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Biomedical subjects

J Vormann

Publications and source records attributed to J Vormann.

At least 37 records · Page 2Linked to original sources
PubMed1995

Magnesium deficiency induces joint cartilage lesions in juvenile rats which are identical to quinolone-induced arthropathy.

Quinolones accumulate in cartilage, and because they form chelate complexes with divalent cations, they possess the potential to induce a deficiency of functionally available magnesium. To test the hypothesis that quinolone-induced arthropathy is caused (or aggravated) by magnesium deficiency in cartilage, we induced magnesium deficiency by feeding juvenile rats a magnesium-deficient diet for 9 days and treated the rats with single oral doses of ofloxacin (0, 100, 300, 600, or 1,200 mg/kg of body weight) during this period. Additional groups of juvenile rats on a normal diet were treated with ofloxacin correspondingly. Typical cartilage lesions (e.g., swollen matrix, cleft formation) were found in knee joints of all magnesium-deficient rats, including those without ofloxacin treatment. Lesions in these groups were not distinguishable from lesions induced by a single dose of 600 mg of ofloxacin per kg of body weight or higher in rats on a normal diet. Ofloxacin levels in plasma after 600 mg/kg of body weight were approximately 10-fold higher than those in humans during therapy with this quinolone. Lesions in rats treated with ofloxacin plus magnesium deficiency were more pronounced than those in rats with normal magnesium concentrations. After intake of a magnesium-deficient diet for 9 days, the magnesium concentration in serum (mean +/- standard deviation) was 0.18 +/- 0.05 mmol/liter (control on normal diet, 0.82 +/- 0.10 mmol/liter). Magnesium concentrations in bone (femur) and cartilage (processus xiphoideus) samples were 64.7 +/- 10.5 and 14.3 +/- 3.9 mmol/kg of dry weight, respectively, which corresponded to approximately 50% of the concentrations measured in controls on a normal diet. It was concluded that quinolone-induced arthropathy is probably caused by a deficit of available magnesium in joint cartilage due to the formation of quinolone-magnesium chelate complexes. If juvenile patients must be treated with quinolones for serious infections, it seems prudent to ensure that these patients do not have a disturbed magnesium balance.

Animals↗
PubMed1995

Interactions of polyamines with Mg(2+)-sensitive macroelectrodes and Mg2+ buffers.

The polyamines spermine, spermidine and putrescine interact with Mg(2+)-sensitive macroelectrodes based on the neutral carrier ETH 7025; the interaction in decreasing order being spermine, spermidine and putrescine. The effect is small and dependent on the ionized magnesium concentration ([Mg2+]free), only resulting in a significant increase in the measured [Mg2+]free with spermine and spermidine at [Mg2+]free less than 0.5 mM. The polyamines compete with Mg2+ for common binding sites on Mg2+ buffers such as ATP, ADP and citrate, releasing bound Mg2+ and increasing the [Mg2+]free. This effect is most prominent with Mg ATP and the action of the polyamines in decreasing order is spermine, spermidine and putrescine. Increases in polyamines which occur in cell proliferation and cancer could thus secondarily increase the [Mg2+]free resulting in an activation of Mg(2+)-dependent metabolic pathways.

Adenosine Diphosphate↗
PubMed1995

Buffering and activity coefficient of intracellular free magnesium concentration in human erythrocytes.

Human erythrocytes either untreated or Mg2+(-)loaded by means of A23187 in the presence of 3 or 12 mM MgCl2 were haemolysed by freezing and thawing. In the haemolysates the concentration of total Mg2+ (by atomic absorption spectrophotometry), free Mg2+ (by a Mg2+(-)sensitive electrode) and ATP were determined. The increase in the free Mg2+ concentration was also measured when titrating the haemolysates with MgCl2. The experiments yielded a total Mg2+ buffer capacity of 4.85mM with a Ka of 0.9 mM-1, indicating that 2,3 bisphosphoglycerate was the main Mg2+ buffer in haemolysates of erythrocytes which had been ATP-depleted during preparation. The activity coefficient of free Mg2+ in erythrocytes was the same as in the chloride-based calibration solutions.

Buffers↗
PubMed1994

Interactions of polyamines in the measurement of free magnesium concentration by mag-fura-2 and 31P-NMR.

