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Biomedical subjects

J Vormann

Publications and source records attributed to J Vormann.

At least 55 records · Page 3Linked to original sources
PubMed1990

Characterization of Na(+)-dependent Mg2+ efflux from Mg2(+)-loaded rat erythrocytes.

Na(+)-dependent Mg2+ efflux from Mg2(+)-loaded rat erythrocytes was determined from the increase of extracellular Mg2+ concentration or decrease of intracellular Mg2+ content, as measured by means of atomic absorption spectrophotometry. Mg2+ efflux was specifically combined with the uptake of Na+ at a stoichiometric ratio of 2Na+:1Mg2+, indicating electroneutral Na+/Mg2+ antiport. Na+/Mg2+ antiport depended on intracellular ATP and was inhibited by amiloride and quinidine, but was insensitive to strophanthin. Net Mg2+ efflux was only occurring at increased concentration of intracellular Mg2+ ([Mg2+]i), and stopped when the physiological Mg2+ content was reached. Intracellular Mg2+ acted cooperatively with a Hill coefficient of 2.4, which may indicate gating of Na+/Mg2+ antiport at increased [Mg2+]i. At increased intracellular Na+ concentration, Na+ competed with intracellular Mg2+ for Mg2+ efflux and Na+ could leave the rat erythrocyte via this transport system. Na+/Mg2+ antiport was working asymmetrically with respect to extra- and intracellular Na+ and Mg2+, and did not perform net Mg2+ uptake.

Adenosine Triphosphatases↗
PubMed1990

Species-specific Mn2+/Mg2+ antiport from Mg2(+)-loaded erythrocytes.

Mg2(+)-loaded rat erythrocytes performed Mn2+/Mg2+ antiport, which was nonspecifically stimulated by anions and cations. Mn2+/Mg2+ antiport was shown to operate via the Na+/Mg2+ antiporter because extracellular Na+ and Mn2+ inhibited the intracellular uptake of each other's ions competitively. Furthermore, Mn2+/Mg2+ antiport and Na+/Mg2+ antiport were identically inhibited by various amiloride derivatives. Na+/Mg2+ antiport of chicken and human erythrocytes cannot perform Mn2+/Mg2+ antiport although chicken erythrocytes took up more Mn2+ than rat erythrocytes.

Amiloride↗
PubMed1990

Na(+)-dependent Mg2+ efflux from Mg(2+)-loaded rat thymocytes and HL 60 cells.

Mg(2+)-loaded rat thymocytes and HL 60 (human promyelocytic leukemia) cells expressed a high rate of Na(+)-dependent net Mg2+ efflux which was inhibited by two thirds by 1 mM amiloride. During net Mg2+ efflux, extracellular Na+ was taken up at a stoichiometric ratio of 2 Na+ to 1 Mg2+, indicating electroneutral Na+/Mg2+ antiport as found for erythrocytes. Na(+)-independent Mg2+ efflux was not significantly expressed in these cell types.

Animals↗
PubMed1989

Characterization of Mg2+ efflux from human, rat and chicken erythrocytes.

Net Mg2+ efflux from Mg2+-loaded, human, rat and chicken erythrocytes was measured in sucrose, NaCl and choline Cl medium. Thus, Na+-dependent (NaCl minus choline Cl) and Na+-independent Mg2+ efflux (in sucrose) were determined. Na+-dependent Mg2+ efflux amounted to 0.16, 8.9 and 1.57 mmol/l cells x 30 min, Na+-independent Mg2+ efflux amounted to 0.89, 1.55 and 0.37 mmol/l cells x 30 min for human, rat and chicken erythrocytes. Na+-dependent Mg2+ efflux was inhibited by quinidine. Na+-independent Mg2+ efflux was inhibited by SITS and Cl-. A small fraction of Na+-independent Mg2+ efflux (in choline Cl) was resistant to SITS and Cl-. Ca2+ loading increased Mg2+ efflux similar to K+ efflux (Gardos effect). This effect was differently expressed in human and chicken erythrocytes.

Animals↗
PubMed1989

Na+-independent Mg2+ efflux from Mg2+-loaded human erythrocytes.

Net Mg2+ efflux from Mg2+-loaded human erythrocytes was maximal after reincubation in sucrose. Net Mg2+ efflux was not inhibited by furosemide or bumetanide and, therefore, was not performed by the (Na,K,Cl)- or (K,Cl)-cotransport system. A component of net Mg2+ efflux was inhibited by extracellular NaC1, KCl, LiCl, choline Cl and SITS, in analogy to the inhibition of net Cl- and SITS. Therefore, it was concluded that net Mg2+ efflux is dependent on net Cl- efflux for charge compensation. Cl- -dependent net Mg2+ efflux was inhibited by amiloride. Only 10% of the maximal net Mg2+ efflux may depend on extracellular Na+.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Induction of hepatic metallothionein by salicylate in adult rats.

