Biomedical subjects

T Günther

Publications and source records attributed to T Günther.

At least 109 records · Page 6Linked to original sources

PubMed1992

Noise-induced hypertension and magnesium in rats: relationship to microcirculation and calcium.

It has been demonstrated that audiogenic stress (AS) can induce elevation of arterial blood pressure (ABP) in animals and humans and that noise-induced hearing loss may be associated with alterations in Mg metabolism. Experiments were designed to determine whether 1) there is a causal relationship among environmental noise stress, serum and vascular tissue (aortas and portal veins) Mg contents, and development of hypertension and 2) such noise-induced hypertension has a microcirculatory basis and what the mechanism may be. Rats maintained on normal Mg-containing diets for 12 wk (plasma [Mg] = 0.96 +/- 0.02 mM) and subjected to AS (85 dB(A), 12 h/day for 8 wk; 95 dB(A), 16 h/day for 4 wk) demonstrated significant elevation in systolic and diastolic ABP; plasma [Mg] showed a 15% deficit, whereas aortic and portal vein muscle exhibited slight reductions in Mg content and elevation in Ca. Moderate and more severely Mg-deficient animals not subjected to AS also exhibited significant elevations in systolic and diastolic ABP; vascular tissue Mg content decreased, whereas Ca content rose. Animals subjected to combined Mg deficiency and AS for 12 wk exhibited the greatest deficits in plasma and vascular muscle Mg and the greatest elevations in systolic and diastolic ABP; vascular tissue Ca contents also showed the greatest increases. In situ measurements of mesenteric arterioles, venules, and precapillary sphincters in the various subgroups revealed that the lower the plasma [Mg], the more constricted the microvessels, and the higher the ABP, the lower the plasma [Mg]. Capillary blood flow velocities were decreased in relation to the degree of plasma Mg deficit.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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

Application of immobilized cells for biotransformations of steroids.

A survey is given of possible solutions and open-ended questions in the biotransformation of steroids (without side chain degradation of sterols) by using immobilized cells. The data of literature between 1975 and 1990 and results of preliminary experiments from the microbial, biochemical, biophysical, physiological, as well as the biotechnological point of view are summarized and discussed.

Bacteria↗

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↗

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

Correlations between ventricular arrhythmias and electrolyte disturbances after acute myocardial infarction.

Seven 24-hour ECG recordings and blood samples were taken within 3 weeks in 42 patients who had suffered an acute myocardial infarction (AMI). Ca, K and Mg concentrations in serum, and K and Mg in the erythrocytes, were determined by atomic absorption spectroscopy. One half of the patients were infused with 81 mval/day MgSO4 for 3 days. In patients who exhibited intense electrolyte alterations 10-20 days after AMI, there was a significantly higher rate in the frequency of couplets and/or tachycardia in the 2- to 20-day period after AMI. In patients infused with MgSO4, the fluctuation in serum electrolytes and the rate of arrhythmias were significantly reduced.

Aged↗

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

Enhancement of gentamicin-induced nephrotoxicity by Mg deficiency in non-pregnant rats. Morphological, enzyme histochemical and immunohistochemical studies.

Non-pregnant rats fed an Mg-deficient diet showed some degenerated and calcified proximal tubules in the inner region of the medullary rays accompanied by reduced or absent enzyme activities. After gentamicin treatment some damaged convoluted proximal tubules occurred. Enzyme histochemistry revealed decreased activities for brush border and lysosomal hydrolases; using immunohistochemistry lesions were detectable for the cytoskeletal proteins keratin and vimentin. Administration of gentamicin to Mg-deficient rats led to a further decrease of hydrolase activities in obviously intact proximal tubules and drastic structural and enzymatic defects as well as alterations of the cytoskeletal proteins in the convoluted and straight segments of other proximal tubules and to a lesser degree also in glomeruli and further portions of the tubular apparatus including the collecting ducts.

Animals↗

PubMed1989

Lipid peroxidation in mitochondria and microsomes from adult and fetal rat tissues. Effects of Zn deficiency, Fe, and salicylate.

Pregnant female Wistar rats that received a control (100 ppm Zn) or a Zn-deficient diet (1.5 ppm Zn) from d 0 to 21, or nonpregnant normally fed female rats without or with five daily oral doses of 300 mg/kg salicylic acid were used for the experiments. In isolated mitochondria or microsomes from various maternal and fetal tissues, lipid peroxidation was determined as malondialdehyde formation measured by means of the thiobarbiturate method. Zn deficiency increased lipid peroxidation in mitochondria and microsomes from maternal and fetal liver, maternal kidney, maternal lung microsomes, and fetal lung mitochondria. Lipid peroxidation in fetal microsomes was very low. Zn deficiency produced a further reduction of lipid peroxidation in fetal liver microsomes. Salicylate increased lipid peroxidation in liver mitochondria and microsomes after addition in vitro and after application in vivo. The increase of lipid peroxidation by salicylate may be caused by two mechanisms: an increased cellular Fe uptake that, in turn, can increase lipid peroxidation and chelating Fe, in analogy to the effect of ADP in lipid peroxidation. The latter effect of salicylate is particularly expressed at increased Fe content.

Animals↗

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

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↗