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Journal articles on the topic 'Ionic homeostasi'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Coast, G. "Neuroendocrine control of ionic homeostasis." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 150, no. 3 (July 2008): S133. http://dx.doi.org/10.1016/j.cbpa.2008.04.318.

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2

LeFurgey, Ann, Peter Ingram, J. J. Blum, M. C. Carney, L. A. Hawkey, J. F. Kronauge, Melvyn Lieberman, et al. "Ionic homeostasis and subcellular element compartmentation." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 2 (August 12, 1990): 150–51. http://dx.doi.org/10.1017/s042482010013434x.

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Subcellular compartments commonly identified and analyzed by high resolution electron probe x-ray microanalysis (EPXMA) include mitochondria, cytoplasm and endoplasmic or sarcoplasmic reticulum. These organelles and cell regions are of primary importance in regulation of cell ionic homeostasis. Correlative structural-functional studies, based on the static probe method of EPXMA combined with biochemical and electrophysiological techniques, have focused on the role of these organelles, for example, in maintaining cell calcium homeostasis or in control of excitation-contraction coupling. New methods of real time quantitative x-ray imaging permit simultaneous examination of multiple cell compartments, especially those areas for which both membrane transport properties and element content are less well defined, e.g. nuclei including euchromatin and heterochromatin, lysosomes, mucous granules, storage vacuoles, microvilli. Investigations currently in progress have examined the role of Zn-containing polyphosphate vacuoles in the metabolism of Leishmania major, the distribution of Na, K, S and other elements during anoxia in kidney cell nuclel and lysosomes; the content and distribution of S and Ca in mucous granules of cystic fibrosis (CF) nasal epithelia; the uptake of cationic probes by mltochondria in cultured heart ceils; and the junctional sarcoplasmic retlculum (JSR) in frog skeletal muscle.

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3

Lane, Michelle, and David K. Gardner. "Understanding cellular disruptions during early embryo development that perturb viability and fetal development." Reproduction, Fertility and Development 17, no. 3 (2005): 371. http://dx.doi.org/10.1071/rd04102.

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An inability to regulate ionic and metabolic homeostasis is related to a reduction in the developmental capacity of the embryo. The early embryo soon after fertilisation and up until compaction appears to have a reduced capacity to regulate its homeostasis. The reduced ability to regulate homeostasis, such as intracellular pH and calcium levels, by the precompaction-stage embryo appears to impact on the ability to regulate mitochondrial function and maintain adequate levels of energy production. This reduction in ATP production causes a cascade of events leading to disrupted cellular function and, perhaps ultimately, disrupted epigenetic regulation and aberrant placental and fetal development. In contrast, after compaction the embryo takes on a more somatic cell-like physiology and is better able to regulate its physiology and therefore appears less vulnerable to stress. Therefore, for human IVF it would seem important for the establishment of healthy pregnancies that the embryos are maintained in systems that are designed to minimise homeostatic stress, particularly for the cleavage-stage embryos, as exposure to stress is likely to culminate in impaired embryo function.

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4

Volman, Vladislav, Terrence J. Sejnowski, and Maxim Bazhenov. "Topological basis of epileptogenesis in a model of severe cortical trauma." Journal of Neurophysiology 106, no. 4 (October 2011): 1933–42. http://dx.doi.org/10.1152/jn.00458.2011.

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Epileptic activity often arises after a latent period following traumatic brain injury. Several factors contribute to the emergence of post-traumatic epilepsy, including disturbances to ionic homeostasis, pathological action of intrinsic and synaptic homeostatic plasticity, and remodeling of anatomical network synaptic connectivity. We simulated a large-scale, biophysically realistic computational model of cortical tissue to study the mechanisms underlying the genesis of post-traumatic paroxysmal epileptic-like activity in the deafferentation model of a severely traumatized cortical network. Post-traumatic generation of paroxysmal events did not require changes of the structural connectivity. Rather, network bursts were induced following the action of homeostatic synaptic plasticity, which selectively influenced functionally dominant groups of intact neurons with preserved inputs. This effect critically depended on the spatial density of intact neurons. Thus in the deafferentation model of post-traumatic epilepsy, a trauma-induced change in functional (rather than anatomical) connectivity might be sufficient for epileptogenesis.

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5

Zeiske, W. "INSECT ION HOMEOSTASIS." Journal of Experimental Biology 172, no. 1 (November 1, 1992): 323–34. http://dx.doi.org/10.1242/jeb.172.1.323.

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The constant composition of body fluids in insects is maintained by the cooperative interaction of gastrointestinal and urinary tissues. Water follows ionic movements, which are driven by the basolateral Na+/K+-ATPase and/or the apical 'K+(or Na+) pump'. The latter now is thought to be the functional expression of a parallel arrangement of a proton-motive V-ATPase and a K+(or Na+)/nH+ antiport. This review focuses on the pathways for the movement of monovalent inorganic ions through epithelia involved in ion homeostasis. A graphical summary compares the principal findings with respect to cation secretion in lepidopteran caterpillar midgut goblet cells (K+) and in brush-border cells of Malpighian tubules (K+, Na+).

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6

Lane, Michelle, and David K. Gardner. "Regulation of Ionic Homeostasis by Mammalian Embryos." Seminars in Reproductive Medicine 18, no. 02 (2000): 195–204. http://dx.doi.org/10.1055/s-2000-12558.

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7

Pitlik, T. N., P. M. Bulai, A. A. Denisov, D. S. Afanasenkov, and S. N. Cherenkevich. "Redox regulation of ionic homeostasis in neurons." Neurochemical Journal 3, no. 2 (June 2009): 87–92. http://dx.doi.org/10.1134/s1819712409020020.

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8

Walid, Saibi, and Brini Faiçal. "Ion transporters and their molecular regulation mechanism in plants." Journal of Plant Science and Phytopathology 5, no. 2 (May 26, 2021): 028–43. http://dx.doi.org/10.29328/journal.jpsp.1001058.

