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PubMed1983

Potassium metabolism in seawater teleosts. I. The use of 86Rb as a tracer for potassium.

Comparison of the movements of rubidium and potassium between blood and tissues, and between blood and external medium, was undertaken in seawater adapted rainbow trout (Salmo gairdneri) and sculpin (Leptocottus armatus). Qualitative observations suggested that the two ions behaved similarly in exchanges within both fish. More than 90% of an injected dose of both ions disappeared from the blood within 1 h. Complete equilibration of both required about 5 h, and the decrease in blood concentration during the last 4 h followed similar kinetics. After injection and equilibration of 86Rb into trout the specific activity of most tissue pools (c.p.m. 86Rb/microeq tissue K) was close to that of blood (c.p.m. 86Rb/microeq plasma K). Skeletal muscle was the sole exception; its specific activity was less than 15% that of plasma even 4-5 h after injection. Injection of ouabain into trout caused cells to lose both 86Rb and K at similar rates. The same thing occurred when [K] in the external medium was raised abruptly. Exchanges of the two ions between blood and the external medium were also similar. Both ions were extruded and taken up rapidly across the gills. Double-labelling (86Rb and 42K fluxes measured simultaneously) showed that JK/JRb = 1.27 for both influx and efflux in trout. The same value was obtained for effluxes in sculpin. Exposing sculpin to seawater lacking Na and K caused both 42K and 86Rb efflux to fall by 75-80%; 86Rb efflux decreased similarly in trout. Alkali metal-free sea water also caused the voltage across the trout gill to change from +10 mV to -20 mV, and in the sculpin from +25 mV to -25 mV. Addition of either Rb or K to the ion-deficient medium partially repolarized the gill in both fish. Repolarization was slightly greater after K repletion than after Rb repletion. These observations suggest that 86Rb is an adequate tracer for potassium movement in seawater-adapted fish. The gills of trout and sculpin are a little more permeable to K than to Rb, and 86Rb fluxes must be multiplied by 1.3 to provide accurate estimates of transbranchial K movement. The quantitative relationship between JK and JRb within the animal was not established, but some data suggest that cell membranes in fish, like the gills, are somewhat more permeable to K than to Rb.

Animals↗
PubMed2001

Greater effect of dietary potassium tripolyphosphate than of potassium dihydrogenphosphate on the nephrocalcinosis and proximal tubular function in female rats from the intake of a high-phosphorus diet.

We examined whether a difference in potassium dihydrogenphosphate (KH2PO4) and potassium tripolyphosphate (K5P3O10) as dietary phosphorus sources could differentially effect the nephrocalcinosis and proximal tubular function in female rats. Rats were fed on a diet containing KH2PO4 or K5P3O10, at the normal phosphorus level (normal phosphorus diet) or at a high phosphorus level (high-phosphorus diet) for 21 d. Nephrocalcinosis, as confirmed by a histological examination, was apparent in all rats fed on the high-phosphorus diet, and this condition was more severe in those rats fed on K5P3O10 than in those fed on KH2PO4. As indicators of the proximal tubular function, the N-acetyl-beta-D-glucosaminidase activity in urine and the urinary beta2-microglobulin excretion were significantly increased in those rats fed on the high-phosphorus diet containing K5P3O10. These results indicate that the intake of a high-phosphorus diet, more strongly influenced the nephrocalcinosis and proximal tubular function when K5P3O10 rather than KH2PO4 was used as the dietary phosphorus source.

Animals↗
PubMed2003

Evaluation of the effects of penicillin G potassium and potassium chloride on the motility of the large intestine in horses.

