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At least 397 records · Page 22Linked to original sources
PubMed1997

Inhibition of nitric oxide synthase prevents magnesium-free-induced epileptiform activity in guinea-pig piriform cortex neurones in vitro.

The effects of N-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, were examined on Mg2+-free-induced epileptiform activity, in guinea-pig piriform cortex slices in vitro. L-NAME (0.1-1 mM) had no effect on neuronal membrane properties or electrically-evoked postsynaptic potentials (PSPs). In contrast, during superfusion of the slices with Mg2+-free solution neurones exhibited spontaneous and stimulus-evoked epileptiform potentials that were suppressed in the presence of L-NAME (100 microM) or the selective NMDA receptor antagonist DL-APV (100 microM). The inhibitory effects induced by L-NAME were reversibly reduced by L-arginine (1 mM), but not D-arginine (1 mM), the latter drug not being a substrate for NO formation. It was concluded that L-NAME can suppress epileptiform activity induced by Mg2+-free exposure primarily through a decrease in presynaptic transmitter release, although additional actions on the NMDA-receptor complex were also considered.

Animals↗
PubMed2003

Characteristics of MgxZn1-xO thin film bulk acoustic wave devices.

Piezoelectric thin film zinc oxide (ZnO) and its ternary alloy magnesium zinc oxide (MgxZn1-xO) have broad applications in transducers, resonators, and filters. In this work, we present a new bulk acoustic wave (BAW) structure consisting of Al/MgxZn1-xO/n(+)-ZnO/r-sapphire, where Al and n+ type ZnO serve as the top and bottom electrode, respectively. The epitaxial MgxZn1-xO films have the same epitaxial relationships with the substrate as ZnO on r-Al2O3, resulting in the c-axis of the MgxZn1-xO being in the growth plane. This relationship promotes shear bulk wave propagation that affords sensing in liquid phase media without the dampening effects found in longitudinal wave mode BAW devices. The BAW velocity and electromechanical coupling coefficient of MgxZn1-xO can be tailored by varying the Mg composition, which provides an alternative and complementary method to adjust the BAW characteristics by changing the piezoelectric film thickness. This provides flexibility to design the operating frequencies of thin film bulk acoustic wave devices. Frequency responses of devices with two acoustic wave modes propagating in the specified structure are analyzed using a transmission line model. Measured results show good agreement with simulation.

Acoustics↗
PubMed2004

Dietary magnesium depletion does not promote oxidative stress but targets apical cells within the mouse caput epididymidis.

It is well documented that a dietary deficiency in magnesium can induce oxidative stress and an inflammatory response in animal models. In our study, we have investigated these responses in the mouse epididymis after mice had been fed a magnesium-deficient diet for a 2-week duration. The extracellular and intracellular concentrations of magnesium where shown to be depleted on this diet. This was followed, however, only in the liver of the Mg-deficient animals, by an increase in both alpha 2-macroglobulin (alpha-2m), an acute phase marker, and interleukin-6 transcripts suggesting that an inflammatory response had been initiated. These changes were correlated with a decrease in circulating neutrophils. To address the question of whether or not peroxidation was induced in mouse epididymis following hypomagnesia, we have monitored the level of endogenous peroxidation, their ability to respond to induced peroxidation as well as the expression and activity of the enzymatic glutathione peroxidase (GPX) antioxidant family. To evaluate if the epididymis had evolved specific protections against peroxidation, other organs such as the liver and the kidney were monitored in parallel. We detected no evidence for increased peroxidation in any of the mouse organs tested. However, GPX activity was found to be significantly lower in the liver and the kidney of Mg-deficient animals while it was unchanged in the epididymides of the same animals during the deficiency. Histological analysis of the epididymis showed no major difference in the overall cytological aspect of the organ. Segment 2 of the caput, however presented a significant increase in the number of apically located cells or blebbing cells. Immunohistochemical analysis proved that these cells were epididymal apical cells and not infiltrated leukocytes. These observations suggested that the mouse caput epididymidis segment 2 specifically responded to Mg deficiency via the apical cells. Finally, a comparative analysis of stress response genes was conducted in control and magnesium-deficient caput epididymidis samples. It brought forward some genes that might be involved in the peculiar response of the caput epithelium following hypomagnesia.

Animals↗
PubMed2005

Copper- and magnesium protoporphyrin complexes inhibit oxidative modification of LDL induced by hemin, transition metal ions and tyrosyl radicals.

