[Magnesium--the 2d most abundant intracellular cation].
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Biomedical subjects
Publications and source records attributed to T Günther.
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In 57 test persons having worked 1 day under traffic noise (Leq = 85 dB(A) and 1 day without noise (Leq < 50 dB(A), blood pressure and pulse frequency were measured at 1 h intervals and total urine was collected during working hours. Additionally, blood was sampled at the end of each working day. Psychological parameters were assessed by means of questionnaires. Statistically significant reactions to noise were found in the following fields: 1. Ergnomics--decrease of working quality; 2. Psychology--increase of psychical tension; 3. Blood circulation--increase of blood pressure and pulse frequency; 4. Biochemistry--increase of epinephrine, cAMP, urine and serum Mg, protein, cholesterol plus decrease of erythrocyte Na, and renin. Hypothetical mechanisms of the action of traffic noise are discussed.
The effect of ConA on passive 42K+ fluxes in human lymphocytes was analysed by treatment with furosemide and ouabain. Furosemide has no effect on net K+ transport and pump flux. The component of passive efflux of 42K+ which depends on K+-K+ exchange is inhibited by furosemide; its mechanism is discussed in detail. The 42K+ uptake in lymphocytes consists of 1. an ouabain-sensitive pump influx, 2. an ouabain-insensitive leak influx and 3. a furosemide-sensitive K+-K+-exchange. Only the first two components of 42K+ uptake are stimulated by ConA.
Incubation of human lymphocytes with ConA causes an increase in [Na+]i and a decrease in [K+]i. This effect is not due to the experimental washing procedure, but is due to the ConA-induced increase in permeability which is not fully compensated by the increase in active transport. The ConA-induced increase in 42K+ uptake consists of an increase in leak flux which is independent of [Na+]o, and of an increase in pump flux which is dependent on [Na+]o. The increase in leak flux may be caused by increased membrane fluidity. The increase in pump flux may be produced by the increased [Na+]i and by a stimulation of Na+, K+ATPase.
The main literature concerning the physiology and biochemistry as well as the pathophysiology and pathobiochemistry of magnesium is reviewed, including: Distribution and physico-chemical state of magnesium in the extracellular and intracellular fluid as well as in the subcellular organelles (membranes, mitochondria, microsomes, ribosomes). Intestinal resorption, transport across membranes and excretion by the kidney. Hormonal regulation of magnesium distribution and its clinical disturbances. Biochemical mechanism and the clinical effects of hypo- and hypermagnesemia.
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Limb buds of 11-day-old mouse embryos were cultured for 6 days with insulin, dibutyryl cAMP and X 537 A. The cartilage anlage was reduced by insulin and enlarged by dibutyryl cAMP and X 537 A. The effects are due to changes in the amount of intercellular substance.
Spleen cells and thymocytes from Mg-deficient rats, fed a Mg-deficient diet for 10--13 weeks, incorporate [3H]thymidine at half the rate of normal cells. The cells from Mg-deficient rats are less stimulated by lectins than those from normal animals. These effects correspond to the reduced content of gamma-globulins in serum in Mg deficiency. They are caused by the altered electrolyte content of the Mg-deficient cells.
The tissue H2O of rabbit heart and rat liver was partially exchanged in situ with D2O. In rat liver, the loss of ATP, resulting from normothermic ischemia, was decreased after perfusion with D2O. The maximal protective effect was found when the proportion of D2O in the water of the liver tissue was 0.20. In both organs the protective effect of D2O could be correlated with a marked decrease in severe ischemic damage of cellular organelles, in particular mitochondria. D2O also increased the protective action of Mg-ions in the heart.
