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J Vormann

Publications and source records attributed to J Vormann.

69 records · Page 4Linked to original sources
PubMed1986

Characterization of furosemide-sensitive Mg2+ influx in Yoshida ascites tumor cells.

Partially Mg2+-depleted Yoshida ascites tumor cells took up Mg2+ after reincubation in Mg2+- and HCO3(-)-containing media. Mg2+ influx was insensitive to ouabain, amiloride and disulfonic stilbenes, but was noncompetitively inhibited by furosemide (Ki = 0.4 mM) and bumetanide. Mg2+ influx obeyed Michaelis-Menten kinetics with respect to Mg2+ concentration (Km = 1.1 mM) and was sigmoidal with respect to HCO3- concentration. Electroneutral Mg2+, HCO3- cotransport was supposed to be the mechanism of Mg2+ influx.

Amiloride↗
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↗
PubMed1984

Regulation of intracellular magnesium by Mg2+ efflux.

Chicken erythrocytes were loaded with Mg2+ by incubation with the cation ionophore A 23187 in the presence of Mg2+. After removing A 23187 by intensive washing with serum albumin and reincubating the Mg2+-loaded cells, Mg2+ was transported out of the cells until the original Mg2+ content was achieved. The net Mg2+ efflux followed Michaelis-Menten-kinetics and was independent of extracellular and intracellular Ca2+ and calmodulin. The net Mg2+ efflux was not affected by adrenalin, isoproterenol, p-chloromercuribenzenesulfonate, ouabain and tetrodotoxin, but was inhibited by dicyclohexylcarbodiimide, KCN, iodoacetate, high extracellular concentrations of Mg2+, Mn2+ and when extracellular Na+ was substituted by choline or K+. The efflux of 1 Mg2+ was coupled with the uptake of 2 Na+. It is concluded that there exists an additional gating process at the inner cell surface becoming active only at increased concentrations of intracellular free Mg2+ regulating the exit of Mg2+ by the efflux system.

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

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

Influence of decreased and increased magnesium supply on the cardiotoxic effects of epinephrine in rats.

Female Sprague-Dawley rats kept on a standard chow or on a magnesium (Mg)-deficient diet during 6 days received s.c. injections of 0, 25, 50, 100 and 200 micrograms of epinephrine (Ep). 1 h before, they were orally treated with 0, 125 or 250 mg of Mg/kg b.w. given as magnesium aspartate hydrochloride. Drug-induced changes were studied by analyzing serum and cardiac tissue samples (Mg, Ca, K, Na and in addition glucose, FFA, cholesterol and creatine kinase in serum) taken at 7 different times (15 to 420 min) after treatment with Ep; effects were evaluated by considering the respective areas under the concentration-time curves (AUC). AUCs were calculated with linear and logarithmic graduation of the time-scale and were also transformed into logarithms. In additional experiments, animals of both diet groups were treated with Mg and Ep as described above and the hearts, excised after 420 min, were prepared for histological examination. Cardiotoxic effects induced by adrenergic overstimulation were aggravated by Mg deficiency. Most pronounced electrolyte alterations and histologically detectable cardiac necroses were observed in the Mg-deficient animals at 420 min following the s. c. injection of 200 micrograms of Ep. On the other hand, oral Mg treatment induced hypermagnesemia and reduced toxic effects of Ep--especially Ca overload of the heart muscle--in controls and in Mg-deficient rats.

Animals↗
PubMedDate not supplied

Lipid peroxidation and morphology of rat testis in magnesium deficiency.

Male Wistar rats were fed diets with different Mg content, ranging from 70 to 850 ppm Mg, for 30 days. After 0, 10, 20 and 30 days, some of the rats were sacrificed for measuring weight, lipid peroxidation, Fe, vitamin E, Na+, K+, Mg2+ and Ca2+ content of testes. After 30 days, the morphology of the testes was investigated by electron microscopy. Mg deficiency induced an increase in weight, Na+, Ca2+ and Fe content and a reduction of K+ and Mg2+ content. Vitamin E content was reduced and the content of malondialdehyde as an indicator of lipid peroxidation was increased. Mg deficiency induced morphological alterations in up to 40% of the spermatids in the 70 ppm Mg group, which consisted: 1) in injured stretching of spermatids; 2) in an irregular arrangement of coarse fibres with missing microtubulus complex (axoneme) and microtubulus sheath; 3) in the development of up to 4 bundles of outer fibrils in one spermatid. The increase of Fe content, lipid peroxidation and the onset of morphological alterations occurred already at a mild degree of Mg deficiency.

