Patterns of TRPM7 expression in hypothalamic and hippocampal neurons in modeling of nutritional magnesium deficiency.

Patterns of expression of TRPM7, the major cellular magnesium transporters in neurons of the hypothalamic region and hippocampus, were studied immunohistochemically. Multidirectional nature and different levels of the expression of the above antigen were revealed during modeled magnesium deficiency with regard to structural and functional features of neuron organization in the hypothalamic paraventricular and supraoptic nuclei as well as hippocampal field CA1 and CA3. Changes in the structural characteristics of neurons in the studied areas (absolute and relative indicators) and TRPM7 expression patterns were quantitatively analyzed considering the data on the role of the studied antigen in magnesium homeostasis, cell damage, and compensation.

[Cardioprotective properties of zoniporide studied on experimental ischemia and reperfusion models in rat myocardium].

Using the experimental model of rat heart ischemia/reperfusion, it is established that zoniporide (inhibitor of Na+/H+ exchanger) produces a significant (1.4-fold) decrease in the area of myocardial necrosis, 2.1-fold decrease in the serum troponin I level, and 2-fold decrease in the severity of post-reperfusion arrhythmias.

[Correction of isoproterenol-induced myocardial injury with magnesium salts in magnesium-deficient rats].

The effect of Mg L-asparaginate (Mg-L-Asp), Mg chloride (MgCl2) and Mg sulfate (MgSO4) on the severity of isoproterenol-induced myocardial injury in Mg-deficient rats has been evaluated. To induce Mg deficiency, twenty-eight rats were placed on a low Mg diet (Mg content < 15 mg/kg) and demineralized water for 10 weeks. Twelve control rats were fed a basal control diet (Mg content = 500 mg/kg) and water (with Mg content 20 mg/l) for equal duration. On day 49 of low Mg diet, Mg-deficient rats were randomly divided into four groups: 1) group that continued to receive low Mg diet; 2) low Mg diet plus oral MgSO4; 3) low Mg diet plus oral Mg-L-Asp and 4) low Mg diet plus oral MgCl2 (50 mg of Mg per kg of body weight). Isoproterenol was injected subcutaneously (30 mg/kg BW, twice, at an interval of 24 hours) on the day 70 of the study, when plasma and erythrocyte Mg level in rats fed a low Mg diet were significantly decreased by 47% and 45% compared to intact animals. Twenty-four hours after second injection of isoproterenol, tests for activities of creatine kinase (CK), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) were run and histopathological study was carried out. Administration of isoproterenol to rats resulted in significantly elevated plasma CK, LDH and AST, however analyses in Mg deficient group demonstrated more dramatically increased activity of CK and AST compared to control rats (3,06 and 4,67 fold in Mg-deficient group vs. 1,91 and 3,92 fold in intact group). Increased leakage of cardiac injury markers was concomitant to increased volume of fuchsinophilic cardiomyocytes (54.2 +/- 1.7% in Mg-deficient group and 38.9 +/- 1.9% in intact group, p < 0.05). However, pretreatment with of MgCl2, MgSO4 and Mg-L-Asp during 21 days favorably decreased sensitivity of myocardium to isoproterenol-induced ischemic injury. All evaluated salts significantly decreased myocyte marker enzymes as well as protected myocardium against isoproterenol-induced histopathological perturbations.

[Functional reserves of the heart under conditions of alimentary magnesium deficit].

Aim of the study was to assess functional reserves of myocardium in animals with deficit of magnesium during stress tests. Magnesium deficit was modeled by 10 week long magnesium deficient diet. After 54% lowering of magnesium level in erythrocytes we registered left ventricular pressure, myocardial contraction and relaxation rates, heart rate, systolic and diastolic arterial pressure, intensity of structures functioning. Than we subjected hearts of these animals to volume load, graded stimulation of cardiac adrenoreceptors, maximal isometric load by clamping ascending aorta. In animals with magnesium deficit we noted smaller increases of left ventricular pressure, myocardial contraction and relaxation rates under conditions of all functional tests, and of systolic arterial pressure during loading with volume and adrenaline. Lowering of myocardial reactivity under conditions of volume and adrenaline loading as well as isometric work load could constitute a basis of genesis of heart failure in magnesium deficit.

[Magnesium and the oxidative stress].

Magnesium deficiency has been shown to result in alterations of cellular functions and biological activity of molecules. The review discusses possible relationship between Mg2+ deficiency and development of oxidative stress. Decrease of Mg2+ concentration in tissues and blood is accompanied with elevation of the oxidative stress markers, including products of the oxidative modification of lipids, proteins and DNA. The reduction in antioxidant defenses is synchronous with oxidative stress markers elevation. Different mechanisms including systemic reactions (hyperactivation of inflammation and endothelial dysfunction) and cellular changes (mitochondrial dysfunction and excessive production of fatty acids) are supposed to be involved in development and maintenance of the oxidative stress due to Mg2+ deficiency. Therefore the facts consolidated into the review evidence clear relation between Mg2+ deficiency and the oxidative stress development.

Correction of furosemide-induced magnesium deficiency with different stereoisomers of organic magnesium salts: a comparative study.

We compared the efficiency of different stereoisomers of organic magnesium salts (Mg DL-, Mg D-, and Mg L-aspartate and Mg L- and Mg DL-glutamate) after oral administration under conditions of furosemide-induced magnesium deficiency. The time to complete compensation of erythrocyte magnesium level was 5 days for Mg L-aspartate, 10 and 8 days for Mg L-glutamate and Mg D-aspartate, respectively, and 11 days for Mg DL-aspartate and Mg DL-glutamate. These findings attest to better bioavailability of Mg complex with L-stereoisomer of aspartate in comparison with DL and D-stereoisomers and stereoisomers of Mg glutamate.