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Ion Homeostasis (ion + homeostasi)
Selected AbstractsAqueous exposure to 4-nonylphenol and 17,-estradiol increases stress sensitivity and disrupts ion regulatory ability of juvenile Atlantic salmonENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 7 2007Darren T. Lerner Abstract Population declines of wild Atlantic salmon have been attributed to an array of anthropogenic disturbances, including dams, commercial and recreational fishing, habitat loss, and pollution. Environmental contaminants in particular, can act as environmental stressors on fish, typically causing disruption of ion homeostasis due to their close association with the aquatic environment. To examine the effects of the xenoestrogen 4-nonylphenol (NP) or 17,-estradiol (E2) on stress sensitivity and ion regulation, we exposed juvenile Atlantic salmon continuously for 21 d to either 10 or 100 ,g/L NP (NP-L or NP-H), 2 ,g/L E2 (positive control), or vehicle control during the parr-smolt transformation in April. After treatment, fish were sampled in freshwater (FW), transferred to 30, seawater (SW) for 24 h, or subjected to a handling stress. Estradiol and NP-H increased plasma vitellogenin in males and females, and E2 increased gonadosomatic index only in males. In FW, E2 reduced sodium potassium,activated adenosine triphosphatase activity as well as plasma levels of growth hormone, insulin-like growth factor I, and triiodothyronine. Both E2 and NP-H reduced plasma sodium in FW and increased plasma chloride in SW. Plasma Cortisol levels pre- and poststressor were significantly elevated by all treatments relative to controls, but only E2 increased plasma glucose before and after the stressor. These results indicate that exposure of anadromous salmonids to environmental estrogens heightens sensitivity to external stressors, impairs ion regulation in both FW and SW, and disrupts endocrine pathways critical for smolt development. [source] Neocortical Microenvironment in Patients with Intractable Epilepsy: Potassium and Chloride ConcentrationsEPILEPSIA, Issue 2 2006Ali Gorji Summary:,Purpose: The regulation of extracellular ion concentrations plays an important role in neuronal function and epileptogenesis. Despite the many studies into the mechanisms of epileptogenesis in human experimental models, no data are available regarding the fluctuations of extracellular potassium ([K+]o) and chloride ([Cl,]o) concentrations, which could underlie seizure susceptibility in human chronically epileptic tissues in vivo. Methods: By using cerebral microdialysis during surgical resection of epileptic foci, the basic [K+]o and [Cl,]o as well as their changes after epicortical electric stimulation were studied in samples of dialysates obtained from 11 patients by ion-selective microelectrodes. Results: The mean basal values of [K+]o and [Cl,]o in all patients were 3.83 ± 0.08 mM and 122.9 ± 2.6 mM, respectively. However, significant differences were observed in the basal levels of both [K+]o and [Cl,]o between different patients. Statistically, no correlation was found between basal [K+]o or [Cl,]o and electrocorticogram (ECoG) spike activity, but in one patient, dramatically lowered baseline [Cl,]o was accompanied by enhanced ECoG spike activity. Application of epicortical electrical stimulation increased [K+]o but not [Cl,]o in all cases. According to the velocity as well as spatial distribution of [K+]o reduction to the prestimulation levels, three different types of responses were observed: slow decline, fast decline, and slow and fast declines at adjacent sites. Conclusions: These data may represent abnormalities in ion homeostasis of the epileptic brain. [source] Differential expression of PKC beta II in the rat organ of CortiEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2007S. Ladrech Abstract To investigate a possible involvement of protein kinase C (PKC) in cochlear efferent neurotransmission, we studied the expression of the calcium-dependent PKC beta II isoform in the rat organ of Corti at different postnatal ages using immunofluorescence and immunoelectron microscopy. We found evidence of PKC beta II as early as postnatal day (PND) 5 in efferent axons running in the inner spiral bundle and in Hensen cells. At PND 8, we also found PKC beta II in efferents targeting outer hair cells (OHCs), and a slight detection at the synaptic pole in the first row of the basal and middle