Polyamines, particularly spermine, in physiological concentrations interact with mag-fura-2 and the mag-fura-2/Mg2+ complex, resulting in reduced values of free Mg2+ concentration. Similarly, polyamines interact with ATP and MgATP. Thus, free Mg2+ concentration, as measured by 31P-NMR or mag-fura-2, is underestimated in the presence of polyamines, particularly of spermine.

Adenosine Triphosphate↗
PubMed1994

Increased Na+/Mg2+ antiport in erythrocytes of patients with cystic fibrosis.

Na+/Mg2+ antiport and Na(+)-independent Mg2+ efflux were investigated in erythrocytes of 41 patients with cystic fibrosis and 26 controls. Na(+)-independent Mg2+ efflux was unchanged in cystic fibrosis, but a significantly increased activity of Na+/Mg2+ antiport was detected (control: 0.16 +/- 0.02, cystic fibrosis: 0.39 +/- 0.06, Mg2+ efflux, mmol/30 min x 1 cells, mean +/- SEM, p < 0.01). An increased activity of Na+/Mg2+ antiport was only found in patients with severe clinical symptoms. There was no correlation of the increased Na+/Mg2+ antiport to the dF508 genotype. In a patient with increased Na+/Mg2+ antiport, the capacity of this transport system was unchanged 14 weeks after double lung transplantation but reached control values after 53 weeks. The sweat of cystic fibrosis patients with severe clinical symptoms showed a significantly increased Mg2+ concentration (control (n = 12): 0.053 +/- 0.08, cystic fibrosis (n = 9): 0.123 +/- 0.016 mmol/l, mean +/- SEM, p < 0.001).

Adolescent↗
PubMed1994

Magnesium metabolism in erythrocytes of patients with chronic renal failure and after renal transplantation.

Plasma and erythrocyte Mg2+ concentrations were found to be increased in 14 haemodialysis patients with chronic renal failure and in 7 chronic renal failure patients receiving chronic ambulatory peritoneal dialysis. The rate of Na+/Mg2+ antiport was significantly higher in haemodialysis patients, but not in chronic ambulatory peritoneal dialysis patients (control: 0.15 +/- 0.02, haemodialysis: 0.46 +/- 0.08, chronic ambulatory peritoneal dialysis: 0.21 +/- 0.06; Mg2+, mmol/30 min x 1 cells). High erythrocyte Mg2+ content in chronic renal failure results from the increased plasma Mg2+, which induces elevated Mg2+ uptake during haematopoiesis. An increased rate of Na+/Mg2+ antiport, which only performs Mg2+ efflux, leads to a relatively lower erythrocyte Mg2+ content in haemodialysis patients compared with chronic ambulatory peritoneal dialysis patients. The elevated Na+/Mg2+ antiport in erythrocytes from haemodialysis patients was almost normalised after haemodialysis. Incubation of normal erythrocytes with heat-inactivated plasma from haemodialysis patients led to a doubling of Na+/Mg2+ antiport, indicating the presence of a heat-stable, dialysable plasma factor. This factor does not accumulate in chronic ambulatory peritoneal dialysis patients. After renal transplantation all changed quantities of Mg2+ metabolism returned to normal.

Adult↗
PubMed1994

Effect of oxygen free radicals on Mg2+ efflux from erythrocytes.

Hydrogen peroxide destroyed the Na+/Mg2+ antiport in Mg(2+)-loaded human and rat erythrocytes and increased the leakage of intracellular Mg2+ and K+. These effects are opposite to the increase of Na+/Mg2+ antiport and unchanged Na(+)-independent Mg2+ efflux from erythrocytes of patients with cystic fibrosis score 3. Thus, the increase of Na+/Mg2+ antiport in these patients is not caused by increased formation of free radicals.

Animals↗
PubMed1993

Perinatal development of iron and antioxidant defence systems.

The time course of malondialdehyde (MDA), Fe, vitamin E, superoxide dismutase (Cu, Zn-SOD) and glutathione peroxidase (GSH-Px) was measured in serum, liver, kidney and heart from rats between day 17 of gestation and day 20 after birth. MDA was higher in fetal than maternal tissues and showed a transient increase after birth. The low maternal MDA levels were reached later than 3 weeks after birth. Fe was higher in fetal than in maternal serum and liver. Five days after birth Fe drastically dropped in these tissues. The antioxidant factors vitamin E, Cu, Zn-SOD and GSH-Px were low in fetal tissues and rose after birth. It is discussed whether lipid peroxidation is increased in fetal tissues because of less-developed antioxidant defence mechanisms.