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With the global population predicted to grow by at least 25% by 2050, the need for sustainable production of nutritious foods is important for human and environmental health. Recent progress demonstrate that membrane transporters can be used to improve yields of staple crops, increase nutrient content and resistance to key stresses, including salinity, which in turn could expand available arable land. Exposure to salt stress affects plant water relations and creates ionic stress in the form of the cellular accumulation of Na+ and Cl- ions. However, salt stress also impacts heavily on the homeostasis of other ions such as Ca2+, K+, and NO3- and therefore requires insights into how transport and compartmentation of these nutrients are altered during salinity stress. Since Na+ interferes with K+ homeostasis, maintaining a balanced cytosolic Na+/K+ ratio has become a key salinity tolerance mechanism. Achieving this homeostatic balance requires the activity of Na+ and K+ transporters and/or channels. The aim of this review is to seek answers to this question by examining the role of major ions transporters and channels in ions uptake, translocation and intracellular homeostasis in plants.

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9

Deng, Jielin, Yunqiu Jiang, Zhen Bouman Chen, June-Wha Rhee, Yingfeng Deng, and Zhao V. Wang. "Mitochondrial Dysfunction in Cardiac Arrhythmias." Cells 12, no. 5 (February 21, 2023): 679. http://dx.doi.org/10.3390/cells12050679.

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Electrophysiological and structural disruptions in cardiac arrhythmias are closely related to mitochondrial dysfunction. Mitochondria are an organelle generating ATP, thereby satisfying the energy demand of the incessant electrical activity in the heart. In arrhythmias, the homeostatic supply–demand relationship is impaired, which is often accompanied by progressive mitochondrial dysfunction leading to reduced ATP production and elevated reactive oxidative species generation. Furthermore, ion homeostasis, membrane excitability, and cardiac structure can be disrupted through pathological changes in gap junctions and inflammatory signaling, which results in impaired cardiac electrical homeostasis. Herein, we review the electrical and molecular mechanisms of cardiac arrhythmias, with a particular focus on mitochondrial dysfunction in ionic regulation and gap junction action. We provide an update on inherited and acquired mitochondrial dysfunction to explore the pathophysiology of different types of arrhythmias. In addition, we highlight the role of mitochondria in bradyarrhythmia, including sinus node dysfunction and atrioventricular node dysfunction. Finally, we discuss how confounding factors, such as aging, gut microbiome, cardiac reperfusion injury, and electrical stimulation, modulate mitochondrial function and cause tachyarrhythmia.

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10

Bkaily, Ghassan, Levon Avedanian, Johny Al-Khoury, Lena Ahmarani, Claudine Perreault, and Danielle Jacques. "Receptors and ionic transporters in nuclear membranes: new targets for therapeutical pharmacological interventions." Canadian Journal of Physiology and Pharmacology 90, no. 8 (August 2012): 953–65. http://dx.doi.org/10.1139/y2012-077.

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Work from our group and other laboratories showed that the nucleus could be considered as a cell within a cell. This is based on growing evidence of the presence and role of nuclear membrane G-protein coupled receptors and ionic transporters in the nuclear membranes of many cell types, including vascular endothelial cells, endocardial endothelial cells, vascular smooth muscle cells, cardiomyocytes, and hepatocytes. The nuclear membrane receptors were found to modulate the functioning of ionic transporters at the nuclear level, and thus contribute to regulation of nuclear ionic homeostasis. Nuclear membranes of the mentioned types of cells possess the same ionic transporters; however, the type of receptors is cell-type dependent. Regulation of cytosolic and nuclear ionic homeostasis was found to be dependent upon a tight crosstalk between receptors and ionic transporters of the plasma membranes and those of the nuclear membrane. This crosstalk seems to be the basis for excitation–contraction coupling, excitation–secretion coupling, and excitation – gene expression coupling. Further advancement in this field will certainly shed light on the role of nuclear membrane receptors and transporters in health and disease. This will in turn enable the successful design of a new class of drugs that specifically target such highly vital nuclear receptors and ionic transporters.

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11

Janssen, Luke J., Subhendu Mukherjee, and Kjetil Ask. "Calcium Homeostasis and Ionic Mechanisms in Pulmonary Fibroblasts." American Journal of Respiratory Cell and Molecular Biology 53, no. 2 (August 2015): 135–48. http://dx.doi.org/10.1165/rcmb.2014-0269tr.

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12

Ito, Saya, Kazuma Sato, Yukiko Himeno, Yukari Takeda, and Akira Amano. "A Photoreceptor Model Considering Regulation of Ionic Homeostasis." Biophysical Journal 112, no. 3 (February 2017): 531a. http://dx.doi.org/10.1016/j.bpj.2016.11.2871.

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13

Ghelardoni, Sandra, Silvia Suffredini, Sabina Frascarelli, Simona Brogioni, Grazia Chiellini, Simonetta Ronca-Testoni, David K. Grandy, Thomas S. Scanlan, Elisabetta Cerbai, and Riccardo Zucchi. "Modulation of cardiac ionic homeostasis by 3-iodothyronamine." Journal of Cellular and Molecular Medicine 13, no. 9b (February 27, 2009): 3082–90. http://dx.doi.org/10.1111/j.1582-4934.2009.00728.x.

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14

Sousa, Valéria F. de O., Gisele L. dos Santos, Josemir M. Maia, Sebastião de O. Maia Júnior, João P. de O. Santos, José E. Costa, Anselmo F. da Silva, Thiago J. Dias, Sérgio L. Ferreira-Silva, and Carlos A. K. Taniguchi. "Salinity-tolerant dwarf cashew rootstock has better ionic homeostasis and morphophysiological performance of seedlings." Revista Brasileira de Engenharia Agrícola e Ambiental 27, no. 2 (February 2023): 92–100. http://dx.doi.org/10.1590/1807-1929/agriambi.v27n2p92-100.

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ABSTRACT Considering the cashew tree’s relevance and the limitations imposed by salinity stress in semi-arid regions, the use of alternatives capable of mitigating the harmful effects due to salinity is of great importance to the production sector. The use of grafted plants, especially with rootstock made of tolerant materials, influences the accumulation of toxic ions in leaves of grafted seedlings. Thus, the objective of this work was to evaluate morphophysiological characteristics and leaf concentrations of Na+, K+ and Ca+2 of combinations of scion and rootstock of early dwarf cashew, contrasting in terms of salinity tolerance. The experiment was carried out in a completely randomized design with five replicates, in a 4 × 3 factorial arrangement, corresponding to four dwarf cashew scion/rootstock combinations (self-graft CCP 09, CCP 09/CCP 76, self-graft CCP 76, and CCP 76/CCP 09) and three NaCl concentrations (0, 50, and 100 mM L-1). Height, number of leaves, leaf area, dry matter, tolerance index and leaf concentrations of Na+, K+ and Ca+2 were evaluated after 30 days of application of NaCl concentrations. The scion/rootstock combination CCP 76/09 showed tolerance to 50 mM L-1, due to the increase of leaf area and number of leaves. The scion/rootstock combination CCP 76/09 was more suitable, as it kept the leaf K+ concentration and had the lowest Na+ concentration.

