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PubMed1986

Effect of magnesium deficiency on ultrastructural changes in coronary arteries of swine.

The effects of magnesium (Mg) deficiency on the coronary arteries of 27 Yorkshire swine were studied by light and electron microscopy. The experimental animals were divided into 4 groups which received the following supplements: Group I, basal ration with adequate Mg (540 mg/kg diet), Group II, basal ration with insufficient Mg (270 mg/kg diet) Group III, 10% milk powder with adequate Mg (540 mg/kg diet), Group IV, 10% milk powder with insufficient Mg (270 mg/kg diet). Serum analysis indicated that dietary low Mg supplementation decreased cholesterol levels and increased phospholipid concentrations significantly. The highest magnitude and incidence of intimal thickening were observed in the coronary arteries of Group IV (p less than 0.003). No significant intimal thickening was detected in any of the other groups. Ultrastructural studies revealed a greater frequency of degenerated cells in Group III and IV (p less than 0.01). Numerous calcifications were observed in only Group IV. These data suggest that moderate Mg deficiency can promote atherosclerosis in combination with some atherogenic diet, and that the presence of smooth muscle cell degeneration is important in order for a magnesium deficiency to exert an effect on the coronary artery of swine.

Animals↗
PubMedDate not supplied

Fructose precipitates calcium phosphate in the kidneys of female rats fed magnesium-deficient diets.

We have previously shown the synergistic interaction between fructose and magnesium (Mg) deficiency on renal calcification of female rats. The purpose of the present study was to determine whether the calcification formed in the kidneys of female rats fed an Mg-deficient fructose diet is due to phosphate or oxalate precipitates of calcium. The rats were divided into two dietary groups: fructose without Mg and starch with Mg. Rats were fed their respective diets for 9 weeks, and 24 h urine was collected for measuring urinary output, pH, Mg and calcium (Ca). The rats were then fasted overnight and after decapitation, blood was immediately collected for measuring plasma Ca and Mg, and the kidneys were removed. Left kidneys were used to determine their Mg and Ca contents, and right kidneys were dissected and fixed in neutral buffered formalin. Formalin-fixed specimens for microscopy were processed in paraffin using conventional procedures. Histochemical analysis was conducted by staining serial paraffin sections with haematoxylin, eosin, PAS-Schiff, alcian blue and trichrome. The sections were stained by the von Kossa method for calcium phosphate and by the silver hydroperoxide method for calcium oxalate. Only calcium phosphate was detected in the corticomedullary junction of the kidneys of female rats fed Mg-deficient fructose. The hypercalcaemia, hypercalciuria, and hypomagnesuria observed in the fructose group may cause calcium phosphate crystallization. A possible mechanism for the interaction between magnesium deficiency, fructose and oestrogen may be through parathyroid hormone which increases tubular fluid Ca and phosphorus (TF[Ca]x[P]). Further studies are required to prove the mechanism proposed here.

Animals↗
PubMed1982

Magnesium deficiency following jejunoileal bypass operations for obesity.

Skeletal muscle biopsies, blood samples, and 24-hour urines, before and after magnesium infusions, were obtained from 12 patients who had undergone jejuno-ileal bypass surgery several years earlier, selected for probable magnesium deficiency on the basis of repeated hypomagnesemia. The patients retained significant amounts of the infused magnesium, and exhibited elevation of low skeletal muscle magnesium and potassium, with concomitant decreases of muscle sodium and chloride. These changes were accompanied by increased urinary calcium and sodium and decreased urinary phosphorus excretion.

Adult↗
PubMedDate not supplied

Comparison of renal calcium concentration in obese, lean, diabetic, and non-diabetic Zucker rats fed a magnesium-deficient fructose diet.

In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on nephrocalcinosis induced by the interaction between fructose and magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a magnesium-deficient fructose diet. One half of the obese and lean animals, respectively, was injected with streptozotocin to produce diabetes, and the other half was injected with citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high starch or high fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output, protein, oxalate, citrate, MG, and calcium (Ca) measurements. The animals were then decapitated, and blood was collected for glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All fructose-fed animals exhibited significantly more kidney Ca then the starch-fed animals. Lean non-diabetic rats fed fructose showed the greatest kidney Ca along with the greatest urinary protein excretion among all experimental groups. The significant finding in the present study is that diabetes or obesity reduced nephrocalcinosis regardless of the insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in nephrocalcinosis induced by the interaction between fructose and magnesium deficiency. Hyperproteinuria (uromucoid) in combination with hypercalciuria and hypomagnesuria may be responsible for greater nephrocalcinosis in the fructose than the starch group. The possible mechanisms for this interaction on nephrocalcinosis have been discussed.

Animals↗
PubMed1979

[Blood histamine and response of spleen cells to phytohemagglutinins during moderate magnesium deficiency in the rat].

