Activity Of Na Research Articles

Interleukin 6 plus High Salt Increases Systolic Blood Pressure

Cytokines and immune cells are implicated in the development of hypertension (HTN), and clinically, interleukin 6 (IL‐6) is independently correlated with HTN. HTN is also characterized by increased sodium (Na+) reabsorption along the aldosterone‐sensitive distal nephron (ASDN), as well as increased expression and/or activity of Na+ transport proteins, such as the sodium chloride cotransporter (NCC) and the epithelial sodium channel (ENaC). We have previously shown that IL‐6 can activate the mineralocorticoid receptor (MR) in vitro, and intrarenal IL‐6 perfusion significantly increases expression of total and phosphorylated (T53)‐NCC, and ENaC α/γ subunits in vivo. Here, we hypothesize that IL‐6 increases Na+ reabsorption, leading to HTN. To determine whether IL‐6 increases blood pressure (BP), mice (C57Bl6) were implanted with miniosmotic pumps and tail cuff plethysmography used to measure systolic BP during IL‐6 infusion (16 ng/hr, 0.01% BSA in saline) or sham surgery. Mice were fed normal chow (NC) or high salt (HS) food. Mice with systemic IL‐6 infusion (3 days) plus HS diet had significantly increased BP as compared to HS alone (129±6 mmHg vs. 110±5 mmHg, n=4, *p<0.05) with no increases in proteinuria (7 days). No changes in BP was observed in mice treated with IL‐6 and fed NC.To investigate whether intra‐renal IL‐6 activates NCC via the MR, in vivo, jugular catheters were attached to a miniosmotic pump and inserted under the renal capsule. Mice were infused with IL‐6 (16 ng/hr, 0.1% BSA in saline; 3 days) or vehicle. Mice were sacrificed, tissues removed and then cryosectioned for immunofluorescence (IF) studies. We observed a significant increase in phosphor(T53)‐NCC expression (291±12 mean pixel intensity, MPI) vs. vehicle (236±9; p<0.01, n=3). Mice were then given the MR antagonist (spironolactone, [0.6 mg/day] in peanut butter); we observed a significant reduction in the IL‐6‐mediated increase in phosphor(T53)‐NCC expression (210±12 MPI; p<0.001, n=3).Our data suggest that IL‐6 infusion plus HS increases systolic BP, beginning on day 3, without significant renal damage on day 7. Although we observed a significant increase in IL‐6‐mediated MR‐dependent phosphor(T53)‐NCC expression, our metabolic cage data suggest that pressure natriuresis may be occurring by day 3. Together, these data suggest a novel role for cytokines and high salt in the development of HTN.Support or Funding InformationEmory SIRE to GGH and BMW; ASPET SURF to GGH; Emory University SUPERR 5R25DK101390‐05 to HCM; NIDDK085097 and VA MERIT I01BX002322 to RSH and 2T32DK7656‐2 to BMWThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Caste-Specific Expression of Na+/K+-ATPase in the Asian Weaver Ant, Oecophylla smaragdina (Fabricius, 1775).

Social insect colonies adopt different levels of survival strategies and exhibit well-defined reproductive division of labour. Oecophylla smaragdina (Fabricius, 1775) has physiological and behavioral adaptations that enable them to forage at extreme environmental conditions and are lethal to most other insects. Ion homeostasis is the key process in an organism's survival mechanism. Among ion pumps, the ATP-dependent sodium-potassium ion pump is essential for maintaining the Na+ and K+ ionic balance and is well known as the primary consumer of energy. Oecophylla smaragdina plays pivotal role as a model among social insects for understanding ion homeostasis at the organization level of the castes. We have evaluated the expression and activity of Na+/K+-ATPase among various castes of O. smaragdina (worker subcastes, queen and male). Real-time PCR and immunoblotting analyses revealed the differential expression of Na+/K+-ATPase in the castes. Significantly higher expression of Na+/K+-ATPase mRNA and protein were observed in the minor workers, queen, major workers and males respectively. These results suggest that in the weaver ant colony, the castes might have variously adapted and evolved with a well-developed ion transport mechanism which allows them to perform allocated tasks within the nest and could be a key to their adaptive benefits towards division of labour.