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15

Bkaily, Ghassan, Levon Avedanian, and Danielle Jacques. "Nuclear membrane receptors and channels as targets for drug development in cardiovascular diseasesThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue)." Canadian Journal of Physiology and Pharmacology 87, no. 2 (February 2009): 108–19. http://dx.doi.org/10.1139/y08-115.

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The use of confocal microscopy has shown that the nucleus plays an important role in excitation–contraction and excitation–secretion coupling of several excitable and nonexcitable cardiovascular cells. It has shown that the nuclear membranes, like the sarcolemmal membrane, possess ionic transporters as well as G protein-coupled receptors (GPCRs), which play a major role in modulating both cytosolic and nuclear ionic homeostasis and nuclear signalling. During spontaneous contraction of heart cells, the increase in cytosolic Ca2+ was immediately followed by a transient increase in nuclear Ca2+. The nuclear Ca2+ rise during excitation–contraction and excitation–secretion coupling was both dependent and independent of changes in cytosolic Ca2+. Nuclear membrane GPCRs, such as those of angiotensin II, neuropeptide Y, and ET-1, were functional and contributed to modulation of nuclear ionic homeostasis via direct and (or) indirect modulation of nuclear membrane ionic transporters such as channels, pumps, and exchangers. The signalling of nuclear membrane GPCRs may also contribute to modulation of gene expression, which may regulate proliferation and remodelling of cells and, indeed, life and death. Direct or indirect targeting of nuclear membrane ionic transporters and GPCRs may constitute a new target for drug action.

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16

Rahman, Anisur, Mazhar Ul Alam, Md Shahadat Hossain, Jubayer Al Mahmud, Kamrun Nahar, Masayuki Fujita, and Mirza Hasanuzzaman. "Exogenous Gallic Acid Confers Salt Tolerance in Rice Seedlings: Modulation of Ion Homeostasis, Osmoregulation, Antioxidant Defense, and Methylglyoxal Detoxification Systems." Agronomy 13, no. 1 (December 21, 2022): 16. http://dx.doi.org/10.3390/agronomy13010016.

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The worldwide saline-affected area is expanding day by day, and soil salinity restricts crop development and productivity, including rice. Considering this, the current study explored the response of gallic acid (GA) in conferring salinity tolerance in rice seedlings. Fourteen-day-old rice (Oryza sativa L. cv. BRRI dhan52) seedlings were treated with 200 mM NaCl alone or combined with 1 mM GA. Salt stress resulted in osmotic, ionic, and oxidative stress in rice seedlings. Osmotic stress increased proline accumulation and osmotic potential, which decreased the relative water content, chlorophyll contents, and dry weight. Ionic stress interrupted ion homeostasis by Na+ accumulation and K+ leakage. Osmotic and ionic stress, concomitantly, disrupted antioxidant defense and glyoxalase systems by higher production of reactive oxygen species (ROS) and methylglyoxal (MG), respectively. It resulted in oxidative damage indicated by the high amount of malondialdehyde (MDA). The supplementation of GA in salt-treated rice seedlings partially recovered salt-induced damages by improving osmotic and ionic homeostasis by increasing water balance and decreasing Na+ content and Na+/K+ ratio. Supplemental GA enhanced the antioxidant defense system in salt-treated rice seedlings by increasing ascorbate (AsA), glutathione (GSH), and phenolic compounds and the activities of AsA-GSH cycle enzymes, including monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), and glutathione reductase (GR) enzymes that accelerated ROS detoxification and decreased oxidative damage. Gallic acid also enhanced the detoxification of MG by triggering glyoxalase enzyme activities in salt-treated rice seedlings. The present findings elucidated that supplemental GA reversed salt-induced damage in rice seedlings through improving osmotic and ionic homeostasis and upregulating the ROS and MG detoxification system.

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17

Zandawala, Meet, Thomas Nguyen, Marta Balanyà Segura, Helena A. D. Johard, Mirjam Amcoff, Christian Wegener, Jean-Paul Paluzzi, and Dick R. Nässel. "A neuroendocrine pathway modulating osmotic stress in Drosophila." PLOS Genetics 17, no. 3 (March 8, 2021): e1009425. http://dx.doi.org/10.1371/journal.pgen.1009425.

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Environmental factors challenge the physiological homeostasis in animals, thereby evoking stress responses. Various mechanisms have evolved to counter stress at the organism level, including regulation by neuropeptides. In recent years, much progress has been made on the mechanisms and neuropeptides that regulate responses to metabolic/nutritional stress, as well as those involved in countering osmotic and ionic stresses. Here, we identified a peptidergic pathway that links these types of regulatory functions. We uncover the neuropeptide Corazonin (Crz), previously implicated in responses to metabolic stress, as a neuroendocrine factor that inhibits the release of a diuretic hormone, CAPA, and thereby modulates the tolerance to osmotic and ionic stress. Both knockdown ofCrzand acute injections of Crz peptide impact desiccation tolerance and recovery from chill-coma. Mapping of the Crz receptor (CrzR) expression identified three pairs ofCapa-expressing neurons (Va neurons) in the ventral nerve cord that mediate these effects of Crz. We show that Crz acts to restore water/ion homeostasis by inhibiting release of CAPA neuropeptides via inhibition of cAMP production in Va neurons. Knockdown ofCrzRin Va neurons affects CAPA signaling, and consequently increases tolerance for desiccation, ionic stress and starvation, but delays chill-coma recovery. Optogenetic activation of Va neurons stimulates excretion and simultaneous activation of Crz and CAPA-expressing neurons reduces this response, supporting the inhibitory action of Crz. Thus, Crz inhibits Va neurons to maintain osmotic and ionic homeostasis, which in turn affects stress tolerance. Earlier work demonstrated that systemic Crz signaling restores nutrient levels by promoting food search and feeding. Here we additionally propose that Crz signaling also ensures osmotic homeostasis by inhibiting release of CAPA neuropeptides and suppressing diuresis. Thus, Crz ameliorates stress-associated physiology through systemic modulation of both peptidergic neurosecretory cells and the fat body inDrosophila.