OBJECTIVE: To evaluate effects of IV administration of penicillin G potassium (KPEN) or potassium chloride (KCl) on defecation and myoelectric activity of the cecum and pelvic flexure of horses. ANIMALS: 5 healthy horses. PROCEDURE: Horses with 12 bipolar electrodes on the cecum and pelvic flexure received KPEN or KCl solution by IV bolus 4 hours apart. Each horse received the following: 2 X 10(7) U of KPEN (high-dose KPEN) followed by 34 mEq of KCl (high-dose KCl), 1 X 10(7) U of KPEN (low-dose KPEN) followed by 17 mEq of KCl (low-dose KCl), high-dose KCl followed by high-dose KPEN, and low-dose KCl followed by low-dose KPEN. Number of defecations and myoelectric activity were recorded for 60 minutes. The first three 5-minute segments and first four 15-minute segments of myoelectric activity were analyzed. RESULTS: Number of defecations during the first 15-minute segment was greater after high-dose KPEN treatment than after high-dose or low-dose KCl treatment. Compared with reference indexes, myoelectric activity was greater in the pelvic flexure for the first 5-minute segment after high-dose KCl treatment, in the cecum and pelvic flexure for the first 5-minute segment and in the pelvic flexure for the first 15-minute segment after low-dose KPEN treatment, and in the pelvic flexure for the first and second 5-minute segments and the first three 15-minute segments after high-dose KPEN treatment. CONCLUSIONS AND CLINICAL RELEVANCE: IV administration of KPEN stimulates defecation and myoelectric activity of the cecum and pelvic flexure in horses. Effects of KPEN may be beneficial during episodes of ileus.

Animals↗
PubMed2000

[Transtubular potassium gradient in the diagnosis of potassium metabolism disorders].

The transtubular potassium gradient (TTKG) is a simple physiologically based clinical test to study the renal excretion of potassium. This article reviews the most important physiological changes influencing TTKG, the hypokalaemia and hyperkalaemia, the effect of mineralocorticoids, alkalosis, action of diuretics among other drugs etc. The authors studied the abnormalities of TTKG occurring in clinical conditions (renal patients with nephrotic edema, "dry" patients with renal diseases, liver cirrhosis associated with ascites, and primary hyperaldosteronism) and compare them to the results obtained in healthy people. They consider the test to be useful in the recognition of conditions with hypoaldosteronism (including the various types of pseudohypoaldosteronisms and aldosterone resistance) and hyperaldosteronism as well as renal diseases, in accordance with the data published in the literature. On the basis of their own results, they found the method of determination of TTKG informative and helpful also when investigating the site of actions and the effect mechanisms of the diuretics.

Diagnosis, Differential↗
PubMed1991

[Activity of the sodium-potassium pump and values of sodium and potassium in erythrocytes in patients with non-dialyzed renal failure and arterial hypertension treated conservatively].

In 8 non-dialysed patients with chronic renal failure (PNN) and hypertension (NT)-(PNNT group) sodium-potassium pump activity (PSP) and intra-erythrocyte sodium (NaE) and potassium (KE) concentration were measured. No differences were found in PSP, NaE and KE between group PNNT and healthy volunteers (Z). These results do not support an importance of the role of the so-called endogenous PSP inhibitor in the pathogenesis of NT in patients with PNN.

Adult↗
PubMed1984

[Atmospheric radiations. Effects of potassium-inhibitory and potassium-retentive hormones on two types of infective agent].

The glucocorticoids and the estrogens facilitate the loss of potassium from the cells (iK+ hormones). The thyroid hormones, the androgens, the growth hormone and the insulin facilitate the penetration of potassium into the cells (rK+ hormones). The incretion of iK+ hormones follows the course of the intensity of the atmospheric radiations (atmospheric electric field, terrestrial magnetic field), that is it grows or diminishes according to the increase or decrease of the intensity of said radiations, while the incretion of rK+ hormones has an opposite course in comparison with the variations of said intensity. The iK+ hormones cause loss of iodine, decrease of eosinophils, of RNA and antibodies, while the rK+ hormones cause opposite effects. High temperatures produce an increase of iK+ hormones and low temperatures an increase of rK+ hormones. The study of the effects of atmospheric radiations on infectious diseases has shown the existence of two kind of infectious agents: the iK+ agents and the rK+ agents on which the hormones iK+ and rK+ have an effect. The hormones iK+ work jointly with iK+ agents (virus RNA, bacteria Gram-negative) and counteract the rK+ agents (virus DNA, bacteria Gram-positive, protozoa). The rK+ hormones have opposite effects in comparison to those of iK+ hormones, that is they counteract the iK+ agents and work jointly with the rK+ agents.

