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PubMed2000

High prevelance of chronic magnesium deficiency in T cell lymphoblastic leukemia and chronic zinc deficiency in children with acute lymphoblastic leukemia and malignant lymphoma.

Magnesium and zinc are the elements having essential roles in regulation of cell growth, division and differentiation. There have been some studies in the literature suggesting an association between the deficiency of these elements and the development of malignant disorders. In this study hair and serum zinc and magnesium levels were investigated in children with acute lymphoblastic leukemia (ALL) and malignant lymphoma (ML) at the time of initial diagnosis. Ten children with T-cell ALL, 10 children with B-precursor ALL, 5 children with Burkitt's Lymphoma (BL), 11 children with Hodgkin's lymphoma (HL), 10 children with non-Burkitt non-Hodgkin's lymphoma (NBNHL) and 12 age and sex matched healthy children as a control group were included in the study. Mean hair magnesium levels in all of the groups of the patients were lower than the levels in the control group but the difference was statistically significant only in the children with T cell ALL comparable to the controls (28.9+/-3.9 microg/g and 87.6+/-18.5 microg/g respectiveley, p<0,05). Mean serum magnesium levels in all the cohorts were not significantly different than those in controls (p>0.05 in each comparison). Mean hair zinc levels in the patients with T-cell, B-precursor ALL, BL, HL, NBNHL were 103.4+/-14.6 microg/g, 100.9+/-7.8 microg/g, 91.1+/-19 microg/g, 72.5+/-9.1 microg/g, 103.2+/-12.2 microg/g respectively. Each of these levels were significantly lower than the mean hair zinc levels of the control group (141.2+/-9.6 microg/g, p<0.05 in each comparison). Although mean serum zinc levels in all of the groups were also decreased, the differences were statistically significant only in the groups with B-precursor ALL, HL and NBNHL (75.9+/-5.29 microg/dl, 68.6+/-7.3 microg/dl, 85.7+/-5.5 microg/dl respectively) when compared with controls (105.1+/-9.9 microg/dl, p<0.05 in each comparison). Hair magnesium and zinc levels showed a positive correlation with each other in all the groups (r congruent with 0.5). No significant difference was found in the mean hair/serum magnesium and zinc levels between malnourished and nonmalnourished patients. In conclusion, regarding the results of our study and previous data in the literature chronic magnesium and zinc deficiency seems to be associated with the development of ALL and malignant lymphoma in a group of patients.

Child↗
PubMed1978

Preliminary report on the magnesium deficient rat as a model of epilepsy.

Weanling male rats fed a low magnesium diet for 14 days were protected from audiogenic seizures by administration of phenobarbital and diphenylhydantoin. Amphetamine, levo-dopa, and magnesium chloride injected 45 minutes prior to testing did not prevent the seizures. In contrast to weanling male rats which became mortally seizure prone, 3--5 week-old female rats fed a low magnesium diet for 17--21 days varied as to their susceptibility to audiogenic seizures. If thrown into seizures by a loud noise, the females frequently could be revived for subsequent testing, thus affording the opportunity to design experiments using fewer animals.

Age Factors↗
PubMed1996

Protein peroxidation, magnesium deficiency and fibromyalgia.

Lipid and protein peroxidations were investigated in female patients with magnesium deficit (MD), fibromyalgia (FM) and age matched controls: malondialdehyde and protein carbonyls (PC), as well as serum, leucocyte and erythrocyte magnesium (EMg) were assessed in 20 controls, 25 FM and 16 MD patients. MDA are unchanged in MD and FM. PC are significantly increased (P < 0.01) in FM. EMg is significantly decreased in MD. There is a slight, but not significant, negative correlation between PC and EMg, in controls and MD. Protein peroxidations are demonstrated in FM. Further studies are needed in MD.

Adult↗
PubMed1984

Sodium kinetics and membrane potential in aorta of magnesium-deficient rats.

In light of the important role of magnesium (Mg) in vascular smooth muscle function, this study was undertaken to examine effects of dietary Mg deficiency on membrane potential (Em), sodium (Na) efflux and distribution, and total ion content in rat aorta. Rats were fed either Mg-sufficient or Mg-deficient diets for 30 days. The aortic arch was removed and a segment incubated in 22Na to monitor kinetics of Na efflux. Another segment was used for measurement of Em under control conditions and during ouabain suffusion. Total tissue water and ion content were also determined. Results of this work indicate that, in aorta from Mg-deficient rats, Em was less polarized and Na accumulated intracellularly. Although the Em in Mg-deficient aorta was not affected by ouabain, which suggested Na-K pump inhibition, Na efflux was greater in Mg-deficient aorta, suggesting increased passive permeability changes to Na as the mechanism responsible for these changes.

Animals↗
PubMed1994

Consequences of magnesium deficiency on the enhancement of stress reactions; preventive and therapeutic implications (a review).

