Involvement Of Sodium Research Articles

Electric lantern using sea water battery

In this study cathode material is used in the electrochemical process of seawater to suggest a rechargeable saltwater battery system for electric lanterns. Sodium is created from saltwater during battery charge , and oxygen of sea water helps to discharge the battery. As well stand as oxidants to energy production. Hence sodium and cathode can be brought from the sea water. During this procedure it shows the success of 72 percent as the involvement of Sodium and evolution of Cl2 in the presence of O2. This has been increased to 82 percent with a cycle of 40.

The involvement of sodium in the function of the human amino acid transporter ASCT2.

Alanine, serine, cysteine transporter 2 (ASCT2) is a membrane amino acid transporter with relevance to human physiology and pathology, such as cancer. Notwithstanding, the study on the ASCT2 transport cycle still has unknown aspects, such as the role of Na+ in this process. We investigate this issue using recombinant hASCT2 reconstituted in proteoliposomes. Changes in the composition of purification buffers show the crucial role of Na+ in ASCT2 functionality. The transport activity is abolished when Na+ is absent or substituted by Li+ or K+ in purification buffers. By employing a Na+ fluorometric probe, we measured an inwardly directed flux of Na+ and, by combining fluorometric and radiometric assays, determined a 2Na+ : 1Gln stoichiometry. Kinetics of Na+ transport suggest that pH-sensitive residues are involved in Na+ binding/transport. Our results clarify the role of Na+ on human ASCT2 transporter activity.

A greedy classifier optimization strategy to assess ion channel blocking activity and pro-arrhythmia in hiPSC-cardiomyocytes.

Novel studies conducting cardiac safety assessment using human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are promising but might be limited by their specificity and predictivity. It is often challenging to correctly classify ion channel blockers or to sufficiently predict the risk for Torsade de Pointes (TdP). In this study, we developed a method combining in vitro and in silico experiments to improve machine learning approaches in delivering fast and reliable prediction of drug-induced ion-channel blockade and proarrhythmic behaviour. The algorithm is based on the construction of a dictionary and a greedy optimization, leading to the definition of optimal classifiers. Finally, we present a numerical tool that can accurately predict compound-induced pro-arrhythmic risk and involvement of sodium, calcium and potassium channels, based on hiPSC-CM field potential data.

Polyclusters and Substitution Effects in the Na–Au–Ga System: Remarkable Sodium Bonding Characteristics in Polar Intermetallics

A systematic exploration of Na- and Au-poor parts of the Na-Au-Ga system (less than 15 at. % Na or Au) uncovered several compounds with novel structural features that are unusual for the rest of the system. Four ternary compounds Na1.00(3)Au0.18Ga1.82(1) (I), NaAu2Ga4 (II), Na5Au10Ga16 (III), and NaAu4Ga2 (IV) have been synthesized and structurally characterized by single crystal X-ray diffraction: Na1.00(3)Au0.18Ga1.82(1)(I, P6/mmm, a = 15.181(2), c =9.129(2)Å, Z = 30); NaAu2Ga4 (II, Pnma, a = 16.733(3), b = 4.3330(9), c =7.358(3) Å, Z = 4); Na5Au10Ga16 (III, P6(3)/m, a = 10.754(2), c =11.457(2) Å, Z = 2); and NaAu4Ga2 (IV, P2(1)/c, a = 8.292(2), b = 7.361(1), c =9.220(2)Å, β = 116.15(3), Z = 4). Compound I lies between the large family of Bergman-related compounds and Na-poor Zintl-type compounds and exhibits a clathrate-like structure containing icosahedral clusters similar to those in cubic 1/1 approximants, as well as tunnels with highly disordered cation positions and fused Na-centered clusters. Structures II, III, and IV are built of polyanionic networks and clusters that generate novel tunnels in each that contain isolated, ordered Na atoms. Tight-binding electronic structure calculations using linear muffin-tin-orbital (LMTO) methods on II, III, IV and an idealized model of I show that all are metallic with evident pseudogaps at the Fermi levels. The integrated crystal orbital Hamilton populations for II-IV are typically dominated by Au-Ga, Ga-Ga, and Au-Au bonding, although Na-Au and Na-Ga contributions are also significant. Sodium's involvement into such covalency is consistent with that recently reported in Na-Au-M (M = Ga, Ge, Sn, Zn, and Cd) phases.

