteinases. Subcapsular thymocytes lack aminopeptidase A (APA) and AMP and gamma-glutamyltranspeptidase (GGT). Cortical thymocytes show a high activity of APA but no APM and no GGT. Medullar thymocytes possess a high GGT and APM activity but are free of APA. Under Mg deficiency, the APA-negative subcapsular thymocytes are reduced. In lymphoma and beginning lymphoma, APA, APM and GGT are absent. In lymphoma, the alkaline phosphatase activity is increased. Differences are found for dipeptidylpeptidase IV (DPP IV). In some lymphoma, its activity is reduced, in others the DPP IV activity is increased.

Alkaline Phosphatase↗
PubMed1984

Effect of magnesium injection on foetal development.

Pregnant rats were subcutaneously injected twice daily with 1.5 ml 150 mmol/l MgCl2 beginning at day 5 of gestation. By this treatment development of foetal liver and pancreas was enhanced. In the foetal liver, there was a precocious glycogenolysis combined with a precocious development of the smooth endoplasmic reticulum (ER) and an irregular arrangement of the rough ER. In the pancreas, the development of secretory granules was enhanced. In alizarin red-stained and cleared specimens, the foetal skeleton was less calcified. The injected Mg2+ remained extracellular. Altered hormonal secretion and/or an altered activity of the regulatory enzymes of glycogen metabolism induced by the increased extracellular Mg2+ concentration are discussed as possible mechanisms for enhanced foetal liver development.

Animals↗
PubMed1984

Mechanism of the increased cardiac Ca2+ uptake induced by isoprenaline in DOCA-salt pretreated rats.

Desoxycorticosterone acetate (DOCA)-salt supersensitivity to isoprenaline (isoproterenol) was demonstrated by the increase in cardiac Na+ and Ca2+ content and by the decrease in cardiac Mg2+ content that occurs at lower isoprenaline doses in DOCA-salt pretreated rats compared to control rats. The number of beta-adrenoceptors in the myocardium as measured by [3H]-dihydroalprenolol binding amounted to 170 +/- 18 fmol/mg protein in normal rats and to 150 +/- 17 fmol/mg protein in DOCA-salt pretreated rats. The dissociation constant amounted to 2.6 +/- 0.4 nmol/l for normal and to 2.8 +/- 0.5 nmol/l for pretreated rats. The isoprenaline-induced increased cardiac Ca2+ content in DOCA-salt pretreated rats can be explained by the increased adenylate cyclase activity and by the resulting increased Ca2+ influx via phosphorylated calciductin.

Adenylyl Cyclases↗
PubMed1984

Membrane alterations in magnesium-deficiency-induced malignant T cell lymphoma.

Malignant T cell lymphoma cells induced in the thymus by chronic Mg deficiency showed a less ruffled surface in the scanning electron microscope, particularly after intraperitoneal transplantation. Their content of phosphatidylserine and phosphatidylinositol was increased. The content of phosphatidylcholine, cholesterol and the cholesterol/phospholipid ratio, and thus membrane microviscosity, were decreased. The activity of phospholipid methyltransferase I and II was reduced. In parallel to these alterations, 45Ca2+ influx and efflux as well as 45Ca2+ content in mitochondria, microsomes and cytosol of lymphoma cells were enhanced.

Animals↗
PubMed1983

Dependence of noise-induced hearing loss upon perilymph magnesium concentration.

Noise-induced hearing loss (NIHL) is significantly greater in rats fed a magnesium-deficient diet than in rats on a magnesium-rich diet. The hearing loss was found to be negatively correlated with the magnesium concentration of the perilymph. It is suggested that also in man, the magnesium concentration in the perilymph may be of importance in determining susceptibility to NIHL.

Animals↗
PubMed1983

Foetal and maternal magnesium metabolism: effect of magnesium deficiency and isoproterenol.

Pregnant rats were fed diets with an Mg2+ content of 40, 12, 6 and 3 mmol/kg from day 10-19 of pregnancy. There was a linear correlation of non-protein bound Mg2+ between foetal and maternal serum, between amniotic fluid and maternal serum, and between foetal serum and amniotic fluid, the ratios being 2.7, 2.0 and 1.3 respectively, indicating active transport of Mg2+ up to a constant concentration gradient by the placenta. In hearts, increases of Na+ and Ca2+, and decreases of Mg2+ and K+ were observed only in the group receiving the lowest Mg2+ supply. After i.v. injection of MgCl2 to pregnant rats, Mg2+ was slowly transported from maternal to foetal serum and more slowly into the amniotic fluid. The effect of isoproterenol on cardiac electrolyte content in pregnant rats was less than in non-pregnant rats, and the effect of isoproterenol in foetal rats was smaller than in maternal rats. These results are explained by inactivation of isoproterenol in the placenta, by the small diaplacental transport of isoproterenol and by a smaller isoproterenol-stimulation of foetal cardiac adenylate cyclase.