Background Radiation↗
PubMed2001

Regulation of a mammalian Shaker-related potassium channel, hKv1.5, by extracellular potassium and pH.

Using the whole-cell recording mode of the patch-clamp technique we studied the effects of removal of extracellular potassium, [K(+)](o), on a mammalian Shaker-related K(+) channel, hKv1.5. In the absence of [K(+)](o), current through hKv1.5 was similar to currents obtained in the presence of 4.5 mM [K(+)](o). This observation was not expected as earlier results had suggested that either positively charged residues or the presence of a nitrogen-containing residue at the external TEA(+) binding site (R487 in hKv1.5) caused current loss upon removal of [K(+)](o). However, the current loss in hKv1.5 was observed when the extracellular pH, pH(o), was reduced from 7.4 to 6.0, a behavior similar to that observed previously for current through mKv1.3 with a histidine at the equivalent position (H404). These observations suggested that the charge at R487 in hKv1.5 channels was influenced by other amino acids in the vicinity. Replacement of a histidine at position 463 in hKv1.5 by glycine confirmed this hypothesis making this H463G mutant channel sensitive to removal of [K(+)](o) even at pH(o) 7.4. We conclude that the protonation of H463 at pH 7.4 might induce a pK(a) shift of R487 that influences the effective charge at this position leading to a not fully protonated arginine. Furthermore, we assume that the charge at position 487 in hKv1.5 can directly or indirectly disturb the occupation of a K(+) binding site within the channel pore possibly by electrostatic interaction. This in turn might interfere with the concerted transition of K(+) ions resulting in a loss of K(+) conduction.

Amino Acid Sequence↗
PubMed1999

Distinct transient outward potassium current (Ito) phenotypes and distribution of fast-inactivating potassium channel alpha subunits in ferret left ventricular myocytes.

The biophysical characteristics and alpha subunits underlying calcium-independent transient outward potassium current (Ito) phenotypes expressed in ferret left ventricular epicardial (LV epi) and endocardial (LV endo) myocytes were analyzed using patch clamp, fluorescent in situ hybridization (FISH), and immunofluorescent (IF) techniques. Two distinct Ito phenotypes were measured (21-22 degrees C) in the majority of LV epi and LV endo myocytes studied. The two Ito phenotypes displayed marked differences in peak current densities, activation thresholds, inactivation characteristics, and recovery kinetics. Ito,epi recovered rapidly [taurec, -70 mV = 51 +/- 3 ms] with minimal cumulative inactivation, while Ito,endo recovered slowly [taurec, -70 mV = 3,002 +/- 447 ms] with marked cumulative inactivation. Heteropoda toxin 2 (150 nM) blocked Ito,epi in a voltage-dependent manner, but had no effect on Ito,endo. Parallel FISH and IF measurements conducted on isolated LV epi and LV endo myocytes demonstrated that Kv1.4, Kv4.2, and Kv4.3 alpha subunit expression in LV myocyte types was quite heterogenous: (a) Kv4.2 and Kv4.3 were more predominantly expressed in LV epi than LV endo myocytes, and (b) Kv1.4 was expressed in the majority of LV endo myocytes but was essentially absent in LV epi myocytes. In combination with previous measurements on recovery kinetics (Kv1.4, slow; Kv4.2/4.3, relatively rapid) and Heteropoda toxin block (Kv1.4, insensitive; Kv4.2, sensitive), our results strongly support the hypothesis that, in ferret heart, Kv4.2/Kv4.3 and Kv1.4 alpha subunits, respectively, are the molecular substrates underlying the Ito,epi and Ito,endo phenotypes. FISH and IF measurements were also conducted on ferret ventricular tissue sections. The three Ito alpha subunits again showed distinct patterns of distribution: (a) Kv1.4 was localized primarily to the apical portion of the LV septum, LV endocardium, and approximate inner 75% of the LV free wall; (b) Kv4. 2 was localized primarily to the right ventricular free wall, epicardial layers of the LV, and base of the heart; and (c) Kv4.3 was localized primarily to epicardial layers of the LV apex and diffusely distributed in the LV free wall and septum. Therefore, in intact ventricular tissue, a heterogeneous distribution of candidate Ito alpha subunits not only exists from LV epicardium to endocardium but also from apex to base.