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18

Varadarajan, Shankar, Kayoko Tanaka, Joshua L. Smalley, Edward T. W. Bampton, Maurizio Pellecchia, David Dinsdale, Gary B. Willars, and Gerald M. Cohen. "Endoplasmic Reticulum Membrane Reorganization Is Regulated by Ionic Homeostasis." PLoS ONE 8, no. 2 (February 15, 2013): e56603. http://dx.doi.org/10.1371/journal.pone.0056603.

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19

Coast, G. M. "Neuroendocrine control of ionic homeostasis in blood-sucking insects." Journal of Experimental Biology 212, no. 3 (January 16, 2009): 378–86. http://dx.doi.org/10.1242/jeb.024109.

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20

Abhilash, M., Manju Alex, Varghese V. Mathews, and R. Harikumaran Nair. "Chronic Effect of Aspartame on Ionic Homeostasis and Monoamine Neurotransmitters in the Rat Brain." International Journal of Toxicology 33, no. 4 (May 28, 2014): 332–41. http://dx.doi.org/10.1177/1091581814537087.

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Aspartame is one of the most widely used artificial sweeteners globally. Data concerning acute neurotoxicity of aspartame is controversial, and knowledge on its chronic effect is limited. In the current study, we investigated the chronic effects of aspartame on ionic homeostasis and regional monoamine neurotransmitter concentrations in the brain. Our results showed that aspartame at high dose caused a disturbance in ionic homeostasis and induced apoptosis in the brain. We also investigated the effects of aspartame on brain regional monoamine synthesis, and the results revealed that there was a significant decrease of dopamine in corpus striatum and cerebral cortex and of serotonin in corpus striatum. Moreover, aspartame treatment significantly alters the tyrosine hydroxylase activity and amino acids levels in the brain. Our data suggest that chronic use of aspartame may affect electrolyte homeostasis and monoamine neurotransmitter synthesis dose dependently, and this might have a possible effect on cognitive functions.

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21

Abramets, Igor I., Dmitriy V. Evdokimov, Yuriy V. Kuznetsov, and Yuliya V. Sidorova. "Correction of disorders of neuronal homeostatic mechanisms in case of neuropsychiatric diseases as a probable direction of drug exposure." Курский научно-практический вестник «Человек и его здоровье», no. 3 (September 2020): 72–83. http://dx.doi.org/10.21626/vestnik/2020-3/09.

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The improvement of drug therapy for a number of neuropsychiatric diseases requires the search for new directions of action in comparison with those currently used. Most of the drugs used affect molecular targets that modulate interstructural (interneuronal) interactions. Influencing the deeper processes of synaptic and neuronal homeostasis may be a new direction in the treatment of these diseases. This review examines the mechanisms of homeostatic plasticity of synaptic transmission and electrical excitability of neurons, which balance each other and stabilize the functioning of neurons and neural networks. The first type of homeostatic plasticity is regulated by the intracellular Ca2+ concentration and the activity of protein kinases, and the second one - by membrane density of voltage-dependent ionic channels. Analysis of literature data shows that alterations in some neuro-psychiatric diseases reveal disorders of homeostatic plasticity more often in terms of monodirectional alterations of synaptic impacts and neuronal electrical excitability. Thus, mainly in preclinical studies, it was revealed that stress-induced depressive disorders of behavior are accompanied by a unidirectional increase in pyramidal neurons of 2/3 layers of the prefrontal cortex of rodents, or a weakening in neurons of the 5th layer of synaptic drive and electrical excitability. Similar disorders of homeostatic plasticity were observed by other authors in pyramidal neurons of the dorsolateral prefrontal cortex in schizophrenia, depending on the prevalence of positive or negative symptoms. In chronic neuropathic pain, an increase in the excitability of peripheral neurons of the spinal / trigeminal ganglia, neurons of the dorsal horns, and cortical neurons and an increase in incoming synaptic influences were revealed. The observed disturbances were accompanied by changes in the density of ion channels in neuronal membranes. The peculiarities of the distribution and biophysical properties of voltage-dependent potassium channels allow us to consider them as a probable molecular target for the correction of disorders of homeostatic plasticity.

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22

Hu, Hui-Jie, and Mingke Song. "Disrupted Ionic Homeostasis in Ischemic Stroke and New Therapeutic Targets." Journal of Stroke and Cerebrovascular Diseases 26, no. 12 (December 2017): 2706–19. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2017.09.011.

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23

Denda, M., K. Nakanishi, and N. Kumazawa. "Topical Application of Ionic Polymers Affects Skin Permeability Barrier Homeostasis." Skin Pharmacology and Physiology 18, no. 1 (December 10, 2004): 36–41. http://dx.doi.org/10.1159/000081684.

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24

Minghetti, Matteo, and Kristin Schirmer. "Interference of silver nanoparticles with essential metal homeostasis in a novel enterohepatic fish in vitro system." Environmental Science: Nano 6, no. 6 (2019): 1777–90. http://dx.doi.org/10.1039/c9en00310j.

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25

Shatrova, A. N., A. P. Domnina, N. A. Pugovkina, and I. I. Marakhova. "Ionic Homeostasis and Stress-Induced Aging of Human Mesenchymal Stem Cells." Cell and Tissue Biology 16, no. 5 (October 2022): 451–58. http://dx.doi.org/10.1134/s1990519x22050091.

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26

Matsumoto, T., T. P. Obrenovitch, N. A. Parkinson, and L. Symon. "Cortical activity, ionic homeostasis, and acidosis during rat brain repetitive ischemia." Stroke 21, no. 8 (August 1990): 1192–98. http://dx.doi.org/10.1161/01.str.21.8.1192.