Adenosine A2A receptor inhibition restores the normal transport of endothelial glutamate transporters in the brain

Excitatory amino acid transporters (EAATs) on cerebral vascular endothelial cells play an important role in maintaining glutamate homeostasis in the brain. The dysfunction of endothelial EAATs is an important reason for the dramatically elevated brain glutamate levels after brain injury, such as traumatic brain injury (TBI). The adenosine A2A receptor (A2AR) plays an important role in regulating the brain glutamate level after brain injury; however, researchers have not clearly determined whether this role was related to its ability to regulate endothelial EAATs. Activation of A2AR in vitro not only decreased the PKA- and glutamate level-dependent strengthening of the interaction between NKA-α1 and the FXYD1 subunit and the subsequent decrease in the activity of Na+/K+-ATPases (NKAs) but also enhanced its interaction with EAATs and ultimately aggravated the reverse transport function of endothelial EAATs under oxygen-glucose deprivation (OGD) conditions. Conversely, inhibition of A2AR restored the normal transport of EAAT. Moreover, A2AR inhibition increased NKA activity and decreased its interaction with EAATs in isolated brain capillaries after TBI, further confirming its role in endothelial EAATs in vivo. Based on our results, A2AR played an important role in regulating endothelial EAAT function, and strategies that restore the normal transport of endothelial EAATs through the inhibition of A2AR might serve as an effective treatment for brain injury.

Na+, K+-ATPase Activating Antibody Displays in vitro and in vivo Beneficial Effects in the Pilocarpine Model of Epilepsy

Na+, K+-ATPase is an important regulator of brain excitability. Accordingly, compelling evidence indicates that impairment of Na+, K+-ATPase activity contributes to seizure activity in epileptic mice and human with epilepsy. In addition, this enzyme is crucial for plasma membrane transport of water, glucose and several chemical mediators, including glutamate, the major excitatory transmitter in the mammalian brain. Since glucose hypometabolism and increased glutamate levels occur in clinical and experimental epilepsy, we aimed the present study to investigate whether activation of Na+, K+-ATPase activity with specific antibody (DRRSAb) would improve glucose uptake and glutamate release in pilocarpine-treated mice. We found decreased uptake of the glucose fluorescent analog 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-il)amino]-2-desoxi-d-glucose (2-NBDG) in cerebral slices from pilocarpine-treated animals. Interestingly, decreased 2-NBDG uptake was not detected in DRRSAb-treated slices, suggesting a protective effect of the Na+, K+-ATPase activator. Moreover, DRRSAb prevented the increase in glutamate levels in the incubation media of slices from pilocarpine-treated mice. In addition, in vivo intrahippocampal injection of DRRSAb restored crossing activity of pilocarpine-treated mice in the open-field test. Overall, the present data further support the hypothesis that activation of the Na+, K+-ATPase is a promising therapeutic strategy for epilepsy.

Oligoasthenoteratozoospermia and Necrozoospermia: A Study of Sperm Na+, K+-ATPase α4 and Plasma Membrane Ca2+-ATPase 4 Regulation

The oligoasthenoteratozoospermia (OAT) and necrozoospermia are the extreme sperm abnormalities in male infertility. These sperm abnormalities may be related to the imbalance of ion transport which mediated by the ion-transporting P-type ATPases, such as Na+, K+-ATPase and Ca2+-ATPase. Until now, there is limited data about the activity of Na+, K+-ATPase and Ca2+-ATPase in sperms in the OAT and necrozoospermia samples. Therefore, this study investigated the activity of Na+, K+-ATPase and Ca2+-ATPase and the expression of Na+, K+-ATPase α4 and PMCA4 isoforms in both sperm abnormalities. Eighteen semen samples from OAT and necrozoospermia infertile couples were examined in this study. Semen analysis was performed based on WHO 2010, while the enzyme activity was calculated by the released inorganic phosphate. The expression of Na+, K+-ATPase α4 and PMCA4 isoform was defined by Western immunoblotting, whereas the localization of the proteins was analyzed by immunocytochemistry. This study showed that the activity of Na+, K+-ATPase and the expression of Na+, K+-ATPase α4 isoforms in OAT and necrozoospermia group were lower than the normozoospermia group (1.452±0.549 versus 0.559±0.160 versus 1.962±0.56 µmol Pi/mg protein/h, respectively; p>0.05). In addition, the activity of Ca2+-ATPase and the expression of PMCA4 of OAT and necrozoospermia group were also lower compared to the normozoospermia group (2.028±0.524 versus 0.928±0.248 versus 2.657±1.329 µmol Pi/mg protein/h, respectively; p>0.05). For both ATPases, the necrozoospermia group showed lower values compared to the OAT group. The disruption in ATPase and isoform expression in OAT and necrozoospermia may be responsible for sperm structure and functional damage.

Mechanisms of Sodium Transport in Plants-Progresses and Challenges.