cochlear turns. At PND 12, PKC beta II expression declined in the efferent fibres contacting OHCs, whereas expression was concentrated at the postsynaptic membrane, from the basal and middle turns. The adult-like pattern of PKC beta II distribution was observed at PND 20. Throughout the cochlea, we found PKC beta II expression in the Hensen cells, non-sensory cells involved in potassium re-cycling, and lateral efferent terminals of the inner spiral bundle. In addition, we observed expression in OHCs at the postsynaptic membrane facing the endings of the medial efferent system, with the exception of some OHCs located in the most apical region of the cochlea. These data therefore suggest an involvement of PKC beta II in both cochlear efferent neurotransmission and ion homeostasis. Among other functions, PKC beta II could play a role in the efferent control of OHC activity. [source] A respiratory-deficient mutation associated with high salt sensitivity in Kluyveromyces lactisFEMS YEAST RESEARCH, Issue 2 2007Paola Goffrini Abstract A salt-sensitive mutant of Kluyveromyces lactis was isolated that was unable to grow in high-salt media. This mutant was also respiratory-deficient and temperature-sensitive for growth. The mutation mapped in a single nuclear gene that is the ortholog of BCS1 of Saccharomyces cerevisiae. The BCS1 product is a mitochondrial protein required for the assembly of respiratory complex III. The bcs1 mutation of S. cerevisiae leads to a loss of respiration, but, unlike in K. lactis, it is not accompanied by salt sensitivity. All the respiratory-deficient K. lactis mutants tested were found to be salt-sensitive compared to their isogenic wild-type strains. In the presence of the respiratory inhibitor antimycin A, the wild-type strain also became salt-sensitive. By contrast, none of the S. cerevisiae respiratory-deficient mutants tested showed increased salt sensitivity. The salt sensitivity of the Klbcs1 mutant, but not its respiratory deficiency, was suppressed by the multicopy KlVMA13 gene, a homolog of the S. cerevisiae VMA13 gene encoding a subunit of the vacuolar H+ -ATPase. These results suggest that cellular salt homeostasis in K. lactis is strongly dependent on mitochondrial respiratory activity, and/or that the ion homeostasis of mitochondria themselves could be a primary target of salt stress. [source] Contrasts in cortical magnesium, phospholipid and energy metabolism between migraine syndromes.HEADACHE, Issue 4 2003MD Boska Neurology. 2002;58:1227-1233. BACKGROUND: Previous single voxel (31)P MRS pilot studies of migraine patients have suggested that disordered energy metabolism or Mg(2+) deficiencies may be responsible for hyperexcitability of neuronal tissue in migraine patients. These studies were extended to include multiple brain regions and larger numbers of patients by multislice (31)P MR spectroscopic imaging. METHODS: Migraine with aura (MWA), migraine without aura (MwoA), and hemiplegic migraine patients were studied between attacks by (31)P MRS imaging using a 3-T scanner. RESULTS: Results were compared with those in healthy control subjects without headache. In MwoA, consistent increases in phosphodiester concentration [PDE] were measured in most brain regions, with a trend toward increase in [Mg(2+)] in posterior brain. In MWA, phosphocreatine concentration ([PCr]) was decreased to a minor degree in anterior brain regions and a trend toward decreased [Mg(2+)] was observed in posterior slice 1, but no consistent changes were found in phosphomonoester concentration [PME], [PDE], inorganic phosphate concentration ([Pi]), or pH. In hemiplegic migraine patients, [PCr] had a tendency to be lower, and [Mg(2+)] was significantly lower than in the posterior brain regions of control subjects. Trend analysis showed a significant decrease of brain [Mg(2+)] and [PDE] in posterior brain regions with increasing severity of neurologic symptoms. CONCLUSIONS: Overall, the results support no substantial or consistent abnormalities of energy metabolism, but it is hypothesized that disturbances in magnesium ion homeostasis may contribute to brain cortex hyperexcitability and the pathogenesis of migraine syndromes associated with neurologic symptoms. In contrast, migraine patients without a neurologic aura may exhibit compensatory changes in [Mg(2+)] and membrane phospholipids that counteract cortical excitability. Comment: If the theory of hyperexcitability of migraine brain