Involvement of Sodium in Early Phosphatidylserine Exposure and Phospholipid Scrambling Induced by P2X7 Purinoceptor Activation in Thymocytes

Extracellular ATP (ATP(ec)), a possible effector in thymocyte selection, induces thymocyte death via purinoceptor activation. We show that ATP(ec) induced cell death by apoptosis, rather than lysis, and early phosphatidylserine (PS) exposure and phospholipid scrambling in a limited thymocyte population (35-40%). PS externalization resulted from the activation of the cationic channel P2X7 (formerly P2Z) receptor and was triggered in all thymocyte subsets although to different proportions in each one. Phospholipid movement was dependent on ATP(ec)-induced Ca(2+) and/or Na(+) influx. At physiological external Na(+) concentration, without external Ca(2+), PS was exposed in all ATP(ec)-responsive cells. In contrast, without external Na(+), physiological external Ca(2+) concentration promoted a submaximal response. Altogether these data show that Na(+) influx plays a major role in the rapid PS exposure induced by P2X7 receptor activation in thymocytes.

The involvement of sodium and calcium ions in the release of amino acid neurotransmitters from mouse cortical slices elicited by hyperforin

Hyperforin is currently considered to be the major active antidepressant constituent of the medicinal herb St. John’s wort ( Hypericum perforatum L.). The mechanism of action however, is still largely unknown, although the involvement of sodium and calcium has been recently inferred. In the present study hyperforin (5 μM) significantly potentiated the release of endogenous aspartate and glutamate from mouse cortical slices when stimulated by veratridine or potassium. Hyperforin (5 μM) also stimulated the release of aspartate, glutamate, serine, glycine and GABA when perfused on its own. Perfusion of the sodium channel blocker, tetrodotoxin (TTX) inhibited the effect of hyperforin, whereas removal of extracellular calcium potentiated the effect. Our observations suggests that hyperforin increases the overflow of neurotransmitters from mouse cerebral cortex possibly through facilitating the entry of sodium into the neurone which leads to the release of calcium from intracellular stores.

Sodium influx plays a major role in the membrane depolarization induced by oxygen and glucose deprivation in rat striatal spiny neurons.

Striatal spiny neurons are selectively vulnerable to ischemia, but the ionic mechanisms underlying this selective vulnerability are unclear. Although a possible involvement of sodium and calcium ions has been postulated in the ischemia-induced damage of rat striatal neurons, the ischemia-induced ionic changes have never been analyzed in this neuronal subtype. We studied the effects of in vitro ischemia (oxygen and glucose deprivation) at the cellular level using intracellular recordings and microfluorometric measurements in a slice preparation. We also used various channel blockers and pharmacological compounds to characterize the ischemia-induced ionic conductances. Spiny neurons responded to ischemia with a membrane depolarization/inward current that reversed at approximately -40 mV. This event was coupled with an increased membrane conductance. The simultaneous analysis of membrane potential changes and of variations in [Na+]i and [Ca2+]i levels showed that the ischemia-induced membrane depolarization was associated with an increase of [Na+]i and [Ca2+]i. The ischemia-induced membrane depolarization was not affected by tetrodotoxin or by glutamate receptor antagonists. Neither intracellular BAPTA, a Ca2+ chelator, nor incubation of the slices in low-Ca2+-containing solutions affected the ischemia-induced depolarization, whereas it was reduced by lowering the external Na+ concentration. High doses of blockers of ATP-dependent K+ channels increased the membrane depolarization observed in spiny neurons during ischemia. Our findings show that, although the ischemia-induced membrane depolarization is coupled with a rise of [Na+]i and [Ca2+]i, only the Na+ influx plays a prominent role in this early electrophysiological event, whereas the increase of [Ca2+]i might be relevant for the delayed neuronal death. We also suggest that the activation of ATP-dependent K+ channels might counteract the ischemia-induced membrane depolarization.