Stress intensifies release of catecholamines and corticosteroids that increase survival of normal animals when their lives are threatened. When magnesium (Mg) deficiency exists, stress paradoxically increases risk of cardiovascular damage including hypertension, cerebrovascular and coronary constriction and occlusion, arrhythmias and sudden cardiac death (SCD). In affluent societies, severe dietary Mg deficiency is uncommon, but dietary imbalances such as high intakes of fat and/or calcium (Ca) can intensify Mg inadequacy, especially under conditions of stress. Adrenergic stimulation of lipolysis can intensify its deficiency by complexing Mg with liberated fatty acids (FA), A low Mg/Ca ratio increases release of catecholamines, which lowers tissue (i.e. myocardial) Mg levels. It also favors excess release or formation of factors (derived both from FA metabolism and the endothelium), that are vasoconstrictive and platelet aggregating; a high Ca/Mg ratio also directly favors blood coagulation, which is also favored by excess fat and its mobilization during adrenergic lipolysis. Auto-oxidation of catecholamines yields free radicals, which explains the enhancement of the protective effect of Mg by anti-oxidant nutrients against cardiac damage caused by beta-catecholamines. Thus, stress, whether physical (i.e. exertion, heat, cold, trauma--accidental or surgical, burns), or emotional (i.e. pain, anxiety, excitement or depression) and dyspnea as in asthma increases need for Mg. Genetic differences in Mg utilization may account for differences in vulnerability to Mg deficiency and differences in body responses to stress.

Adrenal Cortex Hormones↗
PubMed2004

In vitro application of endotoxin to thoracic aortas from magnesium-deficient rats enhances vascular hyporeactivity to phenylephrine.

OBJECTIVE: Endotoxin-induced vascular hyporeactivity to phenylephrine (PE) is well described in rat aortas, but has not been investigated in those from magnesium (Mg)-deficient rats in vitro. METHODS: Segments of thoracic aorta from control and Mg-deficient rats were incubated in culture medium for 6 hours in the presence or absence of bacterial lipopolysaccharide (LPS; 0.001-10 microg/mL). Contractions to PE were measured with or without an inducible nitric oxide synthase (iNOS) inhibitor (1400W; 0.1 and 1 microM), a guanylate cyclase inhibitor (ODQ; 0.1 and 1 microM), or a potassium channel inhibitor (TEA; 1 and 10 mM). RESULTS: LPS induced hyporeactivity in a concentration-dependent manner under relatively low concentrations (0.001-0.1 microg/mL), however, there was no significant difference at 0.1, 1 and 10 microg/mL. LPS-induced hyporeactivity was not significantly affected by endothelium-denudation. The hyporeactivity was enhanced in thoracic aortas from Mg-deficient rats by LPS (0.01, 0.1 and 1 microg/mL). LPS (1 microg/mL) induced hyporeactivity was reversed with 1400W, ODQ or TEA in both aortas in a concentration-dependent manner, however the degree of reversal was weaker in the Mg-deficient rat aorta than in the control rat one. iNOS mRNA level was increased by LPS (0.1 microg/mL) and the increment was significantly high in Mg-deficient rat thoracic aorta. CONCLUSIONS: From these results it is clearly demonstrated that LPS-induced vascular hyporeactivity to PE is enhanced in thoracic aorta from Mg-deficient rats, and it is suggested that LPS-induced NO production might contribute to the enhancement via stimulation of NO-cyclic GMP-potassium channel pathway.

Animals↗
PubMed1994

Potentiation of magnesium-deficiency-induced foetotoxicity by concomitant iron deficiency and its prevention by adequate supply via drinking water.

Magnesium (Mg) and iron (Fe) deficiency frequently develop during pregnancy. Therefore these factors were studied alone (Mg-L, resp. Fe-L) or in combination (Mg-L/Fe-L) on 16 female and 8 male adult fertile Sprague-Dawley rats. The animals were offered a basal diet containing 30 per cent and 17 per cent of the rat's requirement for magnesium and iron, respectively, starting 21 days before mating (2:1) until 49 days after mating. Offspring were also kept on this regimen during a 3-week lactation period and 7 days post weaning. Drinking water was either enriched with 101 ppm Fe2+ (ferrous gluconate): Mg-L, or 365 ppm magnesium (magnesium-L-aspartate hydrochloride trihydrate, MAH): Fe-L, or with any: Mg-L/Fe-L or with both electrolytes: Controls. Fertility remained unaffected under these conditions. Clinically, Fe-L induced iron deficiency and growth retardation of offspring. Pronounced reproductive toxicity was elicited by Mg-L and was even potentiated by Mg-L/Fe-L. In the parental generation, too, adverse effects of Mg-L were aggravated by Mg-L/Fe-L despite the fact that no iron accumulation occurred. Bioavailability of iron was not impaired by magnesium as MAH. With respect to human pregnancy magnesium supplementation has higher priority over iron supplements. To improve tolerance and compliance both minerals are suggested to be taken simultaneously.

Administration, Oral↗