Blood histamine and spleen cell stimulation index by PHA were determined in either magnesium deficient or control Rats. Between the 10th and 17th days of diet (hyperemia and dermatosis period), histaminemia was significantly higher in deficient animals (485 ng/ml) than in control ones (112 ng/ml), but at the 32nd day it came back to normal values. The mean spleen cell stimulation index by PHA was depressed in deficient animals mainly between the 10th and 17th day of the deficiency; 33% of control mean value. A negative correlation is found between histamine level and stimulation index.

Animals↗
PubMed1997

Histology of magnesium-deficient Norway spruce needles influenced by nitrogen source.

Effects of magnesium deficiency and variation in nitrate to ammonium ratio on needle histology and chlorophyll concentration were investigated in current-year and one-year-old needles of clonal Norway spruce trees (Picea abies (L.) Karst.). Six-year-old trees were grown for one year in sand culture with circulating nutrient solutions containing a sufficient (0.2 mM) or a limiting (0.04 mM) concentration of Mg. The nitrogen concentration was not varied (5 mM), but the NO(3) (-)/NH(4) (+)-ratio was adjusted to 0.76 in Mg-sufficient and to 1.86, 0.76 or 0.035 in Mg-limited plants. Visible symptoms of Mg deficiency occurred only in current-year needles, indicating adequate Mg nutrition before the experiment. Under conditions of Mg limitation, chlorophyll and Mg concentrations were lowest in needles of trees supplied with NH(4) (+) as the major nitrogen source and highest in needles of trees supplied with NO(3) (-) as the major nitrogen source. In current-year and one-year-old needles, starch accumulation induced by Mg deficiency was increased when NH(4) (+) was the major nitrogen source. The accumulation of tannin spherules in current-year needles, which occurred in response to Mg deficiency, also increased with decreasing NO(3) (-)/NH(4) (+)-ratios. Deficient Mg supply caused premature aging in tissues of the vascular bundle, as indicated by modifications of the cambium and increased amounts of collapsed sieve cells. The number of collapsed sieve cells was slightly lower in needles grown in a NH(4) (+)-dominated nutrient regime than in needles grown in a NO(3) (-)-dominated nutrient regime. We conclude that was not directly toxic to Norway spruce trees at the applied concentrations. However, effects of Mg deficiency were considerably greater in an NH(4) (+)-dominated nutrient regime than in a NO(3) (-)-dominated nutrient regime.

Journal Article↗
PubMed1978

Splenic protein synthesis in magnesium deficiency: mechanism of the inhibition.

To investigate the basis for the depressed protein synthesis in vivo in magnesium deficient spleens, the activities of splenic subcellular fractions in polypeptide synthesis were studied in vitro. Splenic ribosomes from Mg deficient animals were normal structurally and functionally. In contrast, supernatant fractions from the deficient spleens had a reduced ability to incorporate labeled amino acids into protein, both in the presence of endogenous mRNA and in the presence of added polyuridylic acid. The specific defects observed in the Mg deficient supernatants were twofold: There was a modest reduction in the rate of acylation of tRNA and a more marked reduction in the activity of the elongation factors, EF-I and EF-II. The reduction in elongation factor activity was quantitatively sufficient to account for the inhibition of protein synthesis in vivo.

Amino Acyl-tRNA Synthetases↗
PubMed1987

Specific change of histamine metabolism in acute magnesium-deficient young rats.

The effects of dietary magnesium (Mg) deficiency on histamine metabolism were studied. Young Wistar rats were fed a Mg-deficient diet (0.001% Mg diet) ad libitum for 8 days with control groups (0.07% Mg diet), food-restricted groups (0.21% Mg diet, but restricted to 5 g/rat/day), and refeeding groups (0.001% Mg diet for 6 days ad libitum, after that fed with a 0.21% Mg diet ad libitum for 2 days). Compared to the other groups, the plasma Mg level was markedly lower in the Mg-deficient group. A return from the lower Mg level to the controls took place after feeding them a 0.21% Mg diet for 2 days. Urinary histamine level increased rapidly after 4 days and reached a maximum on the eighth day of Mg deficiency. The high urinary histamine level in Mg-deficient rats decreased rapidly after feeding them a 0.21% Mg diet for 2 days. Histamine contents in some tissues increased on the eighth day of Mg deficiency. Other groups showed no significant change. The increased histamine content in Mg-deficient rats showed a tendency to return to control levels after feeding them a 0.21% Mg diet for 2 days. Histidine decarboxylase (HDC) activity in some tissues of Mg-deficient rats increased markedly. The increased HDC activity dropped nearly to control levels after feeding them a 0.21% Mg diet for 2 days. Diamine oxidase (DAO) activity in the duodenum was high in control rats. Duodenal DAO activity decreased gradually and reached half the value of controls on the eighth day of Mg deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Amine Oxidase (Copper-Containing)↗
PubMed1986

Dermatosis in magnesium-deficient hairless rats: effects of steroidal and non-steroidal anti-inflammatory drugs.