Understanding the mechanisms of sodium (Na+) influx, effective compartmentalization, and efflux in higher plants is crucial to manipulate Na+ accumulation and assure the maintenance of low Na+ concentration in the cytosol and, hence, plant tolerance to salt stress. Na+ influx across the plasma membrane in the roots occur mainly via nonselective cation channels (NSCCs). Na+ is compartmentalized into vacuoles by Na+/H+ exchangers (NHXs). Na+ efflux from the plant roots is mediated by the activity of Na+/H+ antiporters catalyzed by the salt overly sensitive 1 (SOS1) protein. In animals, ouabain (OU)-sensitive Na+, K+-ATPase (a P-type ATPase) mediates sodium efflux. The evolution of P-type ATPases in higher plants does not exclude the possibility of sodium efflux mechanisms similar to the Na+, K+-ATPase-dependent mechanisms characteristic of animal cells. Using novel fluorescence imaging and spectrofluorometric methodologies, an OU-sensitive sodium efflux system has recently been reported to be physiologically active in roots. This review summarizes and analyzes the current knowledge on Na+ influx, compartmentalization, and efflux in higher plants in response to salt stress.

Effects of the acclimation to high salinity on intestinal ion and peptide transporters in two tilapia species that differ in their salinity tolerance

Tilapiine species, widely distributed across habitats with diverse water salinities, are important to aquaculture as well as a laboratory model. The effects of water salinity on two tilapia species, that differ in their salinity tolerance, was evaluated. Oreochromis niloticus reared in brackish-water, showed a significant decrease in growth and feed efficiency, whereas O. mossambicus reared in seawater did not show any significant changes. The expression and activity of Na+/K+-ATPase (NKA), V-type H+-ATPase (VHA) and carbonic anhydrase (CA), as well as expression levels of genes encoding two HCO3− and three peptide transporters (nbc1, slc26a6, slc15a1a, slc15a1b and slc15a2) were measured in three intestinal sections of these two species, grown in freshwater and brackish/sea-water. Overall, the spatial distribution along the intestine of the genes examined in this study was similar between the two species, with the exception of tcaIV. The salinity response, on the other hand, varied greatly between these species. In O. mossambicus, there was a salinity-dependent increased expression of most of the examined genes (except slc26a6 and slc15a2), while in O. niloticus the expression of most genes did not change, or even decreased (tcaIV, nbc1 and slc15a1b). This study highlighted differences in the intestinal response to salinity acclimation between closely- related species that differ in their salinity tolerance. O. mossambicus, which has a high salinity tolerance, showed expression patterns and responses similar to marine species, and differed from the low-salinity-tolerance O. niloticus, which showed a response that differed from the accepted models, that are based on marine and diadromous fishes.

Abstract WP262: Neuroglobin Mediates Neuroprotection of Hypoxic Postconditioning Against Transient Global Cerebral Ischemia in Rats via Preserving the Activity of Na + /K + ATPases

Introduction: Hypoxic postconditioning (HPC) is an innovative neuroprotective strategy with pro-survival effects on hippocampal neurons against transient global cerebral ischemia (tGCI), but the mechanisms have not yet been completely elucidated. Neuroglobin (Ngb) is an endogenous neuroprotectant with hypoxia-inducible property whose role in experimental stroke has increasingly been attractive. In this study, we explored the role and underlying mechanism of Ngb in HPC-mediated neuroprotection after tGCI. Methods: HPC was carried out with air containing 8% O 2 and 92% N 2 24 h after 10 min tGCI induced by a four-vessel occlusion method in adult male Wistar rats. The level of Ngb and Na + /K + ATPases β1 subunit (Atp1b1) were measured by immunohistochemistry, western blot and immunofluorescence after tGCI and HPC with or without the administration of Ngb antisense oligodeoxynucleotide (AS-ODNs) and lentivirus. Then reactive oxygen species (ROS) was detected via DCFH-DA and immunoprecipitation was performed to measure the glutathionylation of Atp1b1. Finally, the activity of Na + /K + ATPases (NKA) was detected by a Na + K + -ATPase assay kit. Results: HPC increased Ngb expression in CA1 subregion after tGCI. Inhibition of Ngb expression with Ngb AS-ODNs abolished HPC-mediated neuroprotection, whereas overexpression of Ngb ameliorated neuronal damage in hippocampal CA1 subregion after tGCI, confirming that Ngb upregulation is involved in the neuroprotection of HPC against tGCI. Similar to the tendency of Ngb expression, the membranous level of Atp1b1, a Ngb-interacting protein, reduced after tGCI while increased after HPC. Notably, knockdown of Ngb reversed the increase of membranous Atp1b1 mediated by HPC, whereas Ngb overexpression induced an opposite result. Furthermore, we found that Ngb upregulation after HPC maintained membranous Atp1b1 through the direct Ngb-Atp1b1 interaction and reduced the glutathionylation of membranous Atp1b1 via suppression of ROS, finally enhancing the activity of NKA. Conclusions: Our results suggested that Ngb preserved the activity of NKA after tGCI via its regulation on both the level and the glutathionylation of membranous Atp1b1, which contributed to HPC-mediated neuroprotection against tGCI.