Amino Acid Sequence↗
PubMedDate not supplied

Myogenic regulation of arterial diameter: role of potassium channels with a focus on delayed rectifier potassium current.

The phenomenon of myogenic constriction of arterial resistance vessels in response to increased intraluminal pressure has been known for over 100 years, yet our understanding of the molecular mechanisms involved remains incomplete. The focus of this paper concerns the potassium (K+) channels that provide a negative feedback control of the myogenic depolarization of vascular smooth muscle cells that is provoked by elevations in intraluminal pressure, and specifically, the contribution of delayed rectifier (KDR) channels. Our knowledge of the important role played by KDR channels, as well as their molecular identity and acute modulation via changes in gating, has increased dramatically in recent years. Several lines of evidence point to a crucial contribution by heteromultimeric KV1 subunit-containing KDR channels in the control of arterial diameter and myogenic reactivity, but other members of the KV superfamily are also expressed by vascular myocytes, and less is known concerning their specific functions. The effect of pharmacological modulation of KDR channels is discussed, with particular reference to the actions of anorexinogens on KV1- and KV2-containing KDR channels. Finally, the need for a greater understanding of the mechanisms that control KDR channel gene expression is stressed in light of evidence indicating that there is a reduced expression of KDR channels in diseases associated with abnormal myogenic reactivity and vascular remodelling.

Animals↗
PubMed1990

Evidence for increased in vivo sodium-potassium pump activity and potassium efflux in skeletal muscle of spontaneously hypertensive rats.

We have used 87Rb nuclear magnetic resonance spectroscopy (NMR) to study in vivo rubidium kinetics in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) controls, using rubidium as a marker for potassium. We gave 15 male, 13-week-old SHR, mean +/- s.d. blood pressure 180 +/- 10 mmHg, and 15 age-matched normotensive controls, mean blood pressure 120 +/- 9 mmHg, a daily dose of RbCl (2 mmol/kg intraperitoneally). We made repeated NMR measurements of skeletal muscle rubidium concentrations until steady state was reached. We then withdrew rubidium and made further measurements of rubidium concentrations, at intervals, for up to 1 week after the last injection. We also measured plasma and erythrocyte rubidium concentrations by flame atomic absorption spectroscopy at similar intervals after the withdrawal of rubidium. Rubidium concentrations rose at a faster rate in SHR skeletal muscle, but the steady-state muscle rubidium concentration was the same (45 mmol/l) in both SHR and WKY rats. There was also a threefold increase in the rate of rubidium efflux from both muscle and erythrocytes in SHR. These results are consistent with a marked increase in Na+,K(+)-ATPase activity and an increase in the rate of rubidium efflux in vivo in SHR. The increased rate of rubidium efflux in SHR could represent increased K+ efflux via calcium-activated K+ channels and/or result as part of cell volume regulation secondary to increased Na(+)-H+ antiporter activity.

Animals↗
PubMed2004

Potassium depletion improves myocardial potassium uptake in vivo.