Animals↗
PubMed1992

Isoproterenol-induced Mg2+ uptake in liver.

Isoproterenol increased the Mg2+ content of hepatocytes after injection into rats or after addition to collagenase-dispersed hepatocytes. cAMP also the increased cellular Mg2+ content of isolated hepatocytes. This effect was prevented by staurosporine. Phorbol ester had no effect on the Mg2+ content of isolated hepatocytes, and after injection of isoproterenol into rats, protein kinase C of liver was not affected. It was concluded that isoproterenol induced long-term Mg2+ influx via the activation of protein kinase A which can be inhibited by staurosporine.

Alkaloids↗
PubMed1992

Activation of Na+/Mg2+ antiport in thymocytes by cAMP.

Mg2+ efflux from Mg(2+)-loaded rat thymocytes was stimulated by 0.1 mM dibutyryl cAMP (db cAMP). The activation of Mg2+ efflux by db cAMP was more expressed at lower Mg(2+)-loading. cAMP induced only a very small increase in the concentration of intracellular free Mg2+ which cannot explain the activation of Na+/Mg2+ antiport. From these results it was concluded that cAMP increases the affinity of the Na+/Mg2+ antiporter for intracellular Mg2+, probably by phosphorylation.

Animals↗
PubMed1992

Kinetics of beta-glycerophosphate-induced endochondral mineralization in vitro. Calcium accumulation, alkaline phosphatase activity, and effects of levamisole.

Isolated mesenchymal limb bud cells from day-12 mouse embryos grown at high density in organoid culture at the medium/air interphase differentiate into chondrocytes and form cartilage nodules. Upon addition of beta-glycerophosphate (beta-GP), cartilage undergoes endochondral mineralization. This beta-GP-induced mineralization was investigated by measuring the calcium content in the cultures and the activity of alkaline phosphatase (AP) in the cell mass and the medium. Calcium incorporation depended on the amount of beta-GP added. After continuous treatment, mineralization began on day 8 of the culture period and increased linearly until day 15. In long-term cultures, periodical treatment for 6 days caused an increase in mineralization the older the cultures were, but the slope of increase was proportionately less steep. Treatment at the latest period on days 19-24 resulted in a markedly reduced mineralization. After short-term treatment (48 hours), mineralization increased also the older the cultures were and proceeded during further cultivation in beta-GP-free medium. This kinetic behavior indicates a dependency of mineralization on cartilage maturation in this in vitro system. AP activity increased enormously and nearly logarithmically in the cell mass in beta-GP-free medium, whereas beta-GP treatment inhibited this drastic increase. In the medium, considerable activities of AP were also measurable from day 10 onward. It increased in beta-GP-free medium up to day 14, but was diminished after mineralization had been induced. Levamisole inhibited AP activity dose dependently when added directly to the enzyme-containing medium (100% inhibition at 10(-3) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1992

Mineral metabolism in erythrocytes from patients with cystic fibrosis.

In patients with cystic fibrosis plasma concentrations of Zn and Mg were unchanged, plasma Ca concentrations were somewhat decreased, but plasma Fe concentrations were drastically reduced; the ratio Cu/Fe in plasma was increased. The Mg and Zn contents of erythrocytes from patients were unchanged. Therefore, the Mg and Zn content of erythrocytes cannot serve for the detection of patients with cystic fibrosis and their heterozygotes, as has been suggested. Cl(-)-dependent Mg2+ efflux from Mg(2+)-loaded erythrocytes was not affected in cystic fibrosis. Na(+)-dependent Mg2+ efflux was increased only in erythrocytes from patients with the most severe clinical symptoms.

Adolescent↗
PubMed1992

Sex-related effects of zinc deficiency on the selenium metabolism in rats.