Protective effect of ashwagandha (Withania somnifera) against neurotoxicity induced by aluminum chloride in rats

Objective: To evaluate the neuroprotective effect of ashwagandha extract against aluminum chloride-induced neurotoxicity in rats. Methods: Rats were divided into control, aluminum-intoxicated rats treated daily with aluminum trichloride (AlCl3) (100 mg/kg, orally) for 30 d and aluminum-intoxicated animals protected by receiving daily ashwagandha extract (200 mg/kg, orally) one hour before AlCl3 administration for 30 d. Levels of lipid peroxidation, nitric oxide, reduced glutathione and tumor necrosis factor-α were measured in the cortex, hippocampus and striatum. In addition, the activities of Na+, K+, ATPase and acetylcholinesterase were determined in the three studied brain regions. Results: Aluminum increased the levels of lipid peroxidation and nitric oxide in the cortex, hippocampus and striatum and decreased the reduced glutathione level in the hippocampus and striatum. In rats protected with ashwagandha extract, non significant changes were observed in lipid peroxidation, nitric oxide and reduced glutathione. In addition, ashwagandha extracts prevented the increased activity of acetylcholinesterase and Na+, K+, ATPase induced by AlCl3 in the cortex, hippocampus and striatum. The present findings also showed that the significant increase in tumor necrosis factor-α induced by AlCl3 in the cortex and hippocampus was prevented by ashwagandha extract. Conclusions: The present results suggest that ashwagandha extract possesses antioxidant and anti-inflammatory effects against aluminum neurotoxicity. In addition, ashwagandha extract could prevent the decline in cholinergic activity by maintaining normal acetylcholinesterase activity. The later effect could recommend the use of ashwagandha as a memory enhancer.

Effects of salinity on osmotic pressure and nonspecific immune enzymes in juvenile Eniocheir sinensis