Animals↗
PubMedDate not supplied

Iron-induced injury of rat testis.

Male Wistar rats were intraperitoneally injected twice with 0.4 mmol kg-1 FeSO4. One, 2 and 4 days after the second Fe injection, Fe and malondialdehyde (MDA) content in testis was measured, the morphology studied by light and electron microscopy and the number of spermatids counted. After Fe injection, Fe and MDA content had increased in parallel. Light microscopic inspection on days 1 and 2 after Fe injection revealed numerous necroses in the different cell types of the germ epithelium. Four days after Fe injection, fewer alterations were found. Electron microscopic investigations revealed that some spermatids contained up to three nuclei and at least three axonemes. In some sperm tails up to 11 axonemes were found. In some midpieces two or three complexes of axonemes, outer dense fibres and mitochondria were observed. In other midpieces axonemes were absent and replaced by granular and filamentous material. The number of spermatids was reduced 4 days after Fe treatment. The increase in the number of axonemes was similar to that seen in Mg and Zn deficiency, indicating that the increase in Fe content and oxygen free radicals is the major reason for the biochemical and morphological alterations in Mg and Zn deficiency.

Animals↗
PubMedDate not supplied

Comparative evaluation of ultrastructural changes in articular cartilage of ofloxacin-treated and magnesium-deficient immature rats.

Ultrastructural changes in immature articular cartilage were studied after treatment of 5-wk-old rats with ofloxacin-a fluoroquinolone-and in magnesium deficiency. Magnesium deficiency was induced by feeding a magnesium-deficient diet for 9 days; the condition was confirmed by measuring the concentrations of the mineral in plasma, bone, and cartilage samples of the animals by atomic absorption spectrophotometry. Oral administration of single doses of 600 or 1,200 mg ofloxacin/kg body weight and magnesium deficiency were sufficient to induce gross structural cartilage defects. Alterations observed on the ultrastructural level showed striking similarities in magnesium-deficient rats and in rats treated with single doses of 600 mg ofloxacin/kg body weight. Typical observations were (a) bundle-shaped, electron-dense aggregates on the surface and in the cytoplasm of chondrocytes, (b) detachment of the cell membrane from the matrix and necrotic chondrocytes, (c) reduction of the extracellular matrix, and (d) swelling of cell organelles such as mitochondria. These findings further substantiate the histological finding that quinolone treatment and a dietarily induced magnesium-deficiency induce indistinguishable pathological conditions in immature joint cartilage, and they suggest that quinolone-induced arthropathy is probably caused by a reduction of functionally available magnesium (ionized Mg2+) in cartilage (42). Furthermore, they provide a basis for aimed studies with human cartilage samples from quinolone-treated patients that might be available postmortally or after hip replacement surgery.

Aging↗
PubMedDate not supplied

Mg2+ influx into Mg(2+)-depleted reticulocytes.

Mg(2+)-depleted rat reticulocytes reincubated in Mg(2+)-containing media expressed net Mg2+ influx, which was the same in NaCl, choline Cl and sucrose medium. Km of Mg2+ influx amounted to 1.2 mM and Vmax to 0.9 mmol/l cells x h. Mg2+ influx into reticulocytes was inhibited by amiloride, quinidine and imipramine. Mg2+ uptake together with Cl- for charge compensation could be excluded. However, the cation which must be exchanged for Mg2+ in Mg2+ uptake could not be identified because of the low rate of Mg2+ influx.

Animals↗
PubMedDate not supplied

Intracellular Ca(2+)-Mg2+ interactions.

To ascertain possible interactions of intracellular Mg2+ and Ca2+, the concentration of intracellular free Ca2+ ([Ca2+]i) and intracellular free Mg2+ ([Mg2+]i) were experimentally increased within physiological ranges and it was measured by means of fura-2 and mag-fura-2 whether the increased concentration of one divalent cation affected the concentration of the other. A four-fold increase of [Ca2+]i in rat thymocytes by concanavalin A or thapsigargin had no significant effect on [Mg2+]i. Incubation of rat thymocytes in Na(+)-free medium increased [Mg2+]i from 0.35 to 0.7 mM. This increase in [Mg2+]i did not affect [Ca2+]i or the action of thapsigargin on [Ca2+]i.

Amiloride↗