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At least 199 records · Page 11Linked to original sources
PubMed2000

Spectroscopic studies of some novel CuI and CuII complexes derived from the tribochemistry reactions of Kbr, KI and CaI2 with CuII-Girard's T complex [Cu(GT)Cl2(H2O)2(EtOH)]Cl.H2O.

Novel CuI and CuII complexes derived from the tribochemistry reactions of [Cu(GT)Cl2(H2O)2(EtOH)Cl.H2O with KBr, KI and CaI2 have been isolated and characterized. The reactions of KI and CaI2 with [Cu(GT)Cl2(H2O)2(EtOH)]Cl.H2O in the solid state are accompanied by colour change, reduction of CuII to CuI and substitution of the chloride by iodide ions. Also, the tribochemistry reaction of KBr with the CuII-GT complex is accompanied by change in colour, substitution of chloride by bromide ions but no reduction has been occurred. All the isolated solid complexes have been characterised by spectral (UV-vis, IR, 1H-NMR), magnetic and thermal measurements. The effect of the variation of the ratio between alkali and/or alkaline earth metal halides (KI, KBr, and CaI2) and the CuII-GT complex has also been investigated.

Betaine↗
PubMed2006

Reactions of potassium bis(phosphinimino)methanide with group 11 compounds.

Transmetalation of the potassium methanide complex, K{CH(PPh2NSiMe3)2}, with [(Ph3P)2CuI] afforded the corresponding copper complex [{CH(PPh2NSiMe3)2}CuPPh3] (1), whereas the reaction of K{CH(PPh2NSiMe3)2} with [Ph3PAuCl] resulted in the dinuclear gold complex [(Ph3PAu)2{C(PPh2NSiMe3)2}] (2). The solid-state structure of 1 shows the formation of a six-membered metallacycle (N1-P1-C1-P2-N2-Cu) that has a twist boat conformation. In contrast, compound 2 is an alpha,alpha-diaurated species, in which the two gold atoms are coordinated in a linear fashion onto the ligand backbone. Photoluminescence measurements show that the latter compound has a strong violet emission.

Journal Article↗
PubMed1991

Bioavailability of potassium and magnesium, and citraturic response from potassium-magnesium citrate.

The bioavailability of potassium and magnesium, and the citraturic response were determined for the new compound, potassium-magnesium citrate, in 14 normal volunteers. Results were compared to those of potassium citrate and magnesium citrate. Each subject participated in 4 phases of study: potassium-magnesium citrate, potassium citrate, magnesium citrate and potassium chloride. After stabilization on a metabolic diet, each subject ingested a single load of a test medication followed by timed urine collections for the next 24 hours. Test loads included potassium-magnesium citrate (49 mEq. potassium, 24.5 mEq. magnesium and 73.5 mEq. citrate), potassium citrate (50 mEq.), potassium chloride (50 mEq.) and magnesium citrate (25 mEq.) Urinary potassium, magnesium and citrate were measured for each collection period. Potassium-magnesium citrate provided an equivalent potassium bioavailability as potassium citrate and potassium chloride, and a comparable magnesium bioavailability as magnesium citrate. However, it gave the highest citraturic response, since the cumulative increment in urinary citrate post-load was 129 mg. daily for potassium-magnesium citrate, 105 mg. daily for potassium citrate and 35 mg. daily for magnesium citrate. Thus, potassium-magnesium citrate gave an optimum citraturic response in addition to providing absorbable potassium and magnesium.

Adult↗
PubMed2000

The interference of uptake of thallium-201 in cultured rat myocardial cells with existence of potassium related pharmaceuticals--a preliminary report.