PDF HTML阅读 XML下载 导出引用 引用提醒 盐度对中华绒螯蟹仔蟹渗透压和非特异性免疫酶的影响 DOI: 作者: 作者单位: 1. 中国水产科学研究院东海水产研究所, 上海 200090;2. 上海海洋大学水产与生命学院, 上海 201306 作者简介: 徐静静(1992-),女,硕士研究生,从事水生动物生理生态学研究.E-mail:xujingdhs@163.com 通讯作者: 中图分类号: S93 基金项目: 农业农村部财政专项（CJDC-2017-23）；中央级公益性科研院所基本科研业务费项目（2016M05）；上海市中华绒螯蟹产业技术体系项目（沪农科产字2017-4号）. Effects of salinity on osmotic pressure and nonspecific immune enzymes in juvenile Eniocheir sinensis Author: Affiliation: 1. East China Sea Fisheries Research Institute, Chinese Academy of Fishery Science, Shanghai 200090, China;2. College of Fisheries and Life Science, Shanghai Ocean University, Shanghai 201306, China Fund Project: 摘要 | 图/表 | 访问统计 | 参考文献 | 相似文献 | 引证文献 | 资源附件 | 文章评论 摘要:设置盐度梯度0、4、8、12、16、20和24，测定不同盐度下中华绒螯蟹（-ATPase活性、氧合血蓝蛋白含量以及超氧化物歧化酶（SOD）、碱性磷酸酶（AKP）、酚氧化酶（PO）活性，研究盐度对仔蟹成活率、渗透压调节和非特异性免疫酶活性的影响，探讨仔蟹对盐度的适应性。结果表明，盐度8实验组中华绒螯蟹仔蟹成活率和氧合血蓝蛋白含量最高，分别为（90.00±1.00）%和（0.253±0.023） mg/mL，显著高于其他实验组（+浓度，Na+-K+-ATPase活性和非特异性免疫酶活性在盐度0~8时呈下降趋势，而在盐度8~12时逐渐上升，当盐度大于12时趋于稳定；这些指标值在盐度8实验组降到最低，Na+、Cl-和K+浓度分别为（40.897±1.700） mmol/mL、（8.340±2.130） mmol/mL和（1.842±0.158） mmol/mL，Na+-K+-ATPase酶活性为（3.153±0.735） U/mg，非特异性免疫酶SOD、AKP和PO活性分别为（129.026±3.496） U/mg、（1.326±0.173） U/mg和（16.366±0.065） ng/mL。综合各项实验指标表明，不同盐度对中华绒螯蟹仔蟹渗透压和非特异性免疫酶活性具有一定影响，中华绒螯蟹仔蟹在盐度4~8水体中有较好的生理适应性，淡水和高盐度水体会降低其渗透压调节和免疫防御功能，这为长江口仔蟹资源变动评估和繁育场保护提供了参考。 Abstract:Salinity is an important ecological factor in the environment. It not only affects growth but also survival rate, osmotic pressure, and non-specific enzymes in juveniles of E. sinensis in the Yangtze Estuary, the effects of salinity on survival rate, osmotic pressure, and non-specific enzymes of juvenile were studied. Juveniles were added to circular glass fiber cylinders with different salinity levels (0, 4, 8, 12, 16, 20, and 24) and maintained under the following conditions:average water temperature 23-24; pH 7.2℃ -7.8; and average DO>5 mg/L. The survival rate, tissue homogenate supernatant Na+, Cl-, and K+ concentrations, Na+-K+-ATPase activity, oxyhemoglobin content, and the activities of total superoxidase (SOD), alkaline phosphatase (AKP), and phenoloxidase (PO) were analyzed after 3 days of the experiment. The results showed that the salinity 8 experimental group had the highest survival rate and hemocyanin content, which were 89% and (0.253±0.023) mg/mL, respectively, and were significantly higher than those of other experimental groups (<0.05) but were minimized in the freshwater and salinity 24 groups. Na+, Cl-, and K+ concentrations, Na+-K+-ATPase activity, and non-specific immune enzyme activity were divided into three stages. Firstly, these indicators decreased significantly with increasing salinity (0-8), gradually increased with higher salinity (8-12), and finally stabilized at the highest salinity (12-24). It had its lowest index values in the salinity 8 experimental group, the concentrations of Na+, Cl- and K+ were (40.897±1.700) mmol/mL, (8.340±2.130) mmol/mL, and (1.842±0.158) mmol/mL, and the activity of Na+-K+-ATPase was (3.153±0.735) U/mg, and the activities of SOD, AKP, and PO were (129.026±3.496) U/mg, (1.326±0.173) U/mg, and (16.366±0.065) ng/mL, respectively. Together, the results revealed that the juveniles were highly adaptable in low salinity (4-8), whereas fresh water and high salinity water weakened its osmotic regulation and immune defense function. The goals of this study were to reveal the physiological characteristics during feed-bait migration and provide a scientific basis for resource conservation and environmental assessment of juvenile . 参考文献 相似文献 引证文献

Allostatic Compensatory Mechanisms Enable the Mutant KCNT1 Channels to Induce Seizures and Hyperexcitability

Mutations in the sodium-activated potassium channel (KCNT1) gene are linked to epilepsy. Surprisingly, all KCNT1 mutations examined to date increase K current amplitude. These findings present a major neurophysiological paradox: how do gain-of-function KCNT1 mutations expected to silence neurons cause epilepsy? Here, we use Drosophila to show that expressing mutant KCNT1 in GABAergic neurons leads to seizures, consistent with the notion that silencing inhibitory neurons tips the balance towards hyperexcitation. Unexpectedly, mutant KCNT1 expressed in excitatory neurons also causes seizures. Further observations reveal that mutant KCNT1 causes abnormally large and spontaneous excitatory junction potentials (sEJPs), which are shown to be resulting from local depolarization of synaptic terminals due to a reduction in Shaker and Eag channel levels and more active Na and Ca2 channels. Such compensatory changes are likely mediated by the transcriptional factor Islet. Hence, we provide the first in vivo evidence that both disinhibition of inhibitory neurons and allostatic compensatory plasticity in excitatory neurons might account for the paradoxical effects of gain-of-function mutant KCNT1 in epilepsy.

Renal potassium handling in rats with subtotal nephrectomy: modeling and analysis.