The oxidative modification of LDL may play an important role in the early events of atherogenesis. Thus the identification of antioxidative compounds may be of therapeutic and prophylactic importance regarding cardiovascular disease. Copper-chlorophyllin (Cu-CHL), a Cu(2+)-protoporphyrin IX complex, has been reported to inhibit lipid oxidation in biological membranes and liposomes. Hemin (Fe(3+)-protoporphyrin IX) has been shown to bind to LDL thereby inducing lipid peroxidation. As Cu-CHL has a similar structure as hemin, one may assume that Cu-CHL may compete with the hemin action on LDL. Therefore, in the present study Cu-CHL and the related compound magnesium-chlorophyllin (Mg-CHL) were examined in their ability to inhibit LDL oxidation initiated by hemin and other LDL oxidizing systems. LDL oxidation by hemin in presence of H(2)O(2) was strongly inhibited by both CHLs. Both chlorophyllins were also capable of effectively inhibiting LDL oxidation initiated by transition metal ions (Cu(2+)), human umbilical vein endothelial cells (HUVEC) and tyrosyl radicals generated by myeloperoxidase (MPO) in presence of H(2)O(2) and tyrosine. Cu- and Mg-CHL showed radical scavenging ability as demonstrated by the diphenylpicrylhydracylradical (DPPH)-radical assay and estimation of phenoxyl radical generated diphenyl (dityrosine) formation. As assessed by ultracentrifugation the chlorophyllins were found to bind to LDL (and HDL) in serum. The present study shows that copper chlorophyllin (Cu-CHL) and its magnesium analog could act as potent antagonists of atherogenic LDL modification induced by various oxidative stimuli. As inhibitory effects of the CHLs were found at concentrations as low as 1 mumol/l, which can be achieved in humans, the results may be physiologically/therapeutically relevant.

Atherosclerosis↗
PubMed1999

Effect of dietary phytate on magnesium bioavailability and liver oxidant status in growing rats.

Male albino rats (initial average weight 60 g) were fed semi-synthetic diets based on casein, corn starch and sunflower oil over 21 days. All diets were supplemented with 300 mg magnesium from MgSO4x7H2O and 0,7.5 and 15 g phytic acid (PA) from sodium phytate per kg. The addition of PA to the diets resulted in a dose-dependent decrease of apparent Mg absorption and Mg concentration in the plasma and femur. Impaired Mg bioavailability due to 15 g PA/kg diet was accompanied by an increase of hepatic thiobarbituric acid reactive substances and protein carbonyls as well as by a moderate decline in liver reduced glutathione (GSH) levels. The liver homogenates of rats receiving the diets with 7.5 and 15 g PA/kg, respectively, were much more susceptible to iron-induced lipid peroxidation than those of the controls. Hepatic antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), glucose-6-phosphate dehydrogenase (G6PDH)], alpha-tocopherol concentration and phenyl-N-tert-butylnitrone (PBN) adducts using electron spin resonance spectroscopy remained unchanged by the different dietary treatments. Under the conditions of a marginal dietary Mg supply, phytate had pro-oxidative rather than antioxidative effects in the case of liver metabolism.

Absorption↗
PubMed2002

Magnesium influx enhanced by nitric oxide in hypertensive rat proximal tubule cells.

An abnormal handling of renal magnesium has been suggested to cause salt-sensitive hypertension. The filtered magnesium is first reabsorbed in the proximal tubule. Amiloride has been shown to enhance renal magnesium conservation, but the regulatory mechanisms are unknown yet. High-salt (8% NaCl) diet decreased serum magnesium concentration, while increased urinary magnesium in Dahl salt-sensitive (DS) rat. Furthermore, the expression of nitric oxide synthase type 3 and nitric oxide (NO) content were decreased in high-salt loaded DS rat. In isolated proximal tubule cells, amiloride (0.1 mM) increased intracellular free magnesium concentration ([Mg(2+)](i)). However, the net [Mg(2+)](i) increase in the high-salt loaded DS rat was smaller than other groups. NOR1 (0.1 mM), a NO donor, restored the increase of [Mg(2+)](i) to the same level of other groups. On the contrary, L-NMMA (0.1 mM), an inhibitor of NO production, inhibited the increase of [Mg(2+)](i) in all groups. These results suggest that intracellular NO has an important role to up-regulate amiloride-elicited magnesium influx.

Animals↗
PubMed2006

Characterization of the surface properties of Mg/Al oxides by the solvation parameter model.

The oxides of different Mg/Al ratios (Mg/Al = 0, 0.1, 5, 10 and infinity) were prepared, and the characterization of these oxides was attempted by estimating characteristic interaction parameters based on the solvation parameter model. The magnitudes of the regression coefficients varied with the increase of Mg/Al ratio. For the oxide of Mg/Al = 0.1 and Al2O3, the contribution of these characteristic interactions for solutes' retention was similar to that of the common silica, and the dipolarity/polarizability (pi*), the solute hydrogen bond donating (alpha2(H)) and accepting (beta2(H)) abilities played an important role. Yet, the retention behavior at a higher Mg/Al ratio (Mg/Al = 5, 10 and MgO) drastically changes, and V(i)/100 (the intrinsic molar volume), pi*, alpha2(H) and beta2(H) all favored the solutes retention. By comparison of the regression coefficients on various normal-phase (NP) and reversed-phase (RP) columns, a new model was developed to correlate the solute retention factors on Mg/Al = 5, 10 and MgO columns with the data of NP and RP columns.

Aluminum Oxide↗
PubMed2006

Controlling self-assembled perovskite-spinel nanostructures.