The effects of a low zinc status on selenium metabolism were investigated in female and male rats which were fed diets with low and adequate zinc contents and a suboptimal selenium content. For the selenium content and glutathione peroxidase activity in the liver and plasma of the female animals no differences were found between the low zinc group and the pair-fed zinc-adequate control group. In the male rats zinc depletion resulted in testis atrophy and decreased testicular contents of selenium and glutathione peroxidase. In the pair-fed and ad libitum-fed control groups the levels of hepatic selenium and glutathione peroxidase and plasma glutathione peroxidase in the males were lower than those in the females. In the low zinc group, however, they rose to the levels of the females. The results indicate that these effects of zinc deficiency on selenium metabolism are sex-specific and suggest that they are related to changes in the sex hormone status of the male animals.

Animals↗
PubMed1991

Protection against salicylate-induced hepatic injury by zinc. A histochemical and biochemical study.

Female Wistar rats received an oral dose of 700 mg salicylic acid/kg body wt., given as sodium salicylate. Some of the salicylate-treated rats received two subcutaneous injections of 100 mumol kg-1 ZnCl2 (24 h before and simultaneously with the salicylate administration). Other animals were given one subcutaneous injection of 100 mumol kg-1 ZnCl2 simultaneously with the salicylate treatment. Control rats were similarly injected with ZnCl2. Twenty four hours after salicylate treatment, serum and livers were taken for histochemical and biochemical analysis. The most remarkable effects of the treatment were enrichment of lipid droplets and iron and a reduction of glycogen, particularly in the periportal hepatocytes. The effects of salicylate were partially prevented by two ZnCl2 injections. The protective effects of ZnCl2 may be due to lower iron uptake into hepatocytes and by the induction of zinc metallothionein, which can serve as a scavenger for oxygen radicals.

Alanine Transaminase↗
PubMed1991

Effects of Fe, salicylate and Zn on metallothionein and lipid peroxidation in vivo.

Control rats and rats pretreated with two i.p. injections of 15 mg/kg Fe, given as FeCl3, received either one oral dose of 700 mg/kg salicylic acid, given as Na salicylate, or 100 mumol ZnCl2/kg s.c., or salicylate and ZnCl2. In the rats given Fe this treatment was simultaneous with the second iron injection. Salicylate and Fe alone caused a small increase in lipid peroxidation (LPO) measured as malondialdehyde formation in the liver by means of the thiobarbiturate method. When given together, however, Fe and salicylate caused a drastic increase of LPO in liver, which was reduced by the simultaneous injection of ZnCl2. Hepatotoxicity as determined histochemically by lipid storage paralleled LPO. The protective effect of Zn on LPO and hepatotoxicity was not correlated to metallothionein induction in liver. The protective effect of Zn can be explained by the competition of Fe with Zn for binding to salicylate which reduces Fe-salicylate-induced LPO and hepatotoxicity.

Animals↗
PubMed1990

Characterization of Na(+)-independent Mg2+ efflux from erythrocytes.

Na(+)-independent Mg2+ efflux from Mg2(+)-loaded human, rat and chicken erythrocytes was reduced by extracellular Cl-. Na(+)-independent Mg2+ efflux at low extracellular Cl- concentration (sucrose medium) was inhibited by SITS and was nearly insensitive to SITS in 150 mM choline Cl medium. The inhibition of Mg2+ efflux by extracellular Cl- and DIDS could be overcome by the lipophilic permeant tetraphenylphosphonium cation. Na(+)-independent Mg2+ efflux from human and rat erythrocytes in sucrose and choline Cl medium was inhibited by cAMP and by amiloride and amiloride analogues. The results indicate that Na(+)-independent Mg2+ efflux in high Cl- medium is performed by a similar or the same Mg2+ efflux system, operating in sucrose medium in which the efflux of Mg2+ is accompanied by the efflux of Cl- for charge compensation.

Animals↗
PubMed1990

Induction of Mn2+/H+ antiport in chicken erythrocytes by intracellular Mg2+ and Mn2+.

Chicken erythrocytes preloaded with Mg2+ exchange one extracellular Mn2+ for two intracellular H+. Chicken erythrocytes preloaded with Mn2+ alone or with Mg2+ plus Mn2+ performed efflux of Mn2+, which was higher at pH 6 than at pH 7.4, indicating reversibility of Mn2+/H+ antiport. Mn2+/H+ antiport was not inhibited by 1 mM KCN plus 1 mM iodoacetic acid or 1 mM amiloride. Mn2+ influx was activated by anions. Mn2+ efflux via Mn2+/H+ antiport was inhibited by competition between H+ and K+.

Animals↗