We sought to decipher the mechanisms underlying the kidney's response to changes in K+ load and intake, under physiological and pathophysiological conditions. To accomplish that goal, we applied a published computational model of epithelial transport along rat nephrons in a sham rat, an uninephrectomized (UNX) rat, and a 5/6-nephrectomized (5/6-NX) rat that also considers adaptations in glomerular filtration rate and tubular growth. Model simulations of an acute K+ load indicate that elevated expression levels and activities of Na+/K+-ATPase, epithelial sodium channels, large-conductance Ca2+-activated K+ channels, and renal outer medullary K+ channels, together with downregulation of sodium-chloride cotransporters (NCC), increase K+ secretion along the connecting tubule, resulting in a >6-fold increase in urinary K+ excretion in sham rats, which substantially exceeds the filtered K+ load. In the UNX and 5/6-NX models, the acute K+ load is predicted to increase K+ excretion, but at significantly reduced levels compared with sham. Acute K+ load is accompanied by natriuresis in sham rats. Model simulations suggest that the lesser natriuretic effect observed in the nephrectomized groups may be explained by impaired NCC downregulation in these kidneys. At a single-nephron level, a high K+ intake raises K+ secretion along the connecting tubule and reabsorption along the collecting duct in sham, and even more in UNX and 5/6-NX. However, the increased K+ secretion per tubule fails to sufficiently compensate for the reduction in nephron number, such that nephrectomized rats have an impaired ability to excrete an acute or chronic K+ load.

Changes in erythrocyte ATPase activity under different pathological conditions.

Studies have shown that Na+-K+ ATPase activity was altered in disrupted red blood cell membranes and this enzyme is believed to be the site of active transport of Na+ and K+ in intact red blood cells. The enzyme is often referred to as Na+-K+ pump because it pumps Na+ out and K+ into the cell against gradients with the concomitant hydrolysis of intracellular ATP. The aim of this study was to find out the possibility of using Na+-K+-ATPase activity as a biomarker for the diagnosis of individuals with different physiological conditions. The activity of Na+-K+ ATPase was determined in blood samples collected from different pathological and physiological conditions such as pregnancy, smoking, diabetes and renal dysfunction compared with healthy subjects matched for age and sex. The Na+-K+ ATPase activity in pregnancy (0.094 ± 0.0051 µM Pi/min. mg protein), smoking (0.064 ± 0.0011 µM), diabetes (0.047 µM 0.002 µM) and kidney disease (0.069 ± 0.0014 µM) was higher compared to the measurements in healthy individuals (0.0081 ± 0.0031 µM). Na+-K+ATPase specific activity is a biomarker for the diagnosis of individuals with different physiological diseases.

Thermodynamic Analysis of Secondary Minerals Stability in Altered Carbonatites of the Oldoinyo Lengai Volcano, Northern Tanzania

Carbonatites from the Oldoinyo Lengai volcano, northern Tanzania, are unstable under normal atmospheric conditions. Owing to carbonatite interaction with water, the major minerals—gregoryite Na2(CO3), nyerereite Na2Ca(CO3)2, and sylvite KCl—are dissolved and replaced with secondary low-temperature minerals: thermonatrite Na2(CO3) · H2O, trona Na3(CO3)(HCO3) · 2H2O, nahcolite Na(HCO3), pirssonite Na2Ca(CO3)2 · 2H2O, calcite Ca(CO3), and shortite Na2Ca2(CO3)3. Thermodynamic calculations show that the formation of secondary minerals in Oldoinyo Lengai carbonatites are controlled by the pH of the pore solution, H2O and CO2 fugacity, and the ratio of Ca and Na activity in the Na2O–CaO–CO2–H2O system.

The developmental effects of low-level procymidone towards zebrafish embryos and involved mechanism

Procymidone (PCM), a dicarboximide fungicide, is widely used in agriculture to control plant diseases. In the present study, zebrafish embryos were exposed to PCM at 0, 10, 100 and 1000 ng/L for 72 h, the development and cardiac functioning of larvae were observed and determined. The results showed that hatching rate was significantly decreased in the 1000 ng/L treatment, and pericardial edema rate and spine curvature rate were significantly increased in the 100 and 1000 ng/L groups. The PCM-treated larvae exhibited an increased heart rate as well as arrhythmia, and shortened low jaw. The transcription levels of cardiac development-related genes tbx5, nkx2.5, tnnt2, gata4, myh6, myl7, cdh2, ryr2 were altered, which might be responsible for the cardiac developmental and functioning defects in the larvae. The deformation in bone development might be related with the impaired transcription levels of ihh, shh, bmp2b, bmp4, gh, igf1, sox9, gli2. The activities of Na+/K+-ATPase and Ca2+-ATPase were significantly inhibited by 100 ng/L and 1000 ng/L PCM exposure, which might be a cause for the occurrence of pericardial edema and skeletal deformation. The results of this study will be helpful in evaluating the potential threat of PCM to fish population in the aquatic environment.

