Amino acid efflux and cell volume regulation in cerebrocortical minislices prepared from chronically hyponatraemic and hypernatraemic rats

The rates of efflux of pre-loaded amino acids, and associated steady-state volumes, were measured in cells in cerebrocortical minislices prepared from chronically (4 day) hypo- and hypernatraemic rats. The findings were compared with those obtained when cells from normonatraemic rats were acutely exposed to comparable levels of anisosmotic stress. In the presence of 122 mmol/l Na⁺ cells from normal rats showed increases in the rates of efflux of -aspartate and GABA, and significant swelling (both by comparison with levels in media containing 142 mmol/l Na⁺). Conversely there was no acceleration of efflux in cells from hyponatraemic rats (plasma Na⁺=119–126 mmol/l) and volumes were preserved at levels comparable with those in isomotically incubated cells from normal rats. In media containing 164 mmol/l Na⁺ amino acid efflux in cells from normal rats was retarded, and shrinkage occurred. In cells from chronically hypernatraemic rats (plasma Na⁺=160–166 mmol/l) the rates of efflux of -aspartate and -glutamate were accelerated by comparison with cells from normal rats, with volume preservation. However there was no increase in the rate of GABA or glycine efflux, and cell swelling was observed. It is concluded (i) that during chronic hyponatraemia the presence of -aspartate or GABA is associated with cell volume preservation, (ii) during chronic hypernatraemia acidic, but not neutral, amino acids are also effective in this respect, and (iii) that the markedly differing patterns of efflux responses to acute and chronic anisosmotic stress are likely to reflect chronic volume-regulatory adaptations of the efflux mechanism(s).     

Effect of chronic hypernatremic dehydration and rapid rehydration on brain carbohydrate, energy, and amino acid metabolism in weanling mice

Abstract: This is a study of the effects of chronic hypernatremic dehydration and rehydration on carbohydrate, energy, and amino acid metabolism in the brains of weanling mice. Chronic hypernatremic dehydration induced by 4 days of water deprivation and salt loading was associated with severe weight loss (no other observed clinical effects), increased brain Na⁺ levels, and a decreased brain water content. Changes in the concentrations of brain glucose, glycolytic and citric acid cycle metabolic intermediates, and phosphocreatine were compatible with reduced cerebral metabolic rate. In adaptation to chronic hypernatremia, there was a significant increase in the content of the measured brain amino acids. Rapid rehydration over a 4-h period with 2.5% dextrose in water returned plasma Na⁺ levels and brain Na⁺ and water contents to normal. After rehydration, metabolites were altered in a manner consistent with increased fluxes through the glycolytic pathway and citric acid cycle; the brain glycogen content almost tripled. Brain taurine and glutamine levels were not lowered by rehydration, and the total content of the measured amino acids in brain was still significantly higher than in controls. We speculate that these metabolic perturbations may relate to the development of cerebral edema and seizures or coma following rapid rehydration of humans with chronic hypernatremic dehydration.     

Physiological responses to salt stress in young umbu plants

Soil salinity affects plant growth and development due to harmful ion effects and water stress caused by reduced osmotic potential in the soil solution. In order to evaluate the effects of salt stress in young umbu plants, research was performed in green house conditions at the Laboratory of Plant Physiology at Federal Rural University of Pernambuco, Brazil. Growth, stomatal behaviour, water relations, and both inorganic and organic solutes were studied aiming for a better understanding of the responses of umbu plants to increasing salinity. Plants were grown in washed sand with Hoagland and Arnon nutrient solution with 0, 25, 50, 75, and 100 mM NaCl. Growth, leaf water potential, transpiration, and diffusive resistance were evaluated. Na⁺, K⁺, Cl⁻, soluble carbohydrates, and free amino acid contents were measured in several plant organs. Most variables were affected with salinity above 50 mM NaCl showing decreases in: number of leaves, plant height, stems diameter, and dry masses, and increases in root-to-shoot ratio. Reductions in ψ_pd were observed in plants grown under 75 and 100 mM NaCl. All salt levels above zero increased Na⁺ and Cl⁻ contents in leaves. However, K⁺ content was not affected. Na⁺ and Cl⁻ in stems and roots reached saturation in treatments above 50 mM NaCl. Organic solute accumulation in response to salt stress was not observed in umbu plants. These results suggest that umbu plants tolerate salt levels up to 50 mM NaCl without showing significant physio-morphological alterations.     