Amniotic Fluid↗
PubMed1983

Role of magnesium in cardiac disease.

Some aspects of the pathogenesis of cardiac disease are reviewed in the light of current knowledge of the physiological and biochemical actions of magnesium (Mg2+) on heart function. Several authors have reported a reduction of the human myocardial Mg2+ content in areas with (Mg2+ poor) soft water, without a significant alteration of Mg2+ in serum or skeletal muscle. In human during myocardial infarction, there is a reduction of Mg2+ content even in noninfarcted areas of the myocardium, followed by a transient reduction of serum Mg2+ concentration. These effects are explained by the action of catecholamines on the myocardial cells, resulting in a loss of Mg2+ accompanied by a catecholamine-induced urinary Mg2+ loss and/or increased lipolysis which binds Mg2+ as Mg2+ soaps in the adipocytes. As a consequence serum Mg2+ may be decreased. A reduced serum Mg2+ concentration may enhance the action of catecholamines on the heart muscle as well as the action of vasopressive hormones, thus provoking contraction of coronary artery smooth muscle cells and favouring the development of arrhythmia.

Arrhythmias, Cardiac↗
PubMed1982

Development and properties of malignant lymphoma induced by magnesium deficiency in rats.

Female wistar rats were fed on an Mg-deficient diet. After 8 to 10 weeks, the thymus glands were strongly degenerated and the number of lymphocytes was reduced, especially in the cortex. Thymus degeneration was associated with a decreased rate of DNA, RNA, and protein biosynthesis and necrosis and phagocytosis of lymphocytes. The degeneration was normalized after feeding on an Mg-rich diet. After 10 or 11 weeks of Mg deficiency, local cell proliferations of immature lymphocytes with a great number of free ribosomes were found in some thymus glands. The local cell proliferations developed into infiltrating tumors without metastases. In lymphoma cells the Na+ and Ca2+ content, the turnover of cellular Na+ and K+, and the aerobic production of CO2 and lactate were increased.

Animals↗
PubMed1982

Increased noise trauma in guinea pigs through magnesium deficiency.

Mg-deficient guinea pigs developed significantly increased hearing loss during 4 weeks of noise exposure [95 dB(A)] as compared to animals fed a Mg-rich diet. The hearing loss was negatively correlated to the Mg content of the perilymph (r = -0.86). Besides this auditory effect, there was a decrease of intracellular Mg and an increase of collagen in the myocardium, both of which were correlated to the hearing loss and caused by Mg deficiency and noise stress.

Animals↗
PubMed1981

Embryotoxic effects of magnesium deficiency and stress on rats and mice.

Pregnant rats an mice received a magnesium (Mg)-deficient diet with different Mg contents from 40 t 360 ppm. The control received 2,000 ppm. At the end of gestation, the Mg concentration in the maternal serum was found to have decreased by up to 0.3 mmole/liter, depending on the Mg content of the food. Mg-dose-dependent embryotoxic effects (resorptions, retardation, disturbed bone development, and skeletal malformations) were observed only below a threshold value of 0.7 mmole/liter of the maternal serum Mg concentration. Noise stress in rats, in addition to a mild Mg deficiency (360 ppm Mg), which by itself had no effects, increased the rate of resorptions only.

Animals↗
PubMed1981

Biochemistry and pathobiochemistry of magnesium.

The kinetic and thermodynamic effects of Mg2+ on enzyme reactions and the effects of Mg2+ on nucleic acids and phospholipids are reviewed. Since the action of Mg2+ is depending on the Mg2+ concentration, the distribution, and the metabolism of Mg2+ in the extracellular, and the various intracellular compartments are discussed. The main result is that the intracellular Mg2+ is buffered at a level of pMg 3. In experimental Mg deficiency, cell permeability increases, as a consequence of which intracellular Na+, Ca2+ and secondarily, cAMP become elevated, whereas intracellular K+ decreases. Catecholamines are released to a higher extent, an effect that is potentiated by stress. The metabolic consequences of Mg deficiency are caused by the altered intracellular electrolyte, especially the Ca2+ concentration.

Calcium↗