Potassium depletion (KD) is a very common clinical entity often associated with adverse cardiac effects. KD is generally considered to reduce muscular Na-K-ATPase density and secondarily reduce K uptake capacity. In KD rats we evaluated myocardial Na-K-ATPase density, ion content, and myocardial K reuptake. KD for 2 wk reduced plasma K to 1.8 +/- 0.1 vs. 3.5 +/- 0.2 mM in controls (P < 0.01, n = 7), myocardial K to 80 +/- 1 vs. 86 +/- 1 micromol/g wet wt (P < 0.05, n = 7), increased Mg, and induced a tendency to increased Na. Myocardial Na-K-ATPase alpha(2)-subunit abundance was reduced by approximately 30%, whereas increases in alpha(1)- and K-dependent pNPPase activity of 24% (n = 6) and 13% (n = 6), respectively, were seen. This indicates an overall upregulation of the myocardial Na-K pump pool. KD rats tolerated a higher intravenous KCl dose. KCl infusion until animals died increased myocardial K by 34% in KD rats and 18% in controls (P < 0.05, n = 6 for both) but did not induce different net K uptake rates between groups. However, clamping plasma K at approximately 5.5 mM by KCl infusion caused a higher net K uptake rate in KD rats (0.22 +/- 0.04 vs. 0.10 +/- 0.03 micromol x g wet wt(-1) x min(-1); P < 0.05, n = 8). In conclusion, a minor KD-induced decrease in myocardial K increased Na-K pump density and in vivo increased K tolerance and net myocardial K uptake rate during K repletion. Thus the heart is protected from major K losses and accumulates considerable amounts of K during exposure to high plasma K. This is of clinical interest, because a therapeutically induced rise in myocardial K may affect contractility and impulse generation-propagation and may attenuate increased myocardial Na, the hallmark of heart failure.

Animals↗
PubMed1998

Calcitonin gene-related peptide stimulates potassium efflux through adenosine triphosphate-sensitive potassium channels and produces membrane hyperpolarization in osteoblastic UMR106 cells.

In previous studies, we have shown that calcitonin gene-related peptide (CGRP) acutely inhibits 45Ca2+ uptake in osteoblastic UMR106 cells, and we have proposed that ATP-sensitive potassium (K(ATP)) channels are involved in mediating this action of CGRP. To directly test this proposed mechanism, we have now examined the effects of CGRP on both membrane potential (Em) and K+ mobilization in UMR106 cells, using specific fluorometric dye assays. CGRP (0.01-100 nM) induced membrane hyperpolarization in a dose-dependent manner, with a half maximal effect (ED50) at approximately 0.2 nM and a maximal effect at 100 nM. Both pinacidil (Pina; a K(ATP) channel opener) and forskolin (FSK) induced similar membrane hyperpolarization, but the actions of these three agents could be easily distinguished: both CGRP and Pina actions were well antagonized by glibenclamide (Glib; a selective K(ATP) channel blocker), whereas FSK action was strongly attenuated only by tetraethylammonium (a K(Ca) channel blocker) or compound H-89 (an inhibitor of cAMP-dependent protein kinases). Cells pretreated with Pina no longer responded to CGRP, but they could still respond to FSK; furthermore, pretreatment with FSK failed to block successive treatment with either CGRP or Pina. In parallel with observed changes in Em, CGRP (0.01-100 nM) decreased intracellular K+ concentrations ([K+]i) in a dose-dependent manner, with an ED50 identical to that obtained for alterations in Em. This action of CGRP was sensitive to Glib and had only slight sensitivity to tetraethylammonium; this CGRP effect was mimicked by Pina but not by FSK. Interestingly, CGRP significantly elicited changes in cell shape by a Glib-sensitive mechanism that included notable decreases in cross-sectional cytoplasmic area. These observations strongly support our proposal that CGRP primarily stimulates K+ efflux via activation of K(ATP) channels and thereby induces membrane hyperpolarization in UMR106 cells. Furthermore, our data also suggest that this cascade of initial cellular events may result in rapid changes in cell morphology and decreases in cellular area of the type that are thought to act as triggers for proliferation and/or differentiation in many cellular phenotypes.

