Moderate Magnesium Deficiency Research Articles

The Plasma is a Suitable Sample for Moderate Magnesium Deficiency Assessment but the Poor Accuracy of Colorimetric Technique Limits its Use

Background: The broadly disseminated notion that plasmatic concentration of magnesium is not a good indicator of its corporal status bases on the fact that normal magnesemia is reported in people with magnesium deficiency. The aim of this study was to identify a suitable sample for the assessment of magnesium corporal status in magnesium moderate deficiency. Methods and Findings: Female mice were fed with regular or low magnesium diet for 45 days. Bone, muscle, platelets and plasma were sampled and magnesium content was determined by atomic absorption spectrophotometry or using a colorimetric assay. As expected, magnesium content in bones was significantly diminished in animals fed with low magnesium diet when compared with those fed with normal diet (14.6 ± 0.5 versus 16.7 ± 0.2 mmol/100 g, p<0.05). Magnesium moderate deficiency was replicated in plasma (0.76 ± 0.08 versus 0.94 ± 0.09 mmol/L, p<0.05) but not in muscle or platelet samples. The correlation between bone and plasma magnesium contents was 0.53. ROC curve analysis revealed 83% specificity and 75% sensitivity for plasma magnesium cut off of 0.84 mmol/L. Conclusion: Plasma is a suitable sample to determine magnesium corporal status when deficiency is moderate. But, poor accuracy of colorimetric technique limits its use.

Magnesium deficiency accelerates cellular senescence in cultured human fibroblasts

Magnesium inadequacy affects more than half of the U.S. population and is associated with increased risk for many age-related diseases, yet the underlying mechanisms are unknown. Altered cellular physiology has been demonstrated after acute exposure to severe magnesium deficiency, but few reports have addressed the consequences of long-term exposure to moderate magnesium deficiency in human cells. Therefore, IMR-90 human fibroblasts were continuously cultured in magnesium-deficient conditions to determine the long-term effects on the cells. These fibroblasts did not demonstrate differences in cellular viability or plating efficiency but did exhibit a decreased replicative lifespan in populations cultured in magnesium-deficient compared with standard media conditions, both at ambient (20% O(2)) and physiological (5% O(2)) oxygen tension. The growth rates for immortalized IMR-90 fibroblasts were not affected under the same conditions. IMR-90 fibroblast populations cultured in magnesium-deficient conditions had increased senescence-associated beta-galactosidase activity and increased p16(INK4a) and p21(WAF1) protein expression compared with cultures from standard media conditions. Telomere attrition was also accelerated in cell populations from magnesium-deficient cultures. Thus, the long-term consequence of inadequate magnesium availability in human fibroblast cultures was accelerated cellular senescence, which may be a mechanism through which chronic magnesium inadequacy could promote or exacerbate age-related disease.

Potentialisation des effets du Δ9-tétrahydrocannabinol (THC) par la carence magnésique chez le rat

Aggressive behavior can be classified into three major categories: defense, social attack and predatory behavior. The predatory behavior of rats, which prompts them to prey on mice (muricidal behavior) may be induced by injection of high doses (11 mg/kg) of Delta9-tetrahydrocannabinol (THC) or by acute magnesium deficiency. We have studied the effect of a single injection of low doses of THC (2, 4 or 8 mg/kg) in rats with a severe (50 ppm magnesium diet) or moderate (150 ppm) magnesium deficiency. The combination of moderate magnesium deficiency with low doses of THC induced muricidal behavior in all the rats and an increase in aggressiveness at the doses of 4 or 8 mg/kg of THC. Hyperaggressiveness increased with magnesium deficiency severity. Serotonin is probably involved in aggressiveness induced by both moderate magnesium deficiency and low doses of THC, but implication of other neurotransmitters and magnesium deficiency-induced alterations of CB1-and/or CB2-receptor expression are not excluded.

Effect of moderate magnesium deficiency on serum lipids, blood pressure and cardiovascular reactivity in normotensive rats.