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27

Dravis, Christopher, Tao Wu, Michael J. Chumley, Nobuhiko Yokoyama, Shiniu Wei, Doris K. Wu, Daniel C. Marcus, and Mark Henkemeyer. "EphB2 and ephrin-B2 regulate the ionic homeostasis of vestibular endolymph." Hearing Research 223, no. 1-2 (January 2007): 93–104. http://dx.doi.org/10.1016/j.heares.2006.10.007.

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Pokhilko, Alexandra V., Fazoil I. Ataullakhanov, and Ekhson L. Holmuhamedov. "Mathematical model of mitochondrial ionic homeostasis: Three modes of Ca2+ transport." Journal of Theoretical Biology 243, no. 1 (November 2006): 152–69. http://dx.doi.org/10.1016/j.jtbi.2006.05.025.

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29

Guo, Jian-Ying, Jia Lin, Yue-Qiang Huang, Milton Talukder, Lei Yu, and Jin-Long Li. "AQP2 as a target of lycopene protects against atrazine-induced renal ionic homeostasis disturbance." Food & Function 12, no. 11 (2021): 4855–63. http://dx.doi.org/10.1039/d0fo03214j.

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This study shows that atrazine exposure can lead to nephrotoxicity by interfering with ion homeostasis. Lycopene maintains ion homeostasis by regulating the expression of AQPs and the activity of ATPase, and antagonizes the nephrotoxicity induced by atrazine.

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Talaat, Neveen B., and Bahaa T. Shawky. "Synergistic Effects of Salicylic Acid and Melatonin on Modulating Ion Homeostasis in Salt-Stressed Wheat (Triticum aestivum L.) Plants by Enhancing Root H+-Pump Activity." Plants 11, no. 3 (February 2, 2022): 416. http://dx.doi.org/10.3390/plants11030416.

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Salicylic acid (SA) and melatonin (MT) have been shown to play important roles in plant salt tolerance. However, the underlying mechanisms of SA–MT-interaction-mediated ionic homeostasis in salt-stressed plants are unknown. As a first investigation, this study aimed to clarify how SA–MT interaction affects H+-pump activity in maintaining the desired ion homeostasis under saline conditions and its relation to ROS metabolism. Wheat (Triticum aestivum L.) plants were grown under non-saline or saline conditions and were foliar sprayed with 75 mg L−1 SA or 70 μM MT. The SA+MT combined treatment significantly increased N, P, K+, Fe, Zn, and Cu acquisition, accompanied by significantly lower Na+ accumulation in salt-stressed plants compared to non-stressed ones. Additionally, it significantly enhanced ATP content and H+-pump activity of the roots. The mitigation was also detected in the reduced superoxide radical content, electrolyte leakage, and lipoxygenase activity, as well as increased superoxide dismutase, catalase, peroxidase, and polyphenol oxidase activities; K+/Na+, Ca2+/Na+, and Mg2+/Na+ ratios; relative water content; membrane stability index; and free amino acid accumulation in treated plants. The novel evidence shows that the higher root H+-pump activity in treated plants is a tolerance mechanism that increases the salt tolerance via maintaining ionic homeostasis.

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Naz, Riffat, Qamar uz Zaman, Saba Nazir, Nayab Komal, Yinglong Chen, Kamran Ashraf, Asma A. Al-Huqail, et al. "Silicon fertilization counteracts salinity-induced damages associated with changes in physio-biochemical modulations in spinach." PLOS ONE 17, no. 6 (June 9, 2022): e0267939. http://dx.doi.org/10.1371/journal.pone.0267939.

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Plant growth and productivity are limited by the severe impact of salt stress on the fundamental physiological processes. Silicon (Si) supplementation is one of the promising techniques to improve the resilience of plants under salt stress. This study deals with the response of exogenous Si applications (0, 2, 4, and 6 mM) on growth, gaseous exchange, ion homeostasis and antioxidant enzyme activities in spinach grown under saline conditions (150 mM NaCl). Salinity stress markedly reduced the growth, physiological, biochemical, water availability, photosynthesis, enzymatic antioxidants, and ionic status in spinach leaves. Salt stress significantly enhanced leaf Na+ contents in spinach plants. Supplementary foliar application of Si (4 mM) alleviated salt toxicity, by modulating the physiological and photosynthetic attributes and decreasing electrolyte leakage, and activities of SOD, POD and CAT. Moreover, Si-induced mitigation of salt stress was due to the depreciation in Na+/K+ ratio, Na+ ion uptake at the surface of spinach roots, and translocation in plant tissues, thereby reducing the Na+ ion accumulation. Foliar applied Si (4 mM) ameliorates ionic toxicity by decreasing Na+ uptake. Overall, the results illustrate that foliar applied Si induced resistance against salinity stress in spinach by regulating the physiology, antioxidant metabolism, and ionic homeostasis. We advocate that exogenous Si supplementation is a practical approach that will allow spinach plants to recover from salt toxicity.

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Yang, Yiming, Xingjian Zhai, and Yassine El Hiani. "TRPML1—Emerging Roles in Cancer." Cells 9, no. 12 (December 13, 2020): 2682. http://dx.doi.org/10.3390/cells9122682.

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The mucolipin-1 (TRPML1) channel maintains lysosomal ionic homeostasis and regulates autophagic flux. Defects of TRPML1 lead to lysosomal storage diseases and neurodegeneration. In this report, we discuss emerging evidence pertaining to differential regulation of TRPML1 signaling pathways in cancer progression with the goal of leveraging the oncogenic potential of TRPML1 to inspire therapeutic interventions.

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33

Thorsen, Kristian, Tormod Drengstig, and Peter Ruoff. "Transepithelial glucose transport and Na+/K+ homeostasis in enterocytes: an integrative model." American Journal of Physiology-Cell Physiology 307, no. 4 (August 15, 2014): C320—C337. http://dx.doi.org/10.1152/ajpcell.00068.2013.