Gel filtration of the cytoplasmic fraction of homogenate from human peripheral lymphocytes incubated with 65Zn gave five separate peaks with molecular weights of greater than 150,000, 90,000, 65,000, 20,000, and less than 1000 daltons. Peaks I--IV consisted of proteins. The low molecular weight (peak V) may consist of nucleotides, polyamines and amino acids. After gel filtration 75-80% of the 65Zn activity was found in peak V. Lectin-induced stimulation of normal lymphocytes revealed a distribution pattern of 65Zn binding similar to that of unstimulated cells. There was only a slightly enhanced incorporation into the protein peaks I--IV. When peripheral lymphocytes of B lymphocyte origin from patients with chronic lymphocytic leukemia were incubated with 65Zn the same peaks were seen as with supernatants obtained from normal lymphocytes. Lectin-induced stimulation of leukemic lymphocytes had no significant effect on the 65Zn distribution pattern.
Limb buds of 11-day-old mouse embryos were cultured for six days in the presence of 0.1, 0.5 or 2 mg/kg 4-methylumbelliferyl-beta-D-xylopyranoside. A dose-dependent decrease in chondrogenesis could be observed in preparations stained with methylene blue and cleared. A reduction or even disappearance (after 2 mg/kg) of intercellular spaces and a change in shape and size of chondroblasts was striking in the light microscopical picture. The electron microscopical findings reveal a decrease in the number, size, and electron-density of the ruthenium-red-positive proteoglycan granules as well as an alteration in the collagen morphology. Up to 1,000 A thick fibrils occur which partly show a so-called continuous cross-striation. In addition, bundles of thin (50-100 A) collagen filaments without cross-striation occur. The number, distribution and packing density of the cell organelles in the chondroblasts are very variable. The vacuoles of the Golgi apparatus are dilated. These effects may be attributed to the xyloside-induced alterations of proteoglycans.
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Rabbits were fed with thiouracil for 8 months. Subsequently their hearts were examined electron microscopically as well as biochemically for collagen and hexosamine content. Chronic treatment with thiouracil induced an increase in interstitial connective tissue collagen and hexosamine without visible necrosis. As seen by electron microscopy, the increase in collagen content might have been caused by stimulation of the fibrocytes. Furthermore, the heart muscle cells showed deep indentations and bulges of the cell membrane and an enlargement of the T-system.
In chronic Mg-deficiency, there is a decrease in the content of Mg and K+ in the heart muscle. The contents of Ca, Na+ and hydroxyproline increase. There is also an increased urinary excretion of adrenaline and especially noradrenaline. With simultaneous noise stress, these changes are even greater. The magnitude of the changes increases with the degree of Mg-deficiency. The changes in the contents of Na+, K+, Ca, Mg and hydroxyproline correlate with the excretion of noradrenaline. The increase in the collagen content can be verified by electron microscopy, and it is due to a stimulation of the fibrocytes.
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The activity of Mg2+-activated enzymes shows a bell shaped pMg dependency, with a pMg optimum at 3. Intracellular Mg2+ concentrations, determined by different methods, are about 10(-3) mol/1. Thus Mg2+-dependent enzymes are optimally activated, or nearly so, with Mg2+. If the substrates of an enzyme form complexes with Mg2+ of different stabilities, and if free substrate and the substrate-Mg2+ complex react differently with the enzyme, the equilibrium will change with the concentration of Mg2+. When the extracellular concentration of Mg2+ is increased, Mg2+ becomes bound practically exclusively to the cell membrane. In Mg2+ deficiency, the intracellular concentrations of Na+, K+, Ca2+ and cycl. AMP are changed, and the rates of synthesis of DNA, RNA and protein are decreased.
65Zn (7.4 MBq: 200 muCi) was injected intravenously into normal, castrated and castrated, testosterone-substituted rats. After 1, 24 and 48 hours, the distribution of 65Zn-binding proteins in the 100,000 g supernatant of the prostate and seminal vesicles was investigated by separation on Sephadex G 100. The prostate and seminal vesicles from any one rat showed the same distribution pattern of 65Zn-proteins. In castrated rats, the incorporation of 65Zn was, however, 5-6 times lower than in the normal or castrated, testosterone-substituted rats. One hour after the injection, the highest activity of 65Zn was found in proteins in the molecular weight range above 100,000. After 48 hours the greatest proportion of 65Zn was present peak corresponding to 28,000 Daltons.