1. Weanling Wistar rats were pair fed for 10 weeks on a purified diet containing either normal or suboptimal quantities of magnesium (960 or 80 mg/kg respectively). 2. At week 2, hypomagnesaemia was accompanied by hypertriglyceridaemia, an increase in plasma cholesterol and a decrease in high-density-lipoprotein-cholesterol in animals fed on the Mg-deficient diet. At week 10, the increase in triglycerides observed in Mg-deficient animals was less marked while the increase in total cholesterol was more important. 3. During the whole experimental period, Mg-deficient animals never showed hypertension. At week 2, mean arterial blood pressure was significantly lower in Mg-deficient rats than in their respective controls, while heart rate was significantly increased. However, hypotension accompanied by tachycardia was a transitory phenomenon which appeared only in the early phase of deficiency. 4. Vascular reactivity was studied in vagotomized anaesthetized rats after ganglionic blockade with pentolinium and atropine sulphate. The reactivity to noradrenaline was significantly higher in Mg-deficient rats compared with pair-fed controls after 2 weeks on the experimental diet.

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.

Effect of magnesium deficiency on mineral excretion and concentration in rat serum, heart and kidney

Epidemiological evidence suggests that magnesium deficiency may be a factor in the etiology of cardiovascular and renal disease. During moderate magnesium deficiency in rats, caused by feeding 80 mg Mg/kg, however, magnesium levels in the soft tissues were previously shown to vary little. Consequently, in the present study, rats were fed either 80 or 500 mg Mg/kg for 6 weeks, and the concentrations of sodium, potassium, calcium, phosphate and magnesium were determined in serum, heart, kidneys, urine and feces to see whether changes in the levels of these elements, caused by the magnesium deficiency, play a role in the pathogenesis of these diseases. The concentration of oxalate was also determined in the urine. In the heart, both sodium and calcium were increased, while magnesium was decreased slightly in the deficient animals. In the kidney, nephrocalcinosis occurred, along with an increase in sodium and phosphate concentration. The feces contained increased levels of sodium and potassium. The data suggest that magnesium deficiency alters sodium transport. In the case of the heart, this may alter the membrane potential and could account for the cardiac arrhythmias associated with magnesium deficiency.

Influence of Maternal Magnesium Deficiency on Tissue Lead Content of Rats

Diets containing 150 or 600 ppm magnesium with or without 200 ppm lead were fed to rats throughout gestation and lactation to determine the influence of moderate magnesium deficiency on tissue lead content of maternal and offspring tissue. During lactation it was necessary to increase the lowest dietary magnesium level to 225 ppm. Lead caused a significant depression in both gestational weight gain and average pup weight regardless of the level of dietary magnesium. Maternal magnesium deficiency was evidenced by significant reductions in serum and tibia magnesium, a 17-fold increase in kidney calcium, and hyperemia of the ears. In offspring, however, only growth and tibia magnesium were significantly affected by the magnesium deficiency, and the maternal-fetal difference in serum and tibia magnesium concentration was maintained. Maternal magnesium deficiency resulted in significantly higher lead concentrations in dam liver, and offspring erythrocytes, liver and tibia. A mechanism for the enhanced accumulation of lead in maternal and offspring tissue as a result of maternal magnesium deficiency is not defined, but it is likely to involve enhanced intestinal lead absorption.

Effects of Magnesium Deficiency on Parturition and Uterine Involution in the Rat

The effects of moderate magnesium deficiency on the outcome of pregnancy, the process of parturition and uterine involution, were studied in successive experiments using Sherman rats. Females were fed purified diets containing 0.110 or 1.500 g Mg/kg throughout pregnancy and lactation. This magnesium deficient diet decreased the plasma magnesium but did not affect the number of pregnant rats or the weight of females at parturition. There was no change in the weight and size of litter. The number of still births was not significantly increased. The parturition process was observed; abdominal contractions were less obvious in deficient animals than in controls, and they were often not noticeable. Parturition was slightly lengthened in deficient rats. The major effects of magnesium deficiency occurred during lactation when the dam lost weight and the growth of her young was reduced. The uterine weight and its collagen content was higher and the collagen solubility was lower in the deficient rats than in controls between 2 and 10 days post partum. The delay in uterine involution could be prevented by provision of a magnesium supplement after parturition.