Application of salicylate increased the concentration of metallothionein (MT) in liver of pregnant rats as well as of adult male rats, whereas in fetal liver, MT was reduced by salicylate. Induction of MT synthesis by salicylate is an indirect effect because in cultured hepatocytes salicylate did not induce MT synthesis. Salicylate increased MT also in adrenalectomized rats. Indomethacin induced the same concentration of MT in maternal liver as salicylate. However, indomethacin had no effect on MT in fetal liver. Induction of MT in adult liver by salicylate and indomethacin was independent of zinc.

Adrenalectomy↗
PubMed1989

Characterization and development of metallothionein in fetal forelimbs, brain and liver from the mouse.

The presence of the low molecular weight protein metallothionein (MT) has been investigated in fetal forelimbs, brain and liver from the mouse with the aim of using the protein as a biochemical marker for the early recognition of potential teratogenic agents in the future. Forelimbs, brain and liver were taken from mouse fetuses at ages ranging from 12 to 18 d. Each type of organ was homogenized and centrifuged at 9000 x g. The analysis of MT in the supernatants (S9) with the Cd-heme saturation method detected in all three cases the presence of a low molecular weight, Cd-binding protein whose concentration increased with the age of the fetus. Analysis of the S9 fractions using gel- and anion exchange-chromatography and polyacrylamide gel electrophoresis demonstrated the existence of a protein analogue to the hepatic MT in forelimbs and brain.

Animals↗
PubMed1989

Protection against salicylate ototoxicity by zinc.

One day after oral application of 700 mg (5.5 mmol)/kg salicylic acid given as Na salicylate, hearing thresholds in rats, measured by acoustically evoked responses at 10 and 20 kHz, were increased. Salicylate-induced hearing loss was completely prevented by simultaneous s.c. injection of 6 mg (92 mumol)/kg Zn, whereas simultaneous s.c. injection of 1.5 mmol/kg MgCl2 had no effect. Simultaneous s.c. injection of 100 mg (152 mumol)/kg desferrioxamine had only a minor beneficial effect indicating that salicylate-induced Fe accumulation plays no significant role in salicylate ototoxicity.

Animals↗
PubMed1989

Effect of salicylate on copper metabolism in maternal and fetal rats.

Pregnant Wistar rats were treated with 5 oral doses of 100 or 300 mg/kg salicylic acid from day 16 to 20 of gestation. At day 21 of gestation, copper concentrations were measured in serum, liver and cell organelles of liver from dams and litters after cell fractionation. Salicylate caused a reduction of maternal serum Cu and an increase in fetal liver Cu. The increase of Cu in fetal liver was proportional to the Cu content of the organelles. It was concluded that salicylate bound Cu and transferred Cu from maternal serum to the fetus. The increase in fetal liver Cu was explained by displacement of Zn from Zn-metallothionein by Cu, because Zn-metallothionein is high in fetal liver and Cu has a higher affinity to metallothionein than Zn. Such a mechanism was not significant in maternal liver because of the low Zn-metallothionein content in maternal liver.

Animals↗
PubMed1989

Magnesium-induced hypocalcemia in salicylate-treated pregnant rats.

Pregnant and non pregnant rats were fed diets with different Mg content and treated with 5 oral doses of 300 mg/kg salicylic acid for 5 consecutive days or from day 16 to 20 of gestation. One day after the final dosage, serum Mg and Ca concentrations were measured by atomic absorption spectrophotometry. In maternal rats, salicylate caused a strong decrease of serum Ca with increasing serum Mg concentrations (r = -0.8706). In fetal and nonpregnant adult female rats, serum Ca was not significantly decreased by salicylate with increasing serum Mg concentrations. However, the hypocalcemic effect of salicylate was found when nonpregnant young growing rats were fed a Ca-deficient diet.

Animals↗
PubMed1989

Age-dependent accumulation of cadmium in rats exposed to contaminated drinking water; interactions with zinc and copper and subcellular Cd distribution in kidney cells.

One of each pair of female sister rats aging 1, 4, 7 or 10 months was exposed during 3 months to 31.5 mg/L Cd (as CdCl2) in its drinking water and sacrificed immediately after Cd exposure together with its untreated sister. Concentrations of Cd, Zn and Cu were measured in the kidneys (medulla and cortex), the liver, the duodenum and the uterus. Furthermore, the subcellular distribution of Cd was measured in renal tissue. The accumulation of metal ions, defined as the difference between Cd-treated and untreated rats, was pronounced in all tissues except the uterus and was significantly decreased at increasing age. Multivariate analysis of variance revealed significant interaction with Zn and Cu. Higher Cd accumulation in the tissues of young animals probably depends on the higher consumption of contaminated drinking water per kilogram of body weight. High concentrations of Cd detected in cell nuclei may be due to the similarity between Cd2+ and Ca2+.

Aging↗
PubMed1988

Enhanced ototoxicity of gentamicin and salicylate caused by Mg deficiency and Zn deficiency.

In rats, Mg deficiency caused a moderate hearing loss, measured by means of evoked potentials at 10 and 20 kHz, which was repaired after refeeding a normal diet. Application of 700 mg/kg salicylic acid or injection of 5 x 100 mg/kg gentamicin also caused a reversible hearing loss in normally fed rats. Treatment of Zn-deficient rats with salicylic acid produced a stronger although reversible hearing loss than in normally fed salicylate-treated rats. Treatment of Mg-deficient rats with gentamicin induced a strong hearing loss that was nearly complete and irreversible in 9 of 25 rats.