Adenosine Triphosphate↗
PubMed2001

Potassium channels as targets for ethanol: studies of G-protein-coupled inwardly rectifying potassium channel 2 (GIRK2) null mutant mice.

G-Protein-coupled inwardly rectifying potassium channels (GIRKs) regulate synaptic transmission and neuronal firing rates. Selective enhancement of GIRK2 function by intoxicating concentrations of ethanol was recently shown for recombinant homomeric and heteromeric channels. We proposed that specific behavioral actions of ethanol are due to activation of GIRK channels and that these behaviors would be reduced or eliminated in GIRK2 null mutant ("knockout") mice. Three behavioral effects of ethanol were absent in mutant mice as compared with wild-type littermates: stimulation of home cage (habituated) motor activity, anxiolytic action in elevated-plus maze test, and handling-induced convulsions (HIC) after an acute injection of ethanol. In contrast to these reductions of ethanol action, mutant mice displayed greater ethanol-stimulated activity in peripheral regions of an open field. There were no differences between mutant and wild-type mice for ethanol-induced sleep time, acute functional tolerance, or HIC following chronic matched consumption of a liquid diet. Ethanol preference and consumption were equal for wild-type and mutant mice using the standard two-bottle choice test with alternation of the bottles. However, this test was complicated by the strong side preference of the mice. When ethanol was presented constantly in their favored location, the consumption of ethanol was substantially higher for mutant than for wild-type mice. In the absence of ethanol, GIRK2 knockout mice showed more motor activity, less anxiety, and higher HIC. These results provide evidence that GIRK2 channels mediate specific behaviors, including anxiety and convulsions, and may influence effects of ethanol on these behaviors.

Alcohol Drinking↗
PubMed1998

KQT2, a new putative potassium channel family produced by alternative splicing. Isolation, genomic structure, and alternative splicing of the putative potassium channels.

Potassium (K+) channels are critical for a variety of cell functions, including modulation of action potentials, determination of the testing membrane potential, and development of memory and learning. Eleven mouse cDNA clones homologous to the new human putative K+ channel (designated HNSPC, which we recently reported) were isolated from the brain cDNA libraries. All these proteins coded by the isolated cDNAs were identical from the N-terminal to the sixth transmembrane domain, but exhibited differences in the sequence and length of the C-terminal cytoplasmic region. Analyses of the mouse genomic DNAs showed that these clones originated from a single gene located on mouse chromosome 2H3-4, which proved that these clones were generated by alternative RNA splicing. Since all isoforms showed significant structural identity with KVLQT1 (64% identity in the transmembrane domains), which is known to associate with IsK, they were designated mKQT2.1-mKQT2.11. Northern blot analysis indicated that the mRNAs of the mKQT2 isoforms were exclusively expressed in the brain. In the mouse cerebellum region, the localized expression of these clones in the Purkinje cell layer and Golgi cells was shown by in situ hybridization analysis. These transcripts were also detected in the mouse embryonic developmental stage (11th, 15th and 17th day); and in particular, the mRNAs for shorter forms (mKQT2.9, mKQT2.10 or mKQT2.11) were abundantly found on the 11th day after gestation. Although these mKQT2 isoforms had the characteristic structure of voltage-gated K+ channels, functional expression of K+ currents were not detected in Xenopus oocytes.

Alternative Splicing↗
PubMed2004

Geobacillus stearothermophilus V ubiE gene product is involved in the evolution of dimethyl telluride in Escherichia coli K-12 cultures amended with potassium tellurate but not with potassium tellurite.