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The uptake of glucose and the nutrient coupled transcellular sodium traffic across epithelial cells in the small intestine has been an ongoing topic in physiological research for over half a century. Driving the uptake of nutrients like glucose, enterocytes must have regulatory mechanisms that respond to the considerable changes in the inflow of sodium during absorption. The Na-K-ATPase membrane protein plays a major role in this regulation. We propose the hypothesis that the amount of active Na-K-ATPase in enterocytes is directly regulated by the concentration of intracellular Na+ and that this regulation together with a regulation of basolateral K permeability by intracellular ATP gives the enterocyte the ability to maintain ionic Na+/K+ homeostasis. To explore these regulatory mechanisms, we present a mathematical model of the sodium coupled uptake of glucose in epithelial enterocytes. Our model integrates knowledge about individual transporter proteins including apical SGLT1, basolateral Na-K-ATPase, and GLUT2, together with diffusion and membrane potentials. The intracellular concentrations of glucose, sodium, potassium, and chloride are modeled by nonlinear differential equations, and molecular flows are calculated based on experimental kinetic data from the literature, including substrate saturation, product inhibition, and modulation by membrane potential. Simulation results of the model without the addition of regulatory mechanisms fit well with published short-term observations, including cell depolarization and increased concentration of intracellular glucose and sodium during increased concentration of luminal glucose/sodium. Adding regulatory mechanisms for regulation of Na-K-ATPase and K permeability to the model show that our hypothesis predicts observed long-term ionic homeostasis.

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Sá, Francisco V. da S., Ivan E. da Silva, Miguel Ferreira Neto, Yuri B. de Lima, Emanoela P. de Paiva, and Hans R. Gheyi. "Phosphorus doses alter the ionic homeostasis of cowpea irrigated with saline water." Revista Brasileira de Engenharia Agrícola e Ambiental 25, no. 6 (June 2021): 372–79. http://dx.doi.org/10.1590/1807-1929/agriambi.v25n6p372-379.

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HIGHLIGHTS Irrigation using water with electrical conductivity above 2.5 dS m-1 is not adequate for ‘Paulistinha’ cowpea. Increment in phosphorus dose does not increase phosphorus content in cowpea plant. Under salt stress conditions, cowpea plants require lower doses of phosphorus.

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Martynenko, E. V., T. N. Arkhipova, A. A. Belimov, and G. R. Kudoyarova. "IONIC HOMEOSTASIS IN WHEAT PLANTS INOCULATED BY HORMONE-PRODUCING BACTERIA UNDER SALINITY." ÈKOBIOTEH 3, no. 4 (2020): 727–33. http://dx.doi.org/10.31163/2618-964x-2020-3-4-727-733.

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Сytokinins content, concentration of sodium and potassium ions and K+/Na+ratio in wheat plants (Triticum durum Desf., Bashkirskaya 27) were evaluated under salinity during treatment with hormone-producing bacteria Pseudomonas mandelii IB-Ki14 (auxin-producer) or Bacillus subtilis IB-22 (cytokinin-producer). An increased level of cytokinins was observed in the roots on 6th day and then in the shoots (on 11th day) both in the absence of salt and under 100 mM NaCl in the presence of B. subtilis IB-22. The introduction of P. mandelii IB-Ki14 into the rhizosphere did not lead to the accumulation of cytokinins under salinity. The presence of NaCl in the soil led to the expected increase in the concentration of sodium ions both in the roots and in the shoots, and inoculation did not significantly change their values. Salinity decreased the content of potassium ions in the roots by 25% in plants uninoculated with bacteria and in plants treated with P. mandelii IB-Ki14, as a result of which the ratio of K+/Na+ ions decreased by 4 times compared with the control, indicating a disruption of the ionic homeostasis. In plants inoculated with B. subtilis IB-22, no decrease in the concentration of potassium ions was found as compared to the control, and the ratio of K+/Na+ ions in the roots under salinity decreased to a lesser extent than in other variants of the experiment. This indicates the ability of cytokinin-producing bacteria to stabilize ionic balance and reduce the consequences of the negative effects of salinity on photosynthesis, protein synthesis, and growth. Our data indicate that this property of bacteria is associated with their ability to synthesize cytokinins and increase cytokinin content in plants under salinity.

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Donohoe, P. H., T. G. West, and R. G. Boutilier. "Factors affecting membrane permeability and ionic homeostasis in the cold-submerged frog." Journal of Experimental Biology 203, no. 2 (January 15, 2000): 405–14. http://dx.doi.org/10.1242/jeb.203.2.405.

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Frogs (Rana temporaria) were submerged at 3 degrees C in either normoxic (P(O2)=155 mmHg, P(O2)=20 kPa) or hypoxic (P(O2)=60 mmHg; P(O2)=8 kPa) water for up to 16 weeks, and denied air access, to mimic the conditions of an ice-covered pond during the winter. The activity of the skeletal muscle Na(+)/K(+) pump over the first 2 months of hibernation, measured by ouabain-inhibitable (22)Na(+) efflux, was reduced by 30 % during normoxia and by up to 50 % during hypoxia. The reduction in Na(+)/K(+) pump activity was accompanied by reductions in passive (22)Na(+) influx and (86)Rb(+) efflux (effectively K(+) efflux) across the sarcolemma. This may be due to a decreased Na(+) permeability of the sarcolemma and a 75 % reduction in K(+) leak mediated by ATP-sensitive K(+) channels (‘K(ATP)’ channels). The lowered rates of (22)Na(+) and (86)Rb(+) flux are coincident with lowered transmembrane ion gradients for [Na(+)] and [K(+)], which may also lower Na(+)/K(+) pump activity. The dilution of extracellular [Na(+)] and intracellular [K(+)] may be partially explained by increased water retention by the whole animal, although measurements of skeletal muscle fluid compartments using (3)H-labelled inulin suggested that the reduced ion gradients represented a new steady state for skeletal muscle. Conversely, intracellular ion homeostasis within ventricular muscle was maintained at pre-submergence levels, despite a significant increase in tissue water content, with the exception of the hypoxic frogs following 4 months of submergence. Both ventricular muscles and skeletal muscles maintained resting membrane potential at pre-submergence levels throughout the entire period of hibernation. The ability of the skeletal muscle to maintain its resting membrane potential, coincident with decreased Na(+)/K(+) pump activity and lowered membrane permeability, provided evidence of functional channel arrest as an energy-sparing strategy during hibernation in the cold-submerged frog.

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de las Heras, Natalia, Adrián Galiana, Sandra Ballesteros, Elena Olivares-Álvaro, Peter J. Fuller, Vicente Lahera, and Beatriz Martín-Fernández. "Proanthocyanidins Maintain Cardiac Ionic Homeostasis in Aldosterone-Induced Hypertension and Heart Failure." International Journal of Molecular Sciences 22, no. 17 (September 4, 2021): 9602. http://dx.doi.org/10.3390/ijms22179602.

