Calculation of free-magnesium concentration in adenosine 5'-triphosphate containing solutions in vitro and in vivo

Biochemistry ◽  
1984 ◽  
Vol 23 (15) ◽  
pp. 3547-3552 ◽  
Author(s):  
Lillian Garfinkel ◽  
David Garfinkel
1996 ◽  
Vol 127 (3) ◽  
pp. 377-385 ◽  
Author(s):  
C. L. Adam ◽  
R. G. Hemingway ◽  
N. S. Ritchie

SUMMARYDietary calcined magnesite supplements of different particle sizes and temperatures of calcination were examined at Glasgow University Veterinary School in 1981. Balance experiments with wether sheep revealed that particle sizes < 75, 75–150, 150–250 and 500–1000 μm diameter of a feed-grade calcined magnesite all increased urinary output of magnesium to a similar extent but the apparent magnesium availability coefficient for the 500–1000 μm diameter fraction (0·03) was significantly less than for fractions of smaller diameter (0·17–0·23) (P < 0·01). A 1000–2000 μm fraction of fertilizer-grade material had an apparent availability of 0·18 but had the least effect on urinary magnesium output. Calcination temperatures of 800, 900 and 1100 °C significantly increased apparent availability (c. 0·46)compared with that for temperatures of 500 and 650 °C (c. 0·12) (P < 0·01), and significantly increased urinary output of magnesium. Losses of magnesium from these supplements incubated in the rumen of cows at grass in 24 μm mesh nylon bags showed some correlations with their apparent availability and urinary magnesium output. Solubility in molar ammonium nitrate showed some good correlations with urinary magnesium output but not with magnesium availability. Supplementation of a low magnesium diet given to lactating ewes with fine particle (< 75μm) calcined magnesite resulted in significantly greater increases in plasma magnesium concentration than when coarse particle material (500–1000 μm) was given (P < 0·05), but magnesites calcined at 650 and 800 °C induced similar changes in plasma magnesium.


1996 ◽  
Vol 271 (1) ◽  
pp. E113-E122 ◽  
Author(s):  
N. D. Vaziri ◽  
X. J. Zhou ◽  
F. Naqvi ◽  
J. Smith ◽  
F. Oveisi ◽  
...  

We studied the mechanism of erythropoietin (EPO)-induced hypertension (HTN) in rats with chronic renal failure (CRF). After partial nephrectomy, rats were randomized into four groups. Group A received EPO, 150 U/kg, two times weekly for 6 wk to prevent anemia; group B received placebo injections and became anemic; group C received EPO but was kept anemic by dietary iron deficiency; and group D received placebo and regular transfusions to match hematocrit (Hct) in group A. Blood pressure (BP), Hct, platelet cytosolic calcium ([Ca2+]i) and magnesium concentration, and pressor and vasodilatory responses were determined. By design, Hct in groups A and D were comparable and significantly greater (P < 0.01) than in groups B and C. Despite divergent Hct values, the EPO-treated groups A and C showed a significant rise in BP compared with the placebo-treated groups B and D. HTN occurred whether EPO therapy was begun immediately or 4 wk after nephrectomy. EPO therapy augmented the elevation of basal [Ca2+]i and restored the defective thrombin-mediated rise of platelet [Ca2+]i in CRF animals. EPO therapy did not alter caudal artery contraction in response to either 68 mM K(+)-induced depolarization, angiotensin II or alpha 1-agonist, methoxamine in vitro, or the pressor response to angiotensin II in vivo. However, EPO therapy impaired the hypotensive response to nitric oxide (NO) donors, sodium nitroprusside and S-nitroso-N-acetyl-D,L-penicillamine, and reversed the CRF-induced upregulation of guanosine 3',5'-cyclic monophosphate production by thoracic aorta in vitro. Thus EPO-induced HTN in CRF rats is Hct independent and is associated with and perhaps causally related to increased basal and stimulated [Ca2+]i and impaired vasodilatory response to NO.


1974 ◽  
Vol 61 (1) ◽  
pp. 53-61 ◽  
Author(s):  
F. W. HEATON ◽  
H. P. HUMPHRAY

SUMMARY The close positive correlation between the magnesium concentration in serum and the activity of the thyroid gland, as indicated by the ratio of (protein-bound 125I): (total serum 125I) 24 h after injection of a tracer dose of [125I]iodide, was investigated in young male rats. Dietary deficiency or loading with magnesium salts had no effect on the concentration of cyclic AMP within the thyroid gland or the release of thyroid hormone from glands incubated in vitro. Accumulation of radioactive iodide by thyroid glands in vivo was stimulated by magnesium loading and inhibited by magnesium deficiency, but there was no selective effect on the synthesis of iodinated tyrosines or thyronines within the gland. As similar differences in radioactive iodide uptake were observed in other soft tissues, this appears to be part of a general influence of magnesium status on iodide transport, rather than a specific action on the thyroid gland.


1995 ◽  
Vol 67 ◽  
pp. 300
Author(s):  
Masahiko Suzuki ◽  
Masami Nishma ◽  
Makoto Endo ◽  
Kazuhiro Matsushita ◽  
Mitsue Telsuka ◽  
...  