Peroxvnitrite Causes Aspartate Release from Dissociated Rat Cerebeliar Granule Neurones

Peroxynitrite (ONOO^-) is a powerful oxidant which is formed from the reaction between nitric oxide (NO) and superoxide anion. It has therefore been proposed to mediate the toxic actions caused by NO. Since ONOO^- may be formed in the central nervous system (CNS) in pathological conditions such as brain ischaemia, we decided to investigate whether this molecule induces the release of the endogenous excitatory amino acids glutamate and aspartate from neurones. We selected as biological model acutely dissociated rat cerebellar granule neurones in suspension to allow a direct interaction between ONOO^- and target cells. Peroxynitrite caused a concentration-dependent release of aspartate but not of glutamate from dissociated cerebellar granule neurones. Peroxyni-triteinduced aspartate release was inhibited by dithiothreitol, tetrodotoxin, and in Na⁺-deprived solutions and not affected by EGTA or pre-incubation with the cytosolic Ca²⁺ chelator BAPTA/ AM. Peroxynitrite also induced an increase in intracellular Ca²⁺ concentration which was not affected in the presence of EGTA. These data show that ONOO^- causes release of aspartate from cerebellar granule neurones and that this effect might arise from an alteration of Na⁺ membrane permeability leading subsequently to reversal of a Na⁺-dependent plasma membrane transporter of this excitatory amino acid. In addition, ONOO^- alters Ca²⁺ homeostasis likely due to Na⁺ overload. Taken together, these findings may help and elucidate some of the intimate mechanisms of NO-induced neuronal damage in pathological circumstances.     

咸水浇灌后持续干旱条件下棉花生长及光合作用的变化

用咸水(不同浓度的NaCl溶液)浇灌盆栽棉花植株,随后进行持续干旱处理.测定干旱处理期间棉花的生长情况、光合速率、叶绿素荧光等参数的变化,并对植株的相对含水量、水势、渗透势等水分状况和Na⁺、K⁺含量进行分析,探索环境Na⁺在棉花适应干旱胁迫中的作用.结果表明: 干旱可以明显抑制植株的生长,降低叶片的净光合速率;用25～100 mmol·L^-1NaCl溶液浇灌后进行持续干旱处理的棉花植株,其株高、生物量、净光合速率和F_v/F_m值均明显高于用水浇灌后进行持续干旱处理的植株.同时,前者的土壤和叶片相对含水量、细胞膨压、Na⁺含量也明显高于后者,但植株水势和组织渗透势则显著低于后者,且组织渗透势的降低与Na⁺含量具有显著相关性.上述结果说明,土壤适量Na⁺的存在能够提高土壤和植株的保水力、增加棉花对Na⁺的吸收和积累、降低组织渗透势,从而增强植株吸水力、保持较高的细胞膨压,维持相对较高的光合速率和生长速度.土壤中存在一定浓度的NaCl可以有效缓解干旱对棉花的不利影响.     

Glycinebetaine-induced modulation of antioxidant enzymes activities and ion accumulation in two wheat cultivars differing in salt tolerance