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Excess aldosterone promotes pathological remodeling of the heart and imbalance in cardiac ion homeostasis of sodium, potassium and calcium. Novel treatment with proanthocyanidins in aldosterone-treated rats has resulted in downregulation of cardiac SGK1, the main genomic aldosterone-induced intracellular mediator of ion handling. It therefore follows that proanthocyanidins could be modulating cardiac ion homeostasis in aldosterone-treated rats. Male Wistar rats received aldosterone (1 mg kg−1 day−1) +1% NaCl for three weeks. Half of the animals in each group were simultaneously treated with the proanthocyanidins-rich extract (80% w/w) (PRO80, 5 mg kg−1 day−1). PRO80 prevented cardiac hypertrophy and decreased calcium content. Expression of ion channels (ROMK, NHE1, NKA and NCX1) and calcium transient mediators (CAV1.2, pCaMKII and oxCaMKII) were reduced by PRO80 treatment in aldosterone-treated rats. To conclude, our data indicate that PRO80 may offer an alternative treatment to conventional MR-blockade in the prevention of aldosterone-induced cardiac pathology.

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Zhang, Mu, Chengxiao Hu, Xuecheng Sun, Xiaohu Zhao, Qiling Tan, Ying Zhang, and Na Li. "Molybdenum Affects Photosynthesis and Ionic Homeostasis of Chinese Cabbage under Salinity Stress." Communications in Soil Science and Plant Analysis 45, no. 20 (October 15, 2014): 2660–72. http://dx.doi.org/10.1080/00103624.2014.941855.

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39

Tortiglione, Anna, Barbara Picconi, Ilaria Barone, Diego Centonze, Silvia Rossi, Cinzia Costa, Massimiliano Di Filippo, et al. "Na + /Ca 2+ Exchanger Maintains Ionic Homeostasis in the Peri-Infarct Area." Stroke 38, no. 5 (May 2007): 1614–20. http://dx.doi.org/10.1161/strokeaha.106.478644.

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40

Wang, Yuan, Ren-Jie Tang, Xiyan Yang, Xiaojiang Zheng, Qiaolin Shao, Qing-Lin Tang, Aigen Fu, and Sheng Luan. "Golgi-localized cation/proton exchangers regulate ionic homeostasis and skotomorphogenesis in Arabidopsis." Plant, Cell & Environment 42, no. 2 (November 25, 2018): 673–87. http://dx.doi.org/10.1111/pce.13452.

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41

El Chemaly, Antoun, and Nicolas Demaurex. "Do Hv1 proton channels regulate the ionic and redox homeostasis of phagosomes?" Molecular and Cellular Endocrinology 353, no. 1-2 (April 2012): 82–87. http://dx.doi.org/10.1016/j.mce.2011.10.005.

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42

Gibson, J. S., P. I. Milner, R. White, T. P. A. Fairfax, and R. J. Wilkins. "Oxygen and reactive oxygen species in articular cartilage: modulators of ionic homeostasis." Pflügers Archiv - European Journal of Physiology 455, no. 4 (September 12, 2007): 563–73. http://dx.doi.org/10.1007/s00424-007-0310-7.

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43

Franco, Rodrigo, Wayne I. DeHaven, Maria I. Sifre, Carl D. Bortner, and John A. Cidlowski. "Glutathione Depletion and Disruption of Intracellular Ionic Homeostasis Regulate Lymphoid Cell Apoptosis." Journal of Biological Chemistry 283, no. 52 (October 21, 2008): 36071–87. http://dx.doi.org/10.1074/jbc.m807061200.

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44

Fernandes de Lima, V. M., and W. Hanke. "27. Ionic homeostasis within a working neuropil and short-term neuronalglial interactions." Journal of Neuroscience Methods 52, no. 1 (April 1994): A13. http://dx.doi.org/10.1016/0165-0270(94)90087-6.

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45

Panayiotidis, Mihalis I., Rodrigo Franco, Carl D. Bortner, and John A. Cidlowski. "Ouabain-induced perturbations in intracellular ionic homeostasis regulate death receptor-mediated apoptosis." Apoptosis 15, no. 7 (April 27, 2010): 834–49. http://dx.doi.org/10.1007/s10495-010-0494-8.

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46

Mu, Yuqing, Zhibin Du, Lan Xiao, Wendong Gao, Ross Crawford, and Yin Xiao. "The Localized Ionic Microenvironment in Bone Modelling/Remodelling: A Potential Guide for the Design of Biomaterials for Bone Tissue Engineering." Journal of Functional Biomaterials 14, no. 2 (January 19, 2023): 56. http://dx.doi.org/10.3390/jfb14020056.

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Bone is capable of adjusting size, shape, and quality to maintain its strength, toughness, and stiffness and to meet different needs of the body through continuous remodeling. The balance of bone homeostasis is orchestrated by interactions among different types of cells (mainly osteoblasts and osteoclasts), extracellular matrix, the surrounding biological milieus, and waste products from cell metabolisms. Inorganic ions liberated into the localized microenvironment during bone matrix degradation not only form apatite crystals as components or enter blood circulation to meet other bodily needs but also alter cellular activities as molecular modulators. The osteoinductive potential of inorganic motifs of bone has been gradually understood since the last century. Still, few have considered the naturally generated ionic microenvironment’s biological roles in bone remodeling. It is believed that a better understanding of the naturally balanced ionic microenvironment during bone remodeling can facilitate future biomaterial design for bone tissue engineering in terms of the modulatory roles of the ionic environment in the regenerative process.

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Bharti, Hina, Aakriti Singal, Mohsin Raza, P. C. Ghosh, and Alo Nag. "Ionophores as Potent Anti-malarials: A Miracle in the Making." Current Topics in Medicinal Chemistry 18, no. 23 (January 10, 2019): 2029–41. http://dx.doi.org/10.2174/1568026619666181129125950.

