Synthesis of Lactones by Baeyer-Villiger Oxidation with Magnesium Monoperphthalate Hexahydrate.
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The ground- and excited-state species of acridine adsorbed on (NH(4))(2)SO(4), SiO(2), Al(2)O(3), and MgO surfaces were investigated in order to determine the precursor species and electronic states responsible for acridine photodegradation on particles serving as models of atmospheric particulate matter. The species present on each solid surface were characterized by comparing the steady-state absorption and fluorescence spectra, time-resolved fluorescence, and absorption measurements on acridine in solution with those corresponding to adsorbed acridine. On silica, the ground-state species present were hydrogen-bonded, neutral, and protonated, while on alumina hydrogen-bonded and neutral species were identified. A comparison of the protonated acridine absorption and emission intensities on silica and alumina with those observed for acridine in acidic water demonstrated that the emission on the surfaces is higher than expected. This was interpreted as resulting from photoprotolytic reactions on silica and alumina. For acridine adsorbed on ammonium sulfate, protonated acridine was the only adsorbed species identified. Since, at a similar ground-state absorbance, the fluorescence intensity of acridine on ammonium sulfate was smaller than for acridine in acidic water, the quenching of the excited state or a rapid photochemical reaction with the surface was proposed. On magnesium oxide, the presence of neutral and hydrogen-bonded acridine species were characterized from the two-component analysis of the fluorescence, the triplet-triplet absorption decay curves, and the time-resolved emission spectra at different time delays. As demonstrated in these studies, acridine adsorbed species and their decay pathways depend on the acidic properties of these models of atmospheric particulate matter. In addition, a comparison of the photodegradation rates of acridine on the different solids tested is presented and discussed in terms of the nature of the species and their decay pathways.
We review recent developments in controlling photoinduced desorption processes of alkali halides. We focus primarily on hyperthermal desorption of halogen atoms and show that the yield, electronic state, and velocity distributions of desorbed atoms can be selected using tunable laser excitation. We demonstrate that the observed control is due to preferential excitation of surface excitons. This approach takes advantage of energetic differences between surface and bulk exciton states and probes the surface exciton directly. We demonstrate that desorption of these materials leads to controlled modification of their surface geometric and electronic structures. We then extend the exciton mechanism of desorption, developed for alkali halides, to metal oxide surfaces, in particular magnesium oxide. In addition, these results demonstrate that laser desorption can serve as a solid-state source of halogen and oxygen atoms, in well-defined electronic and velocity states, for studying chemical processes in the gas phase and at surfaces.
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To improve the dynamic in-vitro evaluation of the effects of antacids, we have developed the 'artificial stomach' model by adding a 'duodenal reservoir' to receive the gastric emptying flux and simulated bicarbonate secretion, thus constituting an 'artificial stomach-duodenum' model. With this model we measured antacid-induced resistance to gastric acidification, and simultaneously evaluated the effect of antacid activity on the duodenal milieu. The model also permitted evaluation of the antacid effects of proteins (as natural antacids), and of drugs containing aluminium phosphate, alone or combined with magnesium oxide, or aluminium and magnesium hydroxides. At the gastric site, these drugs, as well as the proteins (that is, meat extract), induced a strong resistance to acidification due to the gastric emptying flux and to antacid composition. At the duodenal site, the decrease of the acid load penetrating into the duodenum varied, depending on the efficacy of gastric antacid activity. Duodenal pH was related to the equilibrium between bicarbonate secretion and the emptying of acid load. Proteins and aluminium phosphate induced the same duodenal pH as in the control tests without antacids, but magnesium-containing antacids increased it, thus decreasing bicarbonate consumption. The antacid mechanisms within the stomach, and the fate of antacids in the duodenal milieu, might explain the variation in duodenal pH in response to antacid administration.