Modulation of water relations, activities of antioxidant enzymes and ion accumulation was assessed in the plants of two wheat cultivars S-24 (salt tolerant) and MH-97 (moderately salt sensitive) subjected to saline conditions and glycinebetaine (GB) applied foliarly. Different levels of GB, i.e., 0 (unsprayed), 50 and 100 mM (in 0.10% Tween-20 solution) were applied to the wheat plants at the vegetative growth stage. Leaf water potential, leaf osmotic potential and turgor potential were decreased due to salt stress. Salt stress increased the Na⁺ and Cl⁻ accumulation coupled with a decrease in K⁺ and Ca²⁺ in the leaves and roots of both cultivars thereby decreasing tissue K⁺/Na⁺ and Ca²⁺/Na⁺ ratios. Furthermore, salt stress decreased the activities of superoxide dismutase (SOD), whereas it increased the activities of catalase (CAT) and peroxidase (POD) in both wheat cultivars. However, accumulation of GB in the leaves of both wheat cultivars was consistently increased with an increase in concentration of exogenous GB application under both non-saline and saline conditions. Accumulation of Na⁺ was decreased with an increase in K⁺ accumulation upon a consistent increase in GB accumulation under salt stress conditions thereby resulting in better K⁺/Na⁺ and Ca²⁺/Na⁺ ratios in the leaves and roots. High accumulation of GB and K⁺ mainly contributed to osmotic adjustment, which is one of the factors known to be responsible for improving growth and yield under salt stress. The activities of all antioxidant enzymes, SOD, CAT and POD were enhanced by GB application in cv. MH-97 under saline conditions, whereas all these except SOD were reduced in cv. S-24. It is likely that both applied GB and intrinsic SOD scavenged ROS in the tolerant cultivar thereby resulting into low activities of CAT and POD enzymes under salt stress. In conclusion, the adverse effects of salt stress on wheat can be alleviated by the exogenous application of 100 mM GB by modulating activities of antioxidant enzymes and changes in water relations and ion homeostasis. Furthermore, effectiveness of GB application on regulation of activities of antioxidant enzymes was found to be cultivar-specific.     

盐胁迫下外源褪黑素和Ca2+对甜瓜幼苗的缓解效应

以甜瓜品种‘羊角酥瓜’为试材,利用人工气候室控制环境条件(昼/夜25/18 ℃),研究盐胁迫条件下外源褪黑素(MT)和Ca²⁺对甜瓜幼苗根系和叶片中Cl^-、Na⁺、K⁺、Mg²⁺、Ca²⁺离子含量,Na⁺/K⁺、 Na⁺/Ca²⁺、Na⁺/Mg²⁺值,以及H⁺-ATP酶活性、渗透调节物质积累和细胞膜质过氧化的影响.结果表明: 与对照相比,盐胁迫处理显著抑制甜瓜幼苗生长,增加根系和叶片中Cl^-、Na⁺含量,降低K⁺、Mg²⁺、Ca²⁺含量.盐胁迫下,喷施外源MT或Ca²⁺处理均可以显著降低甜瓜根系和叶片中Cl^-、Na⁺含量,提高K⁺、Mg²⁺、Ca²⁺含量,植株体内Na⁺/K⁺、Na⁺/Ca²⁺和 Na⁺/Mg²⁺值下降;同时也提高了根系和叶片H⁺-ATP酶活性及叶片渗透调节物质的含量,降低盐胁迫对细胞膜的伤害,表现在甜瓜叶片相对电导率和丙二醛含量降低.总之,在盐胁迫条件下,外源MT、Ca²⁺单独和复配处理均可通过提高H⁺-ATP酶活性来降低盐害离子的含量,改善甜瓜幼苗中的离子平衡,同时增加渗透调节物质的含量,降低膜质过氧化水平,从而增强其对盐胁迫的适应性,其中MT和Ca²⁺复配处理时的效果更好.复配外施 MT 和Ca²⁺在诱导甜瓜幼苗提高耐盐方面具有协同增效作用.     