is correct, basic scientists will need to find clear markers for the neuronal abnormalities that underlie this excitability. Using their techniques, these researchers could not find such markers. SJT [source] Quantitative sodium imaging with a flexible twisted projection pulse sequenceMAGNETIC RESONANCE IN MEDICINE, Issue 6 2010Aiming Lu Abstract The quantification of sodium MR images from an arbitrary intensity scale into a bioscale fosters image interpretation in terms of the spatially resolved biochemical process of sodium ion homeostasis. A methodology for quantifying tissue sodium concentration using a flexible twisted projection imaging sequence is proposed that allows for optimization of tradeoffs between readout time, signal-to-noise ratio efficiency, and sensitivity to static field susceptibility artifacts. The gradient amplitude supported by the slew rate at each k -space radius regularizes the readout gradient waveform design to avoid slew rate violation. Static field inhomogeneity artifacts are corrected using a frequency-segmented conjugate phase reconstruction approach, with field maps obtained quickly from coregistered proton imaging. High-quality quantitative sodium images have been achieved in phantom and volunteer studies with real isotropic spatial resolution of 7.5 × 7.5 × 7.5 mm3 for the slow T2 component in ,8 min on a clinical 3-T scanner. After correcting for coil sensitivity inhomogeneity and water fraction, the tissue sodium concentration in gray matter and white matter was measured to be 36.6 ± 0.6 ,mol/g wet weight and 27.6 ± 1.2 ,mol/g wet weight, respectively. Magn Reson Med 63:1583,1593, 2010. © 2010 Wiley-Liss, Inc. [source] The SUI-homologous translation initiation factor eIF-1 is involved in regulation of ion homeostasis in ricePLANT BIOLOGY, Issue 3 2008C. J. Diédhiou Abstract Halophytes survive high salinity by using complex adaptive mechanisms. In a search for novel molecular mechanisms involved in salt acclimation, transcript analyses revealed increased expression of a SUI-homologous translation initiation factor eIF-1 in the salt-tolerant grass species Festuca rubra ssp. littoralis but not in rice. Upon analysis of the cell specificity of eIF-1 transcription by in situ polymerase chain reaction (PCR), predominant signals were detected in rice leaf mesophyll. To further examine the role of eIF-1 in salt tolerance, transgenic rice plants were generated that over-express this factor under the control of the CaMV-35S promoter. The eIF-1 over-expressing lines showed improved growth under salt stress that was correlated with maintenance of photosynthetic activity and reduced Na+ and Cl, accumulation in leaves. The transgenic rice lines also activated expression of the vacuolar H+ -ATPase. In addition, an oxidoreductase that belongs to the aldo/keto reductase family was identified as a gene with modified expression in the eIF-1 over-expressing lines, compared with wild-type rice. Our data suggest that eIF-1 has a central function in salt-stress adaptation in rice by regulating ion accumulation and the intracellular redox status. [source] The plasma membrane Na+/H+ antiporter SOS1 is essential for salt tolerance in tomato and affects the partitioning of Na+ between plant organsPLANT CELL & ENVIRONMENT, Issue 7 2009RAQUEL OLÍAS ABSTRACT We have identified a plasma membrane Na+/H+ antiporter gene from tomato (Solanum lycopersicum), SlSOS1, and used heterologous expression in yeast to confirm that SlSOS1 was the functional homolog of AtSOS1. Using post-transcriptional gene silencing, we evaluated the role played by SlSOS1 in long-distance Na+ transport and salt tolerance of tomato. Tomato was used because of its anatomical structure, more complex than that of Arabidopsis, and its agricultural significance. Transgenic tomato plants with reduced expression of SlSOS1 exhibited reduced growth rate compared to wild-type (WT) plants in saline conditions. This sensitivity correlated with higher accumulation of Na+ in leaves and roots, but lower contents in stems of silenced plants under salt stress. Differential distribution of Na+ and lower net Na+ flux were observed in the xylem sap in the suppressed plants. In addition, K+ concentration was lower in roots of silenced plants than in WT. Our results demonstrate that SlSOS1 antiporter is not only essential in maintaining ion homeostasis under salinity, but also critical for the partitioning of Na+ between plant organs. The ability of tomato plants to retain Na+ in the stems, thus preventing Na+ from reaching the photosynthetic tissues, is largely dependent on the function of SlSOS1. [source] Staphylococcus aureus ClpC ATPase is a late growth phase effector of metabolism and persistencePROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 5 2009Indranil Chatterjee Dr. Abstract Staphylococcus aureus Clp ATPases (molecular chaperones) alter normal physiological functions including an aconitase-mediated effect on post-stationary growth, acetate catabolism, and entry into death phase (Chatterjee et al., J. Bacteriol. 