A female Thai baby born to non-consanguineous parents, presented with primary hypomagnesemia at 10 weeks of age, and suffered recurrent convulsions that responded to magnesium supplementation. She was found to have hypomagnesemia (Mg 0.35-1.02 mEq/L) and a low urinary magnesium excretion of less than 10 mg per day, or urinary Mg/Cr that ranged from 0.005-0.01 mg/mg. Intermittent hypomagnesemia and one episode of hypocalcemia with occasional convulsions developed, due to irregular consumption of oral magnesium sulfate, which had a bitter taste, caused frequent loose stools and black staining of the teeth. Better compliance after switching from magnesium sulfate to magnesium oxide resulted in an increased level of serum magnesium and the gradual disappearance of the black staining of the teeth and frequent loose stools. The patient required an oral elemental magnesium dosage of 15-30 mg/kg/day to maintain the serum magnesium level at between 1.02-1.33 mEq/L and keep her free from convulsions. The follow-up period was 7 years during which the patient showed normal physical growth and a mild degree of mental retardation.
Magnesium deficit and oxidative stress are common features of the diabetic state. This concept supported by another observation that magnesium deficiency is also a state of increased oxidative stress prompted us to study the effect of magnesium supplementation on magnesium status and oxidative stress in diabetic rats. For this purpose, male Wistar rats were made diabetic with a single intraperitoneal injection of Alloxan. Experimental diabetes caused a significant decrease in serum and red blood cell magnesium levels and increased urinary excretion of magnesium. Marked increase in plasma malondialdehyde and corresponding decrease in vitamins C & E, uric acid and total thiols was observed in the diabetic rats as compared to control group. In liver, MDA levels were increased significantly with concomitant decrease in vitamin C, non-protein thiols and antioxidant enzymes (SOD & GST). Magnesium supplementation for four weeks restored serum and RBC magnesium levels to near normal levels with marginal but significant decrease in blood glucose levels. Plasma and liver MDA levels were reduced significantly and vitamin C and total thiols were increased significantly with magnesium supplementation. Antioxidant enzyme activity was also increased significantly with magnesium supplementation in diabetic rats. Our data clearly demonstrates that alloxanic diabetes is associated with decreased magnesium status and increased oxidative stress and that magnesium supplementation can in part restore the antioxidant parameters and decrease the oxidative stress in experimental diabetic rats.
Nanocrystals of magnesium oxide react with organophosphorus compounds at room temperature by dissociative chemisorption, which we term "destructive adsorption". This process involves cleavage of P-O and P-F bonds (but not P-C bonds) and immobilization of the resultant molecular fragments. These ultrafine powders have unusual crystalline shapes and possess high surface concentrations of reactive edge/corner and defect sites, and thereby display higher surface reactivity, normalized for surface area, than typical polycrystalline material. This high surface reactivity coupled with high surface area allows their use for effective decontamination of chemical warfare agents and related toxic substances. Herein data is presented for paraoxon, diisopropylfluorophosphate (DFP), and (CH3CH2O)2P(O)CH2-SC6H5 (DEPTMP). Solid-state NMR and IR spectroscopy indicate that all OR and F groups dissociate; this leaves bound -PO4, -F, and -OR groups for paraoxon, DFP, and DEPTMP, respectively. For paraoxon, it was shown that one monolayer reacts. For DEPTMP, the OR groups dissociate, but not the P-CH2SC6H5 group. The nanocrystalline MgO reacts much faster and in higher capacity than typical activated carbon samples, which physisorb but do not destructively adsorb these phosphorous compounds.
Mechanochemically induced dechlorination of mono-chlorobiphenyl (BP-Cl) on the surfaces of metal oxides was compared with that on metal hydroxides, using the three metals of Mg, Al, and La as examples. The metal oxides, such as gamma-alumina (gamma-Al2O3), magnesium oxide (MgO) and lanthanum oxide (La2O3) showed an efficient ability to dechlorinate the BP-Cl; however, BP-Cl remained in the ground samples when the hydroxides were used. From the product analysis using gas chromatography/mass spectrometry (GC/MS) and electron spin resonance (ESR) measurements, it was confirmed that the charge transfer from the O2- site on the surface of the oxide additives due to the intense grinding has plays a significant role in the decomposition of the chlorinated compound. Based on the observed dependence of the dechlorination on the radical occurrence, some practical methods were proposed to improve the destruction efficiency of the chlorinated organic compounds.