盐胁迫下外源褪黑素和Ca2+对甜瓜幼苗的缓解效应

以甜瓜品种‘羊角酥瓜’为试材,利用人工气候室控制环境条件(昼/夜25/18 ℃),研究盐胁迫条件下外源褪黑素(MT)和Ca²⁺对甜瓜幼苗根系和叶片中Cl^-、Na⁺、K⁺、Mg²⁺、Ca²⁺离子含量,Na⁺/K⁺、 Na⁺/Ca²⁺、Na⁺/Mg²⁺值,以及H⁺-ATP酶活性、渗透调节物质积累和细胞膜质过氧化的影响.结果表明: 与对照相比,盐胁迫处理显著抑制甜瓜幼苗生长,增加根系和叶片中Cl^-、Na⁺含量,降低K⁺、Mg²⁺、Ca²⁺含量.盐胁迫下,喷施外源MT或Ca²⁺处理均可以显著降低甜瓜根系和叶片中Cl^-、Na⁺含量,提高K⁺、Mg²⁺、Ca²⁺含量,植株体内Na⁺/K⁺、Na⁺/Ca²⁺和 Na⁺/Mg²⁺值下降;同时也提高了根系和叶片H⁺-ATP酶活性及叶片渗透调节物质的含量,降低盐胁迫对细胞膜的伤害,表现在甜瓜叶片相对电导率和丙二醛含量降低.总之,在盐胁迫条件下,外源MT、Ca²⁺单独和复配处理均可通过提高H⁺-ATP酶活性来降低盐害离子的含量,改善甜瓜幼苗中的离子平衡,同时增加渗透调节物质的含量,降低膜质过氧化水平,从而增强其对盐胁迫的适应性,其中MT和Ca²⁺复配处理时的效果更好.复配外施 MT 和Ca²⁺在诱导甜瓜幼苗提高耐盐方面具有协同增效作用.     

Seagrass-salinity interactions: Physiological mechanisms used by submersed marine angiosperms for a life at sea

Due to the nature of coastal and estuarine systems, seagrasses must be able to tolerate short-term salinity fluctuations including both hyposaline and hypersaline conditions. Salt tolerance can be achieved, in part, through vacuolar ion sequestering (mostly Na⁺, K⁺, and Cl⁻) and cytosolic osmolyte accumulation (K⁺ and organic osmolytes), with differences in cellular ion levels attributed to selective ion flux and ion partitioning between the cytoplasm and vacuole (with lower cytoplasmic-to-vacuolar ratios favoring higher cellular Na⁺ concentrations). The hydrophilic nature of organic compounds such as organic acids, soluble carbohydrates, and free amino acids allow them to serve as osmoprotectants and low-molecular-weight chaperones which diminishes the inhibitory effects of potentially harmful ions on metabolic processes. Nevertheless, some carbohydrate studies on seagrasses have shown decreased soluble sugar content with increased salinities. During salt stress, carbohydrates are likely converted to other organic compounds that would better facilitate osmotic adjustment in these plants. This is further supported by observed decreases in sucrose-P synthase (a key enzyme involved in sucrose synthesis) activities in seagrass exposed to higher salinities. While modifications in ion flux and organic solute levels often follow changes in environmental salinities, these adjustments are relatively slow (hours to days). Therefore, the initial response to sudden salinity change will include rapid alterations in turgor pressure driven by water flux in the direction of the osmotic gradient. The rate of water movement depends largely on the hydraulic conductivity of the plasmalemma and the elastic properties of the cell wall (bulk elastic modulus; Є). Observations on cell wall elasticity indicate that some seagrasses maintain fairly rigid walls (high Є values), thereby limiting the amount of water influx during hypoosmotic stress. Although high Є would be beneficial to open-water coastal plants living in relatively stable saline environments, in estuaries where salinities fluctuate considerably over shorter intervals, high Є could promote flaccid cells with no turgor pressure during hyperosmotic conditions. Hypo- and hyperosmotic conditions also inhibit photosynthesis in seagrasses. Decreases in photosynthesis have been attributed to declines in chlorophyll content, changes in chloroplast ultrastructure, disruptions of electron flow through photosystems, and inhibitions of key photosynthetic enzymes. The uptake of nutrients can also be strongly influenced by salinity. High affinity Na⁺-dependent nutrient transport systems (for NO₃⁻, H₂PO₄⁻, and HPO₄⁻²) which benefit from the inwardly driving force for Na⁺ have been observed in seagrasses. Nitrate reductase, the key enzyme involved in nitrate reduction/ assimilation, also has elevated activities at higher salinities which would agree with Na⁺-dependent NO₃⁻ transport. While our basic understanding of how seagrasses survive in saline environments is increasing, it still lags well behind marine algae and terrestrial halophytes. It is likely that further investigations will reveal unique physiological adaptations that have not been observed in other plants.     