A 3.8-kb fragment of chromosomal DNA of Geobacillus stearothermophilus V cloned in pSP72 (p1VH) confers resistance to potassium tellurite (K(2)TeO(3)) and to potassium tellurate (K(2)TeO(4)) when the encoded genes are expressed in Escherichia coli K-12. The nt sequence of the cloned fragment predicts three ORFs of 780, 399, and 600 bp, whose encoded protein products exhibit about 80% similarity with the SUMT methyltransferase and the BtuR protein of Bacillus megaterium, and with the UbiE methyltransferase of Bacillus anthracis A2012, respectively. In addition, E. coli/p1VH cells evolved dimethyl telluride, which was released into the headspace gas above liquid cultures when amended with K(2)TeO(3) or with K(2)TeO(4). After 48 h of growth in the presence of these compounds, a protein of about 25 kDa was found at a significantly higher level when crude extracts were analyzed by SDS-PAGE. The N-terminal amino acid (aa) sequence of this protein, obtained by Edman degradation, matched the deduced aa sequence predicted by the G. stearothermophilus V ubiE gene. This gene was amplified by PCR, subcloned in pET21b, and transformed into E. coli JM109(DE3). Interestingly, DMTe evolution occurred when these modified cells were grown in K(2)TeO(4) - but not in K(2)TeO(3) - amended media. These results may be indicative that the two Te oxyanions could be detoxified in the cell by different metabolic pathways.

Anions↗
PubMed1985

The hydrolytic autoxidation of 1,4-naphthoquinone-2-potassium sulphonate: implications for 1,4-naphthoquinone-2-potassium sulphonate-induced oxidative stress in the red blood cell.

1,4-Naphthoquinone-2-potassium sulphonate (NQKS) undergoes an autoxidation reaction in aqueous solution under physiological conditions to produce 3-hydroxy-1,4-naphthoquinone-2-potassium sulphonate (NQKS-OH). Intermediates of dioxygen reduction, superoxide radicals, hydrogen peroxide and hydroxyl radicals, are also detected. The kinetics of the autoxidation of NQKS show a first order dependence on NQKS and hydroxide ion concentration and a zeroth order dependence on oxygen concentration. For the rate equation r = -d[O2]/dt = kappa obs., [NQKS] [-OH], kappa obs. = (6.4 +/- 0.6) X 10(2) M-1s-1 at 37 degrees C. Hydroxide ion attack on NQKS appears to be the rate determining step. The reaction may be conveniently described as a 'hydrolytic autoxidation'. The hydrolytic autoxidation of NQKS occurs in NQKS-treated red blood cells; the hydroxylated quinone NQKS-OH is produced and hydroxyl radical formation is stimulated. The importance of this reaction in NQKS-induced oxidative stress in red blood cells is discussed. The hydrolytic autoxidation of quinones bearing one or more unsubstituted (hydrogen) positions on the quinone centre is a novel mechanism by which such quinones may induce oxidative stress in cellular systems.

Cyclic N-Oxides↗
PubMed1986

Subzero-temperature preservation of reactive fluids in the undercooled state. I. The reduction of potassium ferricyanide by potassium cyanide.

Many reactions show enhanced rates at subzero temperatures due to freeze concentration. The reduction of potassium ferricyanide by potassium cyanide has been studied at subzero temperatures in both the undercooled and the frozen state. The pseudo-first-order rate constants calculated differ greatly from those in previous reports. A high degree of freeze concentration and supersaturation in frozen bulk solutions occurs. It has been clearly demonstrated that undercooled preservation provides a useful method for the long-term storage of reactive mixtures.

Journal Article↗
PubMed2004

Ketone deprotonation mediated by mono- and heterobimetallic alkali and alkaline earth metal amide bases: structural characterization of potassium, calcium, and mixed potassium-calcium enolates.

Potassium, calcium, and mixed potassium-calcium amide combinations have been shown to be efficient reagents in enolization reactions, and a set of representative intermediate mono- and heterobimetallic enolates have been successfully isolated and crystallographically characterized.

Journal Article↗