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PubMed1999

Magnesium-manganese interactions caused by magnesium deficiency in rats.

OBJECTIVE: We investigated the effect of dietary magnesium (Mg) deficiency on the nutritive utilization and tissue distribution of manganese (Mn). METHODS: Wistar rats were fed a Mg-deficient diet (56 mg/kg) for 70 day. Absorbed Mn, Mn balance and Mn content in plasma, whole blood, skeletal muscle, heart, kidney, liver, femoral bone and sternum were determined after 21, 35 and 70 days. RESULTS: The Mg-deficient diet significantly increased Mn apparent absorption and Mn balance from week five until the end of the experimental period. This effect was accompanied by a significant increase in the concentration of Mn in heart at all three time points. Whole blood, skeletal muscle and kidney Mn were significantly increased from day 35, and femur Mn content was increased only at the end of the study (day 70). However, Mn concentration in the sternum decreased significantly from day 35. No changes were found in liver Mn content. CONCLUSION: Mg deficiency increased Mn absorbed, and this favored the deposition of Mn in all tissues studied except the liver and trabecular bone. The lack of response by the liver to increased Mn absorption may have led to the redistribution of this ion to other tissues.

Absorption↗
PubMedDate not supplied

Clinical, EEG, electromyographic and polysomnographic studies in restless legs syndrome caused by magnesium deficiency.

The present paper reports biochemical and neurophysiological investigations in ten cases with restless leg syndrome. Other neuropsychiatric affections and factors which could generate the symptomatology of restless legs syndrome were not included. The EEG recordings demonstrated evident reticular neuronal hypersynchrony generated by hyperpnoea (sinusoidal slow waves). The classical EEG investigations pointed out neuromuscular hyperexcitability, but some modifications of the functional parameters of the neuromuscular excitability and conductibility (signs of neuropathy) were also noticed. In all the cases, continuous 8-hour polysomnographic recordings and monitorization on infrared TV screen were performed. Investigations reported: important disorders of sleep organization, agitated sleep with frequent periods of nocturnal awakenings, increase of the durations and percentages of light slow-wave sleep (LSWS) and rapid and frequent changes of various stages of LSWS, a decrease of duration and percentage of DSWS, a decrease of duration and percentage of REM sleep (as in other parasomnias caused by magnesium deficiency) and nocturnal EEG anomalies (long discharges of sinusoidal slow waves, of sharp waves and of sharp slow waves appearing in the LSWS stages with the disappearance in the REM sleep).

Adult↗
PubMed1987

[Effects of magnesium deficiency on dermal mast cells in rats].

The effects of dietary magnesium (Mg) deficiency on dermal mast cells were studied in young Wistar rats weighing about 50 g. The rats fed with a Mg-deficient diet (0.001% Mg) showed hyperemia on the 3rd or the 4th day after they were fed the diet. The dermal mast cells of the control rats were filled with granules, while the cells of rats fed the Mg-deficient diet for 4 days contained less granules than the controls, but contained extensively dilated rough surfaced endoplasmic reticulum, well-developed Golgi complexes, many mitochondria and ribosomes. These data suggest that hypomagnesemia could induce a release of histamine from dermal mast cells. So, the effect of a low Mg medium on the release of histamine was studied using peritoneal mast cells in vitro. A low Mg medium (0.2 mM Mg) induced much more histamine release than control medium (1 mM Mg) from the peritoneal mast cells obtained from both control and Mg-deficient rats fed with the Mg-deficient diet for 2 days. The peritoneal mast cells obtained on the 8th day of Mg-deficiency released much more histamine than controls in 1 mM Mg medium. These results suggest that hyperemia observed in Mg-deficient rats depends partly on histamine released from dermal mast cells.

Animals↗
PubMed1985

Protection by magnesium of renal calcinosis in furosemide-treated weanling rats with moderate magnesium deficiency.

Prolonged treatment of premature infants with the potent diuretic furosemide has resulted in hypercalciuria, sometimes with renal calcinosis and other complications. Furosemide was administered to weanling rats to explore its effect on magnesium and calcium metabolism. The animals were fed purified diets providing 40 mg magnesium/100 g diet or 10 mg magnesium/100 g. Half of each dietary group (40-F or 10-F) received 18 doses of furosemide, 20 mg/kg body weight, intraperitoneally between days 7 and 35, and half received normal saline intraperitoneally (40-O or 10-O). Furosemide had little effect on the magnesium-sufficient animals (40-F), but comparison of 10-O and 10-F data showed that it aggravated the magnesium-deficiency syndrome. Comparison of data from 40-F and 10-F animals showed the protective effect of magnesium in preserving calcium homeostasis in furosemide-treated animals: the elevation of calcium values in 10-F rats was greater in plasma (p less than 0.0005), heart (p less than 0.0025), and kidney (p less than 0.0005). Stated another way, furosemide was associated with severely disordered calcium metabolism only in animals fed suboptimal magnesium. Studies exploring the role of magnesium in furosemide-treated infants can be recommended.