We report a discovery that self-assembled perovskite-spinel nanostructures can be controlled simply by selecting single-crystal substrates with different orientations. In a model BiFeO(3)-CoFe(2)O(4) system, a (001) substrate results in rectangular-shaped CoFe(2)O(4) nanopillars in a BiFeO(3) matrix; in contrast, a (111) substrate leads to triangular-shaped BiFeO(3) nanopillars in a CoFe(2)O(4) matrix, irrespective of the volume fraction of the two phases. This dramatic reversal is attributed to the surface energy anisotropy as an intrinsic property of a crystal.

Aluminum Oxide↗
PubMed1999

Ceramide generation in nitric oxide-induced apoptosis. Activation of magnesium-dependent neutral sphingomyelinase via caspase-3.

Sodium nitroprusside (SNP), a NO donor, has been recognized as an inducer of apoptosis in various cell lines. Here, we demonstrated the intracellular formation of ceramide, a lipid signal mediator, in SNP-induced apoptosis in human leukemia HL-60 cells and investigated the mechanisms of ceramide generation. The levels of intracellular ceramide increased to, at most, 160% of the control level in a time- and dose-dependent manner when the cells were treated with 1 mM SNP. SNP also decreased the sphingomyelin level to approximately 70% of the control level and increased magnesium-dependent neutral sphingomyelinase (N-SMase) activity to 160% of the control activity 2 h after treatment. Neither acid SMase nor magnesium-independent N-SMase was affected by SNP. Caspases are thought to be key enzymes in apoptotic cell death. Acetyl-Asp-Glu-Val-Asp-aldehyde, a synthetic tetrapeptide inhibitor of caspases, inhibited magnesiumdependent N-SMase, ceramide generation, and apoptosis. Moreover, recombinant purified caspase-3 increased magnesium-dependent N-SMase in a cell-free system. These results suggest that the findings that SNP increased ceramide generation and magnesium-dependent N-SMase activity via caspase-3 are interesting to future study to determine the relation between caspases and sphingolipid metabolites in NO-mediated signaling.

Apoptosis↗
PubMed2002

Changes in gene expression in rat thymocytes identified by cDNA array support the occurrence of oxidative stress in early magnesium deficiency.

Magnesium deficiency in experimental animals leads to inflammation, exacerbated immune stress response and a decrease of specific immune response. It also results in a significant increase in free radical species and subsequent tissue injury. An accelerated thymus involution was observed in Mg-deficient rats in relation to enhanced apoptosis and enhanced susceptibility to oxidative stress. To examine the stress-inducing effects of low Mg status on thymocytes, cDNA arrays were used to evaluate changes in gene expression in weaning rats submitted to Mg deficiency of short duration (2 days). Several genes exhibited changes in their expression caused by Mg deficiency before any perceptible modification in cell integrity and functions. The up-regulated genes included cytochrome c oxidase, glutathione transferase, CuZn superoxide dismutase, genes associated with the stress response (HSP70 and HSP84) and a gene involved in DNA synthesis and repair (GADD45). The down-regulated genes included Na/P cotransporter 1. These findings are consistent with altered cell growth, modifications of ion fluxes and oxidative stress described during Mg deficiency. The observation of induction of genes involved in protection and repair in cells from Mg-deficient animals provides additional evidence of the role of oxidative stress in the pathobiology of this deficiency.

Animals↗
PubMed2000

Magnesium status and parameters of the oxidant-antioxidant balance in patients with chronic fatigue: effects of supplementation with magnesium.

OBJECTIVE: Magnesium deficiency and oxidative stress have both been identified as pathogenic factors in aging and in several age-related diseases. The link between these two factors is unclear in humans although, in experimental animals, severe Mg deficiency has been shown to lead to increased oxidative stress. METHODS: The relationship between Mg body stores, dietary intakes and supplements on the one hand and parameters of the oxidant-antioxidant balance on the other was investigated in human subjects. RESULTS: The study population consisted of 93 patients with unexplained chronic fatigue (median age 38 years, 25% male, 16% smokers and 54% with Chronic Fatigue Syndrome (CFS). Mg deficient patients (47%) had lower total antioxidant capacity in plasma (p=0.007) which was related to serum albumin. Mg deficient patients whose Mg body stores did not improve after oral supplementation with Mg (10 mg/kg/day) had persistently lower blood glutathione levels (p=0.003). In vitro production of thiobarbituric acid reactive substances (TBARS) by non-HDL lipoproteins incubated with copper was related to serum cholesterol (p<0.001) but not to Mg or antioxidants and did not improve after Mg supplementation. In contrast, velocity of formation of fluorescent products of peroxidation (slope) correlated with serum vitamin E (p<0.001), which was, in turn, related to Mg dietary intakes. Both slope and serum vitamin E improved after Mg supplementation (p<0.001). CONCLUSIONS: These results show that the lower antioxidant capacity found in moderate Mg deficiency was not due to a deficit in Mg dietary intakes and was not accompanied by increased lipid susceptibility to in vitro peroxidation. Nevertheless, Mg supplementation was followed by an improvement in Mg body stores, in serum vitamin E and its interrelated stage of lipid peroxidation.

Adolescent↗