Effects of dietary tryptophan levels on performance and biochemical variables of plasma and intestinal mucosa in yellow-feathered broiler breeders.

The effects of dietary tryptophan (Trp) levels on performance and biochemical variables of plasma and intestinal mucosa in broiler breeder hens were investigated in this study. A total of 780 Lingnan yellow-feathered broiler breeder hens were randomly assigned in one of five dietary treatments with six replicates per treatment (26 birds per replicate). The breeder hens were fed either the basal diet (0.11% Trp) or the basal diet supplemented to 0.15%, 0.19%, 0.23% and 0.27% Trp, from 197 to 259days of age. Graded levels of Trp from 0.11% to 0.27% in the diet produced quadratic (p<.05) responses in laying rate, average daily egg production, and feed conversion ratio, and quadratic (p<.01) responses in total large follicle weight and average large follicle weight. An increase in fertilization rate of total eggs was observed in breeders fed 0.27% Trp, and hatchability was higher in breeders fed 0.23% and 0.27% Trp than with 0.19% Trp (p<.05). The content of uric acid N decreased with 0.15% and 0.23% dietary Trp (p<.05). The content of GSH and the GSH-to-GSSG ratio in plasma were reduced by 0.15%, 0.19% and 0.27% Trp diets (p<.05). A higher activity of GST in plasma was observed with 0.15% Trp in relation to 0.23% and 0.27% Trp (p<.05). The activity of Na+ -K+ -ATPase of plasma in birds fed 0.27% Trp was lower than in those fed 0.15% Trp and the control birds (p<.05). There were significant influences of dietary Trp levels on S6K1, B0 AT1, Nrf2, TLR4, TNF-α and IL-6 transcripts of ileal mucosa (p<.05). The optimal dietary Trp level was 0.203% or 254mg per hen per day, for Chinese yellow-feathered broiler breeder hens aged from 197 to 259days.

Vasoconstriction triggered by hydrogen sulfide: Evidence for Na+,K+,2Cl-cotransport and L-type Ca2+ channel-mediated pathway

ObjectivesThis study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC). MethodsIsometric contraction was measured in ring aortas segments from male Wistar rats. Activity of Na+/K+-pump and Na+,K+,2Cl-cotransport was measured in cultured endothelial and smooth muscle cells from the rat aorta as ouabain-sensitive and ouabain-resistant, bumetanide-sensitive components of the 86Rb influx, respectively. ResultsNaHS exhibited the bimodal action on contractions triggered by modest depolarization ([K+]o=30mM). At 10−4 M, NaHS augmented contractions of intact and endothelium-denuded strips by ~ 15% and 25%, respectively, whereas at concentration of 10−3M it decreased contractile responses by more than two-fold. Contractions evoked by 10−4M NaHS were completely abolished by bumetanide, a potent inhibitor of Na+,K+,2Cl-cotransport, whereas the inhibition seen at 10−3M NaHS was suppressed in the presence of K+ channel blocker TEA. In cultured SMC, 5×10−5M NaHS increased Na+,K+,2Cl- - cotransport without any effect on the activity of this carrier in endothelial cells. In depolarized SMC, 45Ca influx was enhanced in the presence of 10−4M NaHS and suppressed under elevation of [NaHS] up to 10−3M. 45Ca influx triggered by 10−4M NaHS was abolished by bumetanide and L-type Ca2+ channel blocker nicardipine. ConclusionsOur results strongly suggest that contractions of rat aortic rings triggered by low doses of NaHS are mediated by activation of Na+,K+,2Cl-cotransport and Ca2+ influx via L-type channels.

S-Adenosylmethionine Promotes Oxidative Stress and Decreases Na+, K+-ATPase Activity in Cerebral Cortex Supernatants of Adolescent Rats: Implications for the Pathogenesis of S-Adenosylhomocysteine Hydrolase Deficiency.