Animals↗
PubMed1988

Effects of salicylate and zinc deficiency on the serum concentrations of magnesium, calcium, and parathyroid hormone.

Oral application of 700 mg/kg salicylic acid to pregnant and non-pregnant female rats caused an increase of serum Mg2+ and a decrease of serum Ca2+ concentration. The salicylate effect was drastically enhanced by Zn deficiency. The increase in serum Mg2+ is probably caused by the nephrotoxicity of salicylate. The decrease of serum Ca2+ concentration is combined with an increase of parathyroid hormone concentration in serum. Probably, salicylate and Zn deficiency inhibit Ca2+ mobilization by parathyroid hormone in bone.

Animals↗
PubMed1988

Maternal and fetal iron accumulation in Zn-deficient and salicylate-treated rats.

Nonhemoglobin Fe (non Hb-Fe) content in fetal serum and liver is much higher than in maternal serum and liver. After feeding a Zn-deficient diet to pregnant rats from d 0 to 21, non Hb-Fe content in maternal and fetal serum and liver was increased. After oral application of salicylic acid (300 mg/kg) from d 16 to 20 to normally fed and Zn-deficient dams, non Hb-Fe content in maternal and particularly in fetal serum and liver was drastically increased. In the kidney, Fe was accumulated to a small amount resulting from Zn deficiency and salicylate treatment. Fe accumulation in the liver occurred in all cell fractions, particularly in microsomes. Fe accumulation was confirmed and extended histochemically by Prussian blue staining. It is assumed that salicylate increases intestinal Fe resorption and fetal transfer of Fe. It is discussed that salicylate nephrotoxicity and its enhancement by Zn deficiency is not caused by an Fe-dependent mechanism.

Animals↗
PubMed1987

Characterization of Na+/Mg2+ antiport by simultaneous 28Mg2+ influx.

During net Mg2+ efflux from Mg2+-preloaded chicken erythrocytes, which occurs via Na+/Mg2+ antiport, 28Mg2+ is taken up intracellularly. Km of 28Mg2+ influx amounted to 1 mM. In Na+-free medium Vmax of 28Mg2+ influx was increased and Km was reduced to 0.2 mM. 28Mg2+ influx was noncompetitively inhibited by amiloride as was found for Na+/Mg2+ antiport. The results indicate that, extracellularly, Mg2+ can compete with Na+ for common binding sites of the Na+/Mg2+ antiporter, resulting in 28Mg2+-24Mg2+ exchange. The rate of Mg2+ exchange depends on extracellular Na+ and on the rate of net Mg2+ efflux.

Amiloride↗
PubMed1987

Enzymatic and morphological response of the thymus to drugs in normal and zinc-deficient pregnant rats and their fetuses.

In the thymus of normally fed pregnant rats the plasma membrane enzymes dipeptidyl peptidase IV (DPP IV) and alkaline phosphatase (alP) were found in cortical and medullary lymphocytes (thymocytes). Plasma membrane aminopeptidase A (APA) and adenosine monophosphate hydrolysing phosphatase (AMPP) were present in cortical reticular cells. In medullary reticular cells, aminopeptidase M (APM), gamma-glutamyl transferase (GGT), adenosine triphosphate (ATPP) and thiamine pyrophosphate (TPPP) cleaving phosphatases were detected. Medullary reticular cells did not contain APA. Lysosomal DPP I and II, acid phosphatase, acid beta-D-galactosidase, beta-D-N-acetyl-glucosaminidase, beta-D-glucuronidase and non-specific esterases occurred especially in macrophages at the corticomedullary junction. The 21-day-old fetal thymus showed a similar reaction pattern as the maternal organ except for APA which was absent before birth. After treatment of the pregnant rats with valproic acid (VPA), salicylic acid (SA), streptozotocin (ST) and retinoic acid (RA) APA showed an increase in activity in the thymic cortex. In addition, ST and RA induced AMPP, ATPP and TPPP activity in cortical reticular cells up to the same pattern as in medullary reticular cells. After ethanol (ET) administration severe damages occurred. The thymic cortex was free of DPP IV-positive lymphocytes; the medullary reticular cells showed reduced or no GGT and occasionally an increased APM activity. Dexamethasone (DEXA) given to normal or zinc-deficient rats produced the most severe lesions; thymocytes with DPP IV activity were completely absent in the cortex and medulla. In Zn-deficient pregnant rats similar alterations were observed as after ET.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Amiloride-sensitive net Mg2+ efflux from isolated perfused rat hearts.

Coronary blood vessels of isolated spontaneously beating rat hearts were perfused with an Mg2+-free solution at a rate of 3 ml/min. 1.5-ml fractions were sampled. Net Mg2+ efflux from heart muscle cells was measured by the increase of Mg2+ concentration in the perfusate. Addition of 0.3 microM isoproterenol to the perfusate resulted in a rapidly occurring transient Mg2+ efflux which was inhibited by amiloride.

Amiloride↗