Dermatosis in magnesium-deficient hairless rats has been described as a reproducible model of skin inflammation. It was therefore felt of interest to search for the effects of various anti-inflammatory compounds on this model. Results showed that 1) Dexamethasone acetate completely abolished the rash, 2) Indomethacin, a Non-Steroidal Anti-Inflammatory Drug (NSAID), inhibitor of the cyclooxygenase pathway was quite inactive, 3) Benoxaprofen, a NSAID inhibitor of both cyclooxygenase and lipoxygenase pathways only slightly modified the development of the pathology. Activity of steroidal anti-inflammatory drugs on this model may be related to their immunosuppressive effects.

Animals↗
PubMed1984

Vigilance states and cerebral monoamine metabolism in experimental magnesium deficiency.

Correlations between cerebral monoamine metabolism and electrophysiological parameters were compared in 18 male Wistar rats subjected to a magnesium-restricted diet and in 14 normal rats. During the 40-day experimental period, plasma and erythrocyte Mg2+ levels and plasma Ca2+ and phosphorus levels were measured, and electroencephalographic tracings as well as clinical data were recorded at regular intervals. At the end of the study, the animals were killed and cerebral concentrations of monoamines and their metabolites were determined. Cerebral monoamine disorders characterized by a rise of dopamine and 5-hydroxyindole-3-acetic acid levels were observed in the magnesium-deficient group. This rise was accompanied by an increase in wakefulness and a decrease in sleep percent. The role played by magnesium in cerebral monoamine metabolism and sleep cycles is discussed.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Impairment of ascorbic acid synthesis in liver extracts of magnesium-deficient rats.

The effect of feeding a magnesium (Mg)-deficient diet for 9-34 days to weanling and young male rats on urinary and tissue ascorbate levels were studied. The concentrations of ascorbic acid in the liver and kidney were significantly reduced in the rats receiving a Mg-deficient diet as compared to those receiving a Mg-supplemented diet. The response to trichloro-2-methyl-2-propanol stimulation of urinary ascorbic acid was found to be considerably suppressed by dietary deficiency of Mg, suggesting that the decrease was not due to feed intake. In in vitro studies, the enzymatic synthesis of the vitamin from glucuronolactone or gulonolactone by liver extracts from Mg-deficient rats was significantly decreased as compared with Mg-supplemented rats. These results suggest that Mg-deficient rats have a reduced capacity to synthesize ascorbate which in turn produces a decrease in ascorbic acid concentrations in the liver.

Animals↗
PubMed1988

Ex vivo study of the vascular reactivity to some vaso-active agents in isolated thoracic aorta from dietary magnesium-deficient rats.

We have reported that dietary magnesium (Mg) deficiency induced both histaminaemia and hypomagnesaemia in rats. In this study, the effects of dietary Mg deficiency on the reactivity of the isolated thoracic aorta to some vaso-active amines were studied ex vivo. Adult male Wistar rats were fed on a Mg-deficient diet (Mg 0.001%) and a control diet (Mg 0.07%) for 30 d. Sensitivity to KCl and adrenaline showed no significant change during Mg deficiency. In Mg-deficient rats, the sensitivity to noradrenaline was higher than in the control group. Removal of calcium ions from the medium in the tissue bath resulted in a greater decay of noradrenaline-induced contraction in Mg-deficient rats than in the control rats. Endothelium-dependent relaxation was also examined in isolated aortic strips precontracted with noradrenaline. In rats which were fed with the Mg-deficient diet for 15 days, histamine produced less relaxation than in the control group, but acetylcholine produced the same degree of relaxation as in the controls. These results showed that hypomagnesaemia and histaminaemia might influence the reactivity of the aorta in vivo.

Acetylcholine↗
PubMed1998

Protective effect of Crassostrea gigas extract on audiogenic seizures in magnesium deficient mice.

Audiogenic seizures associated with loss of weight, prostration, piloerection, palpebral ptosis and motor deficiency were induced after sound stimulation of determined frequency and amplitude in magnesium-deficient DBA/2 mice. These symptoms were maintained when standard diet conditions (1700 ppm Mg2+) were restored. In contrast, mice were protected from audiogenic seizure in a dose related manner when Crassostrea gigas extract (JCOE) were added to the diet for 10 consecutive days. Although a rational explanation for this protective effect has not yet been determined, it is assumed that it might be due to a chelating complex formed between Mg2+ and taurine, which enhance the uptake of Mg2+.

Acoustic Stimulation↗