Effects of ions and ionic channel activators or blockers on release of α-MSH from perifused rat hypothalamic slices

The involvement of sodium and chloride ions in the process of α-melanocyte-stimulating hormone (α-MSH) release from hypothalamic neurons was investigated using perifused rat hypothalamic slices. Three different stimuli were found to increase α-MSH release from hypothalamic slices: high K + concentration (50 mM), veratridine (50 μM), and the Na + K +- ATPase inhibitor ouabain (1 mM). Spontaneous or K +-evoked α-MSH release was insensitive to the specific Na + channel blocker tetrodotoxin (TTX; 1.5 μM) and to the blocker of K + channels tetraethylammonium (TEA; 30 mM) or 4-aminopyridine (4-AP; 4 mM). In contrast, blockage of ouabain-sensitive Na + K +- ATPase increased the resting level of α-MSH and caused a dramatic potentiation of K +-evoked α-MSH release. The Na + channel activator veratridine (50 μM) triggered α-MSH release. This stimulatory effect was blocked by TTX and prolonged by TEA application, indicating the occurrence of voltage-sensitive Na + and K + channels on α-MSH neurons. Replacement of Na + by impermeant choline ions from 95 to 60 mM did not alter K +-evoked α-MSH release. Conversely, dramatic reduction of the external Na + concentration to 16 mM caused a robust increase of α-MSH secretion from hypothalamic neurons, likely through activation of the Na + Ca 2+ exchange system. These data indicate that the depolarizing effect of K + results from direct activation of voltage-operated Ca 2+ channels. The lack of effect of TEA on basal α-MSH release prompted us to investigate the possible involvement of chloride ions in the regulation of the spontaneous activity of α-MSH neurons. Substitution of Cl − for impermeant acetate ions did not affect basal or K +-evoked α-MSH release. In contrast, administration of TEA in low Cl − medium stimulated α-MSH secretion. The response of hypothalamic neurons to TEA in low Cl − medium was totally suppressed by TTX, indicating a Na +-dependent regenerative spontaneous activity. The GABA A agonist, muscimol (100 μM), caused a marked inhibition of the stimulated α-MSH release induced by concomitant administration of veratridine and TEA. The effect of muscimol was reversed by bicuculline (100 μM), a specific GABA A antagonist. Taken together, these data indicate that high K +, veratridine and ouabain trigger α-MSH release through distinct mechanisms: veratridine activates Na + conductance; K + depolarization directly recruits voltage-operated Ca 2+ channels which do not belong to the L-type; ouabain likely increases the internal Na + concentration. Our data also suggest the occurrence of an inhibitory mechanism, dependent on Cl − ions, likely mediated through activation of the GABA A receptor, which may play a pivotal role in the regulation of α-MSH release by hypothalamic neurons.

Energy Restriction or Salt Restriction in the Treatment of Overweight Hypertension. Which one? A Point of View

Body weight reduction in the overweight hypertensive patient was found to reduce blood pressure, irrespective of the daily urinary sodium excretion. Significant blood pressure reductions were achieved while the urine sodium excretion was between 165-185 mEq/day. Salt restriction resulting in a significant decrease of the 24-hour urine sodium from 192-110 mEq/24-hours did not change the blood pressure. Some of the studies indicating a reduction in blood pressure, did not take into account the changes in body weight, while on sodium restriction. Thus sodium restriction in the treatment of hypertension has not been uniformly found to reduce the blood pressure. Although there is much evidence in favour of the involvement of sodium in the regulation of blood pressure, there is no convincing evidence that dietary sodium restriction can be of use as a therapeutic modality in the treatment of hypertension in the overweight hypertensive patient.