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Plasmodium has a complex life cycle that spans between mosquito and human. For survival and pathogenesis it banks upon dynamic alterations in ionic transport across organelle and plasma membrane. Being a fundamental contributor of crucial biological processes in parasite, ionic balance facilitates parasite invasion, augmentation and transmission. Past few decades have witnessed tremendous advancement in understanding the relevance of ionic transit in parasites. Perhaps, not surprisingly, disruption of ionic homeostasis was thought to be detrimental for parasite. Compounds like ionophores are known to facilitate ionic transport across membrane down their electrochemical gradient. Despite continuous effort, malaria treatment is still a challenge particularly due to the development of resistance among parasites against existing therapeutic options. However, repurposing the existing drugs can be advantageous over de novo drug development programs in terms of cost and associated risk factors. Ionophores, being used in coccidiosis have proven to be of significance in the treatment of experimental models of malaria. Several recent reports have highlighted the attractive potential of ionophores such as Monensin, Maduramicin, Valinomycin, etc., that can act against multiple stages of malarial parasite’s life cycle. Improved variety of these molecules may help in mitigating the drug resistance problems as well. This review is an attempt to examine the relevant literature and provide insight into the mechanism and prospects of different classes of ionophores as promising anti-malarial potpourri.

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48

Rivaud, Mathilde R., Mario Delmar, and Carol Ann Remme. "Heritable arrhythmia syndromes associated with abnormal cardiac sodium channel function: ionic and non-ionic mechanisms." Cardiovascular Research 116, no. 9 (April 6, 2020): 1557–70. http://dx.doi.org/10.1093/cvr/cvaa082.

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Abstract The cardiac sodium channel NaV1.5, encoded by the SCN5A gene, is responsible for the fast upstroke of the action potential. Mutations in SCN5A may cause sodium channel dysfunction by decreasing peak sodium current, which slows conduction and facilitates reentry-based arrhythmias, and by enhancing late sodium current, which prolongs the action potential and sets the stage for early afterdepolarization and arrhythmias. Yet, some NaV1.5-related disorders, in particular structural abnormalities, cannot be directly or solely explained on the basis of defective NaV1.5 expression or biophysics. An emerging concept that may explain the large disease spectrum associated with SCN5A mutations centres around the multifunctionality of the NaV1.5 complex. In this alternative view, alterations in NaV1.5 affect processes that are independent of its canonical ion-conducting role. We here propose a novel classification of NaV1.5 (dys)function, categorized into (i) direct ionic effects of sodium influx through NaV1.5 on membrane potential and consequent action potential generation, (ii) indirect ionic effects of sodium influx on intracellular homeostasis and signalling, and (iii) non-ionic effects of NaV1.5, independent of sodium influx, through interactions with macromolecular complexes within the different microdomains of the cardiomyocyte. These indirect ionic and non-ionic processes may, acting alone or in concert, contribute significantly to arrhythmogenesis. Hence, further exploration of these multifunctional effects of NaV1.5 is essential for the development of novel preventive and therapeutic strategies.

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Van Goor, Fredrick, Dragoslava Zivadinovic, and Stanko S. Stojilkovic. "Differential Expression of Ionic Channels in Rat Anterior Pituitary Cells." Molecular Endocrinology 15, no. 7 (July 1, 2001): 1222–36. http://dx.doi.org/10.1210/mend.15.7.0668.

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Abstract Secretory anterior pituitary cells are of the same origin, but exhibit cell type-specific patterns of spontaneous intracellular Ca2+ signaling and basal hormone secretion. To understand the underlying ionic mechanisms mediating these differences, we compared the ionic channels expressed in somatotrophs, lactotrophs, and gonadotrophs from randomly cycling female rats under identical cell culture and recording conditions. Our results indicate that a similar group of ionic channels are expressed in each cell type, including transient and sustained voltage-gated Ca2+ channels, tetrodotoxin-sensitive Na+ channels, transient and delayed rectifying K+ channels, and multiple Ca2+-sensitive K+ channel subtypes. However, there were marked differences in the expression levels of some of the ionic channels. Specifically, lactotrophs and somatotrophs exhibited low expression levels of tetrodotoxin-sensitive Na+ channels and high expression levels of the large-conductance, Ca2+-activated K+ channel compared with those observed in gonadotrophs. In addition, functional expression of the transient K+ channel was much higher in lactotrophs and gonadotrophs than in somatotrophs. Finally, the expression of the transient voltage-gated Ca2+ channels was higher in somatotrophs than in lactotrophs and gonadotrophs. These results indicate that there are cell type-specific patterns of ionic channel expression, which may be of physiological significance for the control of Ca2+ homeostasis and secretion in unstimulated and receptor-stimulated anterior pituitary cells.

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Li, Ping, Meiqin Hu, Ce Wang, Xinghua Feng, ZhuangZhuang Zhao, Ying Yang, Nirakar Sahoo, et al. "LRRC8 family proteins within lysosomes regulate cellular osmoregulation and enhance cell survival to multiple physiological stresses." Proceedings of the National Academy of Sciences 117, no. 46 (November 2, 2020): 29155–65. http://dx.doi.org/10.1073/pnas.2016539117.

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LRRC8 family proteins on the plasma membrane play a critical role in cellular osmoregulation by forming volume-regulated anion channels (VRACs) necessary to prevent necrotic cell death. We demonstrate that intracellular LRRC8 proteins acting within lysosomes also play an essential role in cellular osmoregulation. LRRC8 proteins on lysosome membranes generate large lysosomal volume-regulated anion channel (Lyso-VRAC) currents in response to low cytoplasmic ionic strength conditions. When a double-leucine L706L707motif at the C terminus of LRRC8A was mutated to alanines, normal plasma membrane VRAC currents were still observed, but Lyso-VRAC currents were absent. We used this targeting mutant, as well as pharmacological tools, to demonstrate that Lyso-VRAC currents are necessary for the formation of large lysosome-derived vacuoles, which store and then expel excess water to maintain cytosolic water homeostasis. Thus, Lyso-VRACs allow lysosomes of mammalian cells to act as the cell`s “bladder.” When Lyso-VRAC current was selectively eliminated, the extent of necrotic cell death to sustained stress was greatly increased, not only in response to hypoosmotic stress, but also to hypoxic and hypothermic stresses. Thus Lyso-VRACs play an essential role in enabling cells to mount successful homeostatic responses to multiple stressors.

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