1988 ◽  
Vol 66 (4) ◽  
pp. 929-933
Author(s):  
A. H. Houston ◽  
J. D. Gray

In vivo erythrocytic magnesium concentration was significantly correlated with red cell potassium level and potassium equilibrium potential, but not with specimen weight, plasma magnesium, red cell sodium and chloride, or chloride equilibrium potential. To examine the relationship between magnesium and potassium, potassium levels were manipulated in vitro with catecholamine, furosemide, ouabain, and valinomycin. Over a wide range of normal and supranormal potassium concentrations, a significant correlation between magnesium and potassium levels was evident. However, depletion of potassium following exposure to ouabain and valinomycin led to a shift from the normal high potassium/low sodium relationship to a high sodium/low potassium state with progressive increases in magnesium content. Correlation of magnesium with potassium was lost, and a significant correlation with red cell sodium, but not with sodium equilibrium potential, was evident. Red cell magnesium concentration appears, therefore, to be influenced by the preponderant univalent cellular cation rather than potassium per se.


2003 ◽  
Vol 23 (3) ◽  
pp. 342-354 ◽  
Author(s):  
Alan I. Faden ◽  
Susan M. Knoblach ◽  
Ibolja Cernak ◽  
Lei Fan ◽  
Robert Vink ◽  
...  

The authors developed a novel diketopiperazine that shows neuroprotective activity in a variety of in vitro models, as well as in a clinically relevant experimental model of traumatic brain injury (TBI) in rats. Treatment with 1-ARA-35b (35b), a cyclized dipeptide derived from a modified thyrotropin-releasing hormone (TRH) analog, significantly reduced cell death associated with necrosis (maitotoxin), apoptosis (staurosporine), or mechanical injury in neuronal–glial cocultures. Rats subjected to lateral fluid percussion–induced TBI and then treated with 1 mg/kg intravenous 35b thirty minutes after trauma showed significantly improved motor recovery and spatial learning compared with vehicle-treated controls. Treatment also significantly reduced lesion volumes as shown by magnetic resonance imaging, and decreased the number of TUNEL-positive neurons observed in ipsilateral hippocampus. Unlike TRH or traditional TRH analogs, 35b treatment did not change mean arterial pressure, body temperature, or thyroid-stimulating hormone release, and did not have analeptic activity. Moreover, in contrast to TRH or typical TRH analogs, 35b administration after TBI did not alter free-magnesium concentration or cellular bioenergetic state. Receptor-binding studies showed that 35b did not act with high affinity at 50 classical receptors, channels, or transporters. Thus, 35b shows none of the typical physiologic actions associated with TRH, but possesses neuroprotective actions in vivo and in vitro, and appears to attenuate both necrotic and apoptotic cell death.


Author(s):  
Anique D ter Braake ◽  
Marc G Vervloet ◽  
Jeroen H F de Baaij ◽  
Joost G J Hoenderop

Abstract Vascular calcification is a prognostic marker for cardiovascular mortality in chronic kidney disease (CKD) patients. In these patients, magnesium balance is disturbed, mainly due to limited ultrafiltration of this mineral, changes in dietary intake and the use of diuretics. Observational studies in dialysis patients report that a higher blood magnesium concentration is associated with reduced risk to develop vascular calcification. Magnesium prevents osteogenic vascular smooth muscle cell transdifferentiation in in vitro and in vivo models. In addition, recent studies show that magnesium prevents calciprotein particle maturation, which may be the mechanism underlying the anti-calcification properties of magnesium. Magnesium is an essential protective factor in the calcification milieu, which helps to restore the mineral-buffering system that is overwhelmed by phosphate in CKD patients. The recognition that magnesium is a modifier of calciprotein particle maturation and mineralization of the extracellular matrix renders it a promising novel clinical tool to treat vascular calcification in CKD. Consequently, the optimal serum magnesium concentration for patients with CKD may be higher than in the general population.


Author(s):  
E. J. Kollar

The differentiation and maintenance of many specialized epithelial structures are dependent on the underlying connective tissue stroma and on an intact basal lamina. These requirements are especially stringent in the development and maintenance of the skin and oral mucosa. The keratinization patterns of thin or thick cornified layers as well as the appearance of specialized functional derivatives such as hair and teeth can be correlated with the specific source of stroma which supports these differentiated expressions.


Author(s):  
M.J. Murphy ◽  
R.R. Price ◽  
J.C. Sloman

The in vitro human tumor cloning assay originally described by Salmon and Hamburger has been applied recently to the investigation of differential anti-tumor drug sensitivities over a broad range of human neoplasms. A major problem in the acceptance of this technique has been the question of the relationship between the cultured cells and the original patient tumor, i.e., whether the colonies that develop derive from the neoplasm or from some other cell type within the initial cell population. A study of the ultrastructural morphology of the cultured cells vs. patient tumor has therefore been undertaken to resolve this question. Direct correlation was assured by division of a common tumor mass at surgical resection, one biopsy being fixed for TEM studies, the second being rapidly transported to the laboratory for culture.


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