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PubMed1980

Effect of magnesium deficiency on rat bone and kidney sensitivity to parathyroid hormone.

A series of six experiments was conducted to investigate the effects of Mg deficiency in the young rat on parathyroid hormone (PTH) activity and on response to parathyroid extract (PTE) and to endogenously produced PTH stimulated by dietary Ca deficiency. Major criteria employed were 45Ca release from pre-labeled bone and urinary excretion of cAMP. Mg deficiency was accompanied by lowered 45Ca mobilization and urinary cAMP excretion, indicating either a depression in PTH secretion or tissue insensitivity to it. Administration of PTE resulted in equivalent increases in 45Ca mobilization irrespective of Mg status but increased cAMP excretion only in Mg-adequate animals, thus indicating a depressed sensitivity of kidney to PTH in the Mg-deficient animal. In vitro response of kidney cortex from Mg-deficient animals to PTE added to incubation medium indicated no defect in the adenyl cyclase system. Endogenous stimulation of PTH by low Ca diet increased cAMP in Mg-adequate animals but not in rats with pre-existing Mg deficiency. Mg deficiency did not reduce cAMP previously stimulated by Ca deficiency.

Adenosine Monophosphate↗
PubMed2001

Enhanced production of IL-1beta and IL-6 following endotoxin challenge in rats with dietary magnesium deficiency.

Serum IL-1beta, IL-6 and TNFalpha were not detected in control and Mg-deficient rats. These three cytokine levels in serum were increased after endotoxin challenge (1 mg/kg., i.p.), and the increase of IL-1beta and IL-6, but not TNFalpha, was significantly larger in Mg-deficient rats than in controls. Levels of mRNA for IL-1beta, IL-6 and TNFalpha in alveolar macrophages showed a tendency to decrease during Mg deficiency, but the levels of IL-1beta and TNFalpha mRNAs after endotoxin challenge were higher in Mg-deficient rats than in controls. These results suggest that the increased synthesis of cytokines by alveolar macrophages might contribute, in part, to high sensitivity to endotoxin during Mg deficiency.

Animals↗
PubMed2003

Alterations in osteoclast morphology following osteoprotegerin administration in the magnesium-deficient mouse.

In the present study, we used osteoprotegerin (OPG), which blocks osteoclastogenesis, to correct and thus explain the hypercalcemia that is seen during dietary Mg deficiency in the mouse. Control and Mg-deficient mice received injections for 12 days of either OPG or vehicle only. Serum Ca was similar in Mg-deficient mice treated with OPG and in control mice receiving OPG (9.2 +/- 0.3 mg/dl vs. 9.2 +/- 0.5). Both groups had significantly higher serum Ca than controls or Mg-deficient animals receiving vehicle alone. Surprisingly, Mg-depleted mice that received OPG in doses that inhibit osteoclastic bone resorption remained hypercalcemic. Because mature osteoclasts still present in the marrow might be hyperactive, we examined osteoclast morphology at the light microscopic and ultrastructural level. Light microscopic examination of trabecular bone showed few osteoclasts in OPG-treated mice. Ultrastructural examination revealed that osteoclasts in OPG-treated mice have decreased contact with the endosteal bone surface and absence of a ruffled border. Because the morphology of the existing pool of mature osteoclasts did not enhance resorption, another mechanism, such as increased intestinal absorption of Ca in Mg-deficient mice, likely contributes to the hypercalcemia observed during Mg deficiency.

Acid Phosphatase↗
PubMed1997

Magnesium-deficiency-enhanced post-ischemic myocardial injury is reduced by substance P receptor blockade.

Dietary Mg-deficiency increases the susceptibility of rat hearts to ischemia-reperfusion (I-R) injury in vitro, and also promotes substance P-associated neurogenic inflammation in vivo. The relationship between Mg-deficiency-induced neurogenic inflammation and the subsequently-enhanced free radical-mediated oxidative and functional injury during I-R was examined using the substance P receptor antagonist, L-703,606. Rats maintained on 3-week Mg-deficient (MgD; <1.8 mmol Mg/kg food) or Mg-sufficient (MgS; 25 mmol Mg/kg) diets were treated during this time with either L-703,606 (1.0 or 3.5 mg/sustained-release pellet, s.c.) or a placebo, prior to isolated perfused I-R. Post-ischemic functional recovery (pressure-volume work), myocardial effluent lactate dehydrogenase (LDH) activity, and lipid hydroperoxides (LOOH) were assessed after 30-min global ischemia. Lipid peroxidation-derived free radical production was monitored by alpha-phenyl-N-t-butylnitrone (PBN) spin trap infusion (2-3 mM final) and toluene-extracted effluents were analyzed by electron spin resonance (ESR) spectroscopy. PBN/alkoxyl adducts (alpha(H) = 1.89-1.93 G, alpha(N) = 13.58-13.63 G) were the dominant ESR signals detected in MgS and MgD I-R hearts; however, MgD hearts exhibited greater total LOOH (2.9 x higher) and alkoxyl adduct production (2.3 x higher), higher tissue LDH release (1.8 x ) and lower functional recovery (51% less) than MgS hearts. MgD rats treated with L-703,606 displayed a dose-dependent improvement in myocardial functional recovery (1.5-2 x higher), and reductions in LDH release (42-59% lower), total LOOH content (36-73% lower) and alkoxyl production (40-65% lower). Interestingly. L-703,606 treatment did not reduce functional impairment or lessen the tissue and oxidative injury experienced by MgS I-R hearts. These findings suggest that L-703,606 reduced oxidative injury and improved functional recovery of MgD I-R hearts by retarding substance P-mediated inflammatory/pro-oxidant events during the in vivo development of Mg-deficiency.

Animals↗