The bioavailability was studied of three magnesium preparations-Asmag, Slow-Mag and magnesium oxide (wafer)-administered to healthy volunteers for two weeks. The observed increase of magnesium level in the serum was not statistically significant.
The adsorption of diazepam on magnesium trisilicate, magnesium oxide, aluminium hydroxide, calcium carbonate, magnesium carbonate, bismuth oxycarbonate bismuth subsalicylate, talc, dibasic calcium phosphate, magnesium stearate, kaolin and charcoal was studied at 37 degrees C. With the exception of charcoal, magnesium trisilicate exhibited the highest adsorptive capacity for the drug. Talc and dibasic calcium phosphate had the lowest adsorptive power while the other materials tested had intermediate adsorption properties. In general, low elution values were obtained with both acidic and alkaline solutions. The presence of a specific interaction between diazepam and surface sites of the adsorbing materials was suggested. The Langmuir relationship was obeyed in case of bismuth oxycarbonate. The dissolution of the drug in absence and presence of magnesium trisilicate, which had a very high retention ability, was also studied. The antacid decreased obviously the dissolution of the tranquilizer. The implication of diazepam interaction with antacids and excipients on its bioavailability is to be further confirmed by in vivo testing.
A 51-year-old man who had a past history of gastric resection for medically uncontrollable gastric ulcer has loss of appetite that recurs periodically. And he has frequently presented spontaneous angina early in the morning since 1984. He was diagnosed as having variant angina by the documentation of typical ST elevation during anginal attack and also by showing coronary artery spasm (#2 and #12) during hyperventilation on coronary arteriography. A large quantity of calcium blocking agents and nitrates could not improve his symptoms. Lack of intracellular magnesium by loss of appetite was suspected from a daily excretion of urine magnesium (5.3 mEq) and magnesium tolerance test (56.7%). To confirm the effect of magnesium administration, the second coronary arteriography was performed. After magnesium sulphate (80 mEq, hourly) was injected, coronary artery spasm could not be induced by ergonovine. And orally magnesium oxide, calcium blocking agents and nitrates were started. Anginal attack disappeared with increasing urine magnesium.
For the development of omeprazole buccal adhesive tablets, we studied the release and bioavailability of omeprazole delivered by buccal adhesive tablets composed of sodium alginate, hydroxypropylmethylcellulose (HPMC), magnesium oxide and croscarmellose sodium. Croscarmellose sodium enhanced the release of omeprazole from the tablets. The analysis of the release mechanism showed that croscarmellose sodium changed the release profile of omeprazole from first- to zero-order release kinetics by forming porous channels in the tablet matrix. However, it decreased the bioadhesive forces and stability of omeprazole tablets in human saliva. The tablet is composed of omeprazole-sodium alginate-HPMC-magnesium oxide-croscarmellose sodium (20:24:6:50:10 mg). It may be attached to the human cheek without collapse and it enhanced the stability of omeprazole in human saliva for at least 4 h, giving a fast release of omeprazole. The plasma concentration of omeprazole in hamsters increased to reach a maximum of 370 ng/ml at 45 min after buccal administration and remained at the high level of 146-366 ng/ml for 6 h. The buccal bioavailability of omeprazole in hamsters was 13.7+/-3.2%. These results demonstrate that the omeprazole buccal adhesive tablet would be useful to deliver omeprazole which degrades very rapidly in acidic aqueous medium and undergoes hepatic first-pass metabolism after oral administration.