S-Adenosylmethionine (AdoMet) concentrations are highly elevated in tissues and biological fluids of patients affected by S-adenosylhomocysteine hydrolase deficiency, who are clinically characterized by cerebral symptoms whose pathogenesis is still unknown. In the present work, we investigated the effects of AdoMet on redox homeostasis and on the activity of Na+, K+-ATPase in the cerebral cortex of young rats. AdoMet caused lipid peroxidation (increase of malondialdehyde concentrations) and protein oxidation (increase of carbonyl formation and decrease of sulfhydryl content). AdoMet also reduced the antioxidant defenses (reduced glutathione, GSH) and Na+, K+-ATPase activity. Furthermore, AdoMet-induced lipid peroxidation was fully prevented by the antioxidants trolox, melatonin, and resveratrol, and the decrease of GSH concentrations was abolished by trolox, suggesting the involvement of reactive oxygen species in these effects. In this context, AdoMet induced reactive oxygen (increase of 2',7'-dichloroflurescein-DCFH oxidation) but not nitrogen (nitrate and nitrite levels) species generation. Finally, the decrease of Na+, K+-ATPase activity provoked by AdoMet was totally prevented by trolox, implying a possible oxidation of cysteine groups of the enzyme that are critical for its function and highly susceptible to oxidative attack. It is also noted that adenosine and methionine did not alter the parameters evaluated, suggesting selective effects of AdoMet. Our data strongly indicate that disturbance of redox homeostasis caused by a major metabolite (AdoMet) accumulating in S-adenosylhomocysteine hydrolase deficiency may represent a deleterious mechanism of brain damage in this disease. Finally, reduction of Na+, K+-ATPase activity provoked by AdoMet may lead to impaired neurotransmission, but disturbance of this system should be better clarified in future studies.

Effect of hydrogen peroxide on Na+,K+-ATPase activity in spermatozoa of infertile men

Na+,K+-ATPase plays an essential role in sperm motility, hyperactivation, chemotaxis, acrosome reaction etc. Na+,K+-ATPase is sensitive to ROS insult. Apart from production of highly reactive molecules, H2O2 can exert a number of direct effects on cells, their metabolism and enzymes. In the present study, exposure to exogenous H2O2 was used to characterize the effects of H2O2 on Na+,K+-ATPase activity in spermatozoa of infertile men with different forms of pathospermia. It was shown that Na+,K+-ATPase activities in spermatozoa of infertile men with different forms of pathospermia were inhibited by exposure to H2O2 (50−500 μM). H2O2, one of the most toxic oxygen species, has the ability to depress Na+,K+-ATPase activity in a dose-dependent manner. Severe inhibition of the hydrolytic activity was observed when higher H2O2 were used. The time course of incubation with 100 μM H2O2 showed a sharp decrease in the enzyme activity during the first 5 min of incubation for both normozoospermic and pathozoospermic men. The enzymatic activity of Na+,K+-ATPase in the sperm was completely destroyed at 20 min for asthenozoospermic men and 30 min for normozoospermic men. We show that an administation of H2O2 inhibited Na+,K+-ATPase activity in normozoospermic samples with IC50 of 106.6 ± 7.9 μM. IC50 for patients with asthenozoospermia was two times less than for healthy men with preserved fertility. For other studied groups, the differences in IC50 were not significant. These observations suggest that Na+,K+-ATPase in pathozoospermic samples is more vulnerable to H2O2-induced damage than in normozoospermic men. The Hill coefficient was significantly increased only for patients with asthenozoospermia, indicating increased positively cooperative binding. The decreases in Na+,K+-ATPase hydrolase activity in H2O2-treated sperm cells in men with normozoospermia were largely attenuated by exogenous GSH at 5 mM. This suggests that GSH partially protects the Na+,K+-ATPase from inhibition under experimental oxidative stress. However, treatment of oligo-, astheno- and oligoasthenozoospermic samples with 100 μM H2O2 and 5 mM GSH did not result in protection of Na+,K+-ATPase against induced oxidation, suggesting that the impaired Na+,K+-ATPase in pathozoospermic samples appears to be an irreversible event. In contrast, presence of GSH only after H2O2 treatment does not reverse Na+,K+-ATPase inhibition. This study has provided a deeper insight into the role Na+,K+-ATPase plays in sperm cells,it also could offer clues to the clinical application of antioxidant therapy in male infertility therapy.

Activity of Na+/K+-ATPase and the content of phospholipids in the blue mussel Mytilus edulis L. during environmental temperature changes

Changes in the activity of Na+/K+-ATPase and content of membrane lipids (phospholipids) in the gills and hepatopancreas of the blue mussel Mytilus edulis L. have been studied during a sharp temperature increase under aquarian managed conditions. The most pronounced changes were recorded in mollusk gills. A correlation of changes in the activity of membrane-bound Na+/K+-ATPase and phospholipid content (mainly phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, and lysophosphatidylcholine) was revealed; this correlation evidences their mutual involvement in compensation for the temperature effect to help mussels adapt to sharp temperature changes.