Thallium-201 myocardial perfusion imaging is wildly used to detect and assess the extent of jeopardized myocardial ischemia in the coronary artery disease and the viability of myocardium post infarction. In recent years, there has been a great deal of pharmacological development of blockers and openers of potassium channel. In this study, we will discuss the interference of uptake of thallium-201 ion in cultured neonatal rat myocytes with existence of a variety of pharmacological agents. The cultures of neonatal rat myocardial cells were incubated with different agents such as potassium chloride, sodium-potassium ATPase pump inhibitor (ouabain), cesium compound, variable potassium channel blockers (4 AP, TEA and glibenclamide) and their openers (minoxidil, and cromakalim). The radioactivity of intracellular thallium-201 that could enter rat myocardial cells was detected by gamma counter sixty minutes after thallium-201 was added. In this study we found that thallium and potassium ions behave in an analogous manner in cultured rat myocardial cells. Both 2.5 mM and 5 mM concentration of extracellular potassium ion significantly result in reduction of thallium-201 ion influx in rat myocardial cells. 0.5 mM ouabain, an inhibitor of sodium-potassium ATPase pump, reduced about 40% of influx of thallium-201 ion in cultured rat myocardial cells via active transport. Combination of both potassium ion and ouabain inhibit most of thallium-201 ions influx in myocardial cells, but it is not completely inhibited. Cesium, a potassium antagonist, also interferes with the uptake of thallium-201 in cultured rat myocytes in our study. The most interesting finding in our investigation is that potassium channel blockers such as TEA and glibenclamide, inhibit the influx of thallium-201 in myocytes. However, potassium channel openers have no overt effect on influx of thallium-201 in cultured rat myocytes. We indirectly observe about 60% of influx of thallium-201 ion into cultured rat myocardial cells via active sodium-potassium ATPase pump. Potassium, cesium and potassium channel blockers, such as TEA and glibenclamide, inhibited the different percentage of influx of thallium-201 in cultured rat myocardial cells in this study.

Adenosine Triphosphate↗
PubMed1996

Differential effects of organotin compounds on voltage-gated potassium currents in lymphocytes and neuroblastoma cells.

Effects of organotin compounds were studied on voltage-gated K+ current in whole-cell voltage clamped lymphocytes and in N1E-115 neuroblastoma cells. In human peripheral blood lymphocytes the immunotoxic compounds dibutyltinchloride (DBT, 2.5 microM) and triphenyltinchloride (TPhT, 2.5 microM) decrease the peak amplitude of the K+ current and prolong time to peak. Tributyltinchloride (TBT, 2.5 microM) decreases the K+ current to a greater extent than DBT and TPhT, without affecting the time to peak. The neurotoxic organotin compound trimethyltinchloride (TMT, 2.5 microM) does not affect the voltage-gated K+ current in lymphocytes. Similar effects of DBT were observed in freshly isolated and PHA-activated human lymphocytes and with rat thymocytes. On the other hand, in mouse N1E-115 neuroblastoma cells, none of the organotin compounds altered the voltage-dependent K+ current. In human lymphocytes DBT affects both the peak amplitude and the time to peak of the K+ current in a concentration-dependent manner. At the maximum concentration of 10 microM tested, the peak amplitude of the K+ current was reduced to 22 +/- 4% of the control current. The IC50 and slope factor for block of the peak outward current by DBT amounts to 6.7 +/- 0.4 microM, and 2.7 +/- 0.4, respectively. The delay in K+ current activation does not saturate. At 10 microM DMT increases the time to peak to 332 +/- 12% of the control value. The present results suggest that the effects by DBT originate from two separate interactions with the voltage-gated K+ channel at the extracellular site of the membrane: a direct effect on the closed K+ channel causing a delay in current activation and a membrane-related effect causing inhibition of the K+ current. The differential effects of the organotin compounds may relate to their differential toxicological action.

Animals↗
PubMed1994

Chemical modification of squid axon K+ channel -SH groups with the organic mercurial compound p-hydroxymercuriphenylsulfonic acid (PHMPS).

In internally dialyzed voltage-clamped squid axons, intracellular or extracellular addition of the sulfhydryl group (-SH) specific reagent p-hydroxymercuriphenylsulfonic acid (PHMPS), causes major modifications in the magnitude and kinetic parameters of the delayed rectifier K+ current. PHMPS produces a dramatic slow-down of the macroscopic current activation kinetics with a simultaneous reduction in its amplitude. In addition, it causes a marked increase in the delay of the macroscopic current at various pre-pulse potentials (Cole-Moore shift). The main effect of PHMPS at the single channel level is a sharp decrease in the open probability (4- to 5-fold). There is, however, a small reduction in single channel conductance (20%). Gating current experiments indicate that PHMPS causes a reduction in the voltage dependence of the activation process as well as a shift of the charge/voltage relationship towards more positive potentials. This, together with an increase in the mean open time, suggests that the open state has been destabilized. The results indicate that the reaction of -SH groups with PHMPS differentially affects the gating process. All the above mentioned effects are partially reversed by either dithiotreitol or beta-mercaptoethanol, -SH group reducing agents.

Animals↗