Magnesium modulates endothelium-dependent vasodilation in intact blood vessels. Therefore, the effects of magnesium on nitric oxide (NO) release by isolated endothelial cells and nitric oxide synthase (NOS) activity in endothelial cell homogenates were studied. Unstimulated and bradykinin-stimulated NO release by porcine aortic endothelial cell (PAEC) monolayers were unaffected by 30 min of exposure to magnesium concentrations varying from 0.010 to 10.0 mM. In contrast, when A-23187-stimulated cells were exposed to 0.01, 3.16, and 10.0 mM MgCl2, NO release was decreased by 11.3 +/- 1.8, 11.7 +/- 3.0, and 20.3 +/- 7.2%, respectively, compared with cells exposed to 1.0 mM MgCl2 (P < 0.01). These data suggested that a change in the intracellular magnesium concentration had an effect on NO release, in contrast to a change in the extracellular concentration, which did not have an effect. To further assess this possibility, crude NOS extracts were prepared from PAEC and exposed to MgCl2. NOS activity was measured via the conversion of L-[3H]arginine to L-[3H]citrulline. Increasing the concentration of MgCl2 by 1.0, 3.16, and 10.0 mM caused a 16.0 +/- 6.8, 17.1 +/- 1.7, and 38.6 +/- 5.3% decrease in citrulline formation, respectively (P < 0.05), suggesting a direct inhibition of NOS by MgCl2. No significant difference in the degree of inhibition of NOS activity was found between MgSO4 and MgCl2, thus ruling out a nonspecific chloride effect. In addition, increasing the concentration of NaCl to 15 mM had no effect on NOS activity, ruling out a nonspecific osmotic effect [101.6 +/- 10.5% of control activity, P = not significant (NS)].(ABSTRACT TRUNCATED AT 250 WORDS)
Holstein bull calves were fed 1, 2, and 4% supplemental magnesium as magnesium oxide. The control diet contained .3% magnesium and consisted of ground corn, soybean meal, cottonseed hulls plus mineral, vitamin, and antibiotic supplements. Diarrhea was the most obvious effect of high intake of magnesium. The extent and intensity of the diarrhea was related closely to the dietary magnesium content. High (2 and 4%) magnesium reduced feed consumption and weight gains. Although there were traces of blood in feces, no abnormalities were observed at autopsy. Large tubular sections of mucus were voided in the feces with a greater prevalance among calves fed 2 and 4% supplemental magnesium. Magnesium in plasma rose sharply in response to the increased intake of magnesium. In calves receiving the 4% added magnesium, the plasma values were triple those of controls. When high magnesium was fed, magnesium increased much more in urine than in plasma. Within 1 wk after calves were returned to control diet, magnesium in urine and plasma declined to control.
The adsorption of the antiepileptics sulthiame, phenytoin, mephenytoin, mesuximide, phensuximide, ethosuximide, and primidone on various antacids or adsorbents was studied at 37 degrees C. The antacids or adsorbents used were magnesium trisilicate, aluminium hydroxide, bismuth oxidcarbonate, magnesium oxide, talc, kaolin and calcium carbonate. Magnesium trisilicate was found to be the strongest adsorbent for most of the antiepileptics tested. The other antacids or adsorbents were without an appreciable effect. Sulthiame exhibited the highest degree of interaction with magnesium trisilicate. Mesuximide, phensuximide and primidone showed intermediate adsorption properties. Mephenytoin and phenytoin had lower adsorption characters, while ethosuximide was the least adsorbed antiepileptic tested. The extent of elution was found to be inversely proportional to adsorption. Alkaline solution gave relatively higher eluting power than acid solution. The mechanism of adsorption of the various antiepileptics on antacids was discussed. The effect of magnesium trisilicate on the bioavailability of coadministered antiepileptics has still to be confirmed by in vivo testing.
A simple, efficient, and new method has been developed for the synthesis of alpha-acetoxyphosphonates from aldehydes through a one-pot reaction of aldehydes with diethylphosphite in the presence of acetic anhydride under solvent-free conditions using magnesium oxide. This method is easy, rapid, and high yielding for the one-pot synthesis of alpha-acetoxyphosphonates from aldehydes.