Animals↗
PubMed1994

Magnesium deficiency in alcoholism: possible contribution to osteoporosis and cardiovascular disease in alcoholics.

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin I2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.

Alcoholism↗
PubMed1979

Magnesium deficiency: brain acetylcholine and motor activity.

Deprivation of magnesium ion in the diet caused a significant decrease in whole brain acetylcholine content. At the reginal level, the most pronounced effect was seen in the corpus striatum, diencephalon and cerebellum. The rate of depletion and recovery varied from region to region, and what appeared to be a return to normal acetylcholine in whole brain was the total of regions either higher or lower than control. The data presented here suggest that a positive relationship exists between the lowered cholinergic activity in the corpus striatum and increased nocturnal spontaneous motor activity.

Acetylcholine↗
PubMed1996

Hypocalcaemia and chronic alcohol intoxication: transient hypoparathyroidism secondary to magnesium deficiency.

The authors report the observation of an alcoholic patient admitted for tetanic manifestations, in whom severe hypocalcaemia associated with hyperphosphatemia were suggestive of hypoparathyroidism. Administration of magnesium supplementation alone improved the clinical features and led to the correction of the calcium abnormalities. The mechanisms of hypomagnesemia in alcohol intoxication are reviewed as well as the links with hypocalcaemia.

Aged↗
PubMed2004

Effects of gender on kidney function in magnesium-deficient rats.

This study investigated the gender differences in the kidney function of magnesium (Mg)-deficient rats. Male and female rats were fed a control diet or a Mg-deficient diet for 21 d. Mg-deficient diet had no significant effect on kidney calcium (Ca) or phosphorus (P) concentration in male rats, while Ca and P concentrations in female rats were significantly higher in Mg-deficient rats than in the control rats. With regard to indicators of kidney function, no significant differences in creatinine clearance and serum urea nitrogen concentration were observed among the groups. Serum albumin concentrations were significantly lower in rats fed the Mg-deficient diet than in rats fed the control diet. In both sexes, urinary albumin excretion was significantly higher in rats fed the Mg-deficient diet than in rats fed the control diet. Gender differences had no significant influence on creatinine clearance, serum urea nitrogen concentration, serum albumin concentration and urinary albumin excretion. These results suggest that gender differences have no effect on kidney function in Mg-deficient rats under the condition used.

Albuminuria↗
PubMed1990

Magnesium deficiency detected by intravenous loading test in variant angina pectoris.

To study whether magnesium (Mg) deficiency is present in patients with variant angina, 24-hour Mg retention of low dose Mg (0.2 mEq/kg lean body weight) administered intravenously over 4 hours in 20 patients with variant angina was examined. No patient had received calcium antagonists before or during the study. All had attacks of chest pain associated with ST elevation on electrocardiograms. Twenty-one subjects without ischemic heart disease were studied as control subjects. Ten patients with variant angina were restudied 10 to 529 days (mean 235 +/- 30) after the treatment with calcium antagonists (diltiazem 120 to 240 or nifedipine 40 to 80 mg/day), which resulted in complete suppression of anginal attacks. The mean serum Mg concentrations in the patients with variant angina and the control subjects were 2.1 +/- 0.05 and 2.1 +/- 0.03 mg/dl, respectively (difference not significant). However, 24-hour Mg retention in the patients with variant angina was 60 +/- 5%, while that in the control subjects was 36 +/- 3% (p less than 0.001), suggesting that Mg deficiency is present in at least some patients with variant angina. The mean serum Mg concentrations before and after calcium antagonist treatment in 10 patients with variant angina were 2.1 +/- 0.09 and 2.1 +/- 0.07 mg/dl, respectively (difference not significant). However, 24-hour Mg retention decreased significantly (p less than 0.01) from 60 +/- 6 to 34 +/- 7% after the treatment. There is Mg deficiency in many patients with variant angina and it is corrected after treatment with calcium antagonists.

Adult↗
PubMed1993

Magnesium deficiency affects malaria susceptibility in mice.

One hundred twenty mice were fed control and magnesium-(Mg) deficient diets containing 960 and 50 mg Mg/kg, respectively. After 12 days, mice were inoculated with several strains of Plasmodium (P). Parasitemias and survivals were monitored for 20 days after infection. The Mg-deficient diet protected mice against the nonlethal parasite P. chabaudi as shown by decreased parasitemia. All control mice infected with P. vinckei died from the infection. Mg-deficient mice had a much lower parasitemia and recovered from the infection. In mice infected with the lethal strain P. berghei, the parasitemia showed a biphasic response. In control mice, the first phase resulted in the death of 40% of the animals. After a spontaneous reduction of parasitemia, the surviving animals showed a second increase in parasitemia, which resulted in the death of the remaining animals. In the deficient group, all the animals survived the first phase of infection. By contrast, the evolution of the second phase was similar to that observed in controls. Examination of blood smears showed that the second phase corresponded to an invasion of young reticulocytes by the parasite. The results suggest that the protective effect of Mg deficiency is related to the decrease in erythrocyte Mg and to the prooxidative effect of this mineral deficiency in mature erythrocytes.

Animals↗