2005, 187, 4488,4496). In the present study, the global function of ClpC in physiology, metabolism, and late-stationary phase survival was examined using DNA microarrays and 2-D PAGE followed by MALDI-TOF MS. The results suggest that ClpC is involved in regulating the expression of genes and/or proteins of gluconeogenesis, the pentose-phosphate pathway, pyruvate metabolism, the electron transport chain, nucleotide metabolism, oxidative stress, metal ion homeostasis, stringent response, and programmed cell death. Thus, one major function of ClpC is balancing late growth phase carbon metabolism. Furthermore, these changes in carbon metabolism result in alterations of the intracellular concentration of free NADH, the amount of cell-associated iron, and fatty acid metabolism. This study provides strong evidence for ClpC as a critical factor in staphylococcal energy metabolism, stress regulation, and late-stationary phase survival; therefore, these data provide important insight into the adaptation of S. aureus toward a persister state in chronic infections. [source] Proteomic profiling of antisense-induced exon skipping reveals reversal of pathobiochemical abnormalities in dystrophic mdx diaphragmPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 3 2009Philip Doran Abstract The disintegration of the dystrophin,glycoprotein complex represents the initial pathobiochemical insult in Duchenne muscular dystrophy. However, secondary changes in signalling, energy metabolism and ion homeostasis are probably the main factors that eventually cause progressive muscle wasting. Thus, for the proper evaluation of novel therapeutic approaches, it is essential to analyse the reversal of both primary and secondary abnormalities in treated muscles. Antisense oligomer-mediated exon skipping promises functional restoration of the primary deficiency in dystrophin. In this study, an established phosphorodiamidate morpholino oligomer coupled to a cell-penetrating peptide was employed for the specific removal of exon 23 in the mutated mouse dystrophin gene transcript. Using DIGE analysis, we could show the reversal of secondary pathobiochemical abnormalities in the dystrophic diaphragm following exon-23 skipping. In analogy to the restoration of dystrophin, ,-dystroglycan and neuronal nitric oxide synthase, the muscular dystrophy-associated differential expression of calsequestrin, adenylate kinase, aldolase, mitochondrial creatine kinase and cvHsp was reversed in treated muscle fibres. Hence, the re-establishment of Dp427 coded by the transcript missing exon 23 has counter-acted dystrophic alterations in Ca2+ -handling, nucleotide metabolism, bioenergetic pathways and cellular stress response. This clearly establishes the exon-skipping approach as a realistic treatment strategy for diminishing diverse downstream alterations in dystrophinopathy. [source] Imaging ion flux and ion homeostasis in blood stage malaria parasitesBIOTECHNOLOGY JOURNAL, Issue 6 2009Petra Rohrbach Dr.Article first published online: 8 JUN 200 Abstract The steady-state regulation of intracellular levels of essential ions and ionic gradients is critical for almost all functions within a cell. Thus, it is not surprising to find that ions have been shown to play an important role in numerous parasitic processes, such as invasion, development and possibly drug resistance mechanisms. Live cell imaging has become a widespread technique to visualize and quantify several of these processes, including pH and Ca2+ homeostasis, in an effort to better understand the biology and physiology of cells. This is now also the case for many human pathogens. The aim of this review is to emphasize the importance of this technique and provide an overview of what we have learned so far, using the malaria parasite Plasmodium falciparum as a paradigm. [source] | |||||||||||||