疏叶骆驼刺适应盐渍生境的离子分布、吸收和运输特征

以塔里木盆地南缘关键物种疏叶骆驼刺为材料,研究了不同盐渍土壤生境(轻度盐渍土、中度盐渍土、重度盐渍土)下其器官间Na⁺、K⁺、Ca²⁺、Mg²⁺的分布、吸收及运输特征,以探讨疏叶骆驼刺对自然盐渍生境的适应特性.结果表明: 在轻度和中度盐渍土生境,Na⁺在各器官中的分布规律为茎≈刺>叶>根,而在重度盐渍土生境,Na⁺分布规律为叶>茎≈刺>根;Ca²⁺和Mg²⁺在疏叶骆驼刺体内的分布规律为叶>刺>茎>根.随着土壤含盐量的增加,疏叶骆驼刺体内各器官Na⁺含量都增大,而叶片中K⁺含量呈下降趋势;根和叶器官中K⁺/Na⁺值明显降低,各器官中Ca²⁺/Na⁺、Mg²⁺/Na⁺值都降低.盐渍生境下,疏叶骆驼刺体内Ca²⁺选择性运输系数和Mg²⁺选择性运输系数均为茎-叶>茎-刺>根-茎.疏叶骆驼刺为适应盐渍生境,在土壤含盐量较低时,将Na⁺聚集于茎和刺;而在土壤含盐量较高时,则将Na⁺聚集于叶片.此外,Ca²⁺和Mg²⁺可能是疏叶骆驼适应盐渍生境的无机渗透调节物质.     

Studies on the relationship between osmotic or ionic regulation and thyroid gland activity in two salmonid fishes, Salmo gairdneri Richardson and Oncorhynchus kisutch Walbaum

In freshwater-acclimated rainbow trout a single intraperitoneal injection of ovine TSH significantly elevated plasma thyroxine (T₄) levels within 1 h after the injection. In seawater adapted trout the increase in T₄ after TSH-treatment was not evident until 6 h after the injection. TSH caused a transient fall in plasma Na⁺ and Cl^- between 3 h and 9 h after the injection in seawater-adapted fish and plasma Na⁺ was lowered in freshwater-adapted trout 24 h after the injection. Although there were clear histological changes in the thyroid gland of freshwater-adapted trout after TSH-injection, no such changes were evident in seawater-adapted fish.
Plasma thyroid hormone levels and thyroid histology in freshwater-adapted rainbow trout and coho salmon transferred to sea water, and seawater-adapted trout transferred to fresh water showed no consistent changes compared with controls.
The data are interpreted to indicate that although ambient salinity may have indirect effects on thyroid activity there is no direct involvement in ionic or osmotic regulation in the two species.     

Video enhanced imaging of the fluorescent Na probe SBFI indicates that colonic crypts absorb fluid by generating a hypertonic interstitial fluid

Extracellular accumulation of Na⁷⁺ detected by video-enhanced microscopic imaging of the impenneant fluorescent probe SBFI[1,2] confirms the view that colonic crypts produce a hypertonic absorbate ca 1000 mOsm·kg⁻¹, thereby generating a large osmotic pressure across the crypt wall. This creates a high fluid tension within the crypt lumen, sufficient to dehydrate faeces [3,4]. When bathed in Tyrode the SBFI·Na⁺ fluorescence indicates a [Na⁺) ca 750 mM within the interstitial space of metabolizing rat descending colon. There is no evidence of interstitial Na⁺ accumulation in octanol (2 mM) or in rabbit colon incubated with 1.0 mM ouabain and no evidence of Na⁺ secretion via the crypt lumen during absorption [5].     

Inhibitors of Na+/Ca2+ exchanger prevent oxidant-induced intracellular Ca2+ increase and apoptosis in a human hepatoma cell line

Oxidative stress appears to be implicated in the pathogenesis of various diseases including hepatotoxicity. Although intracellular Ca²⁺ signals have been suggested to play a role in the oxidative damage of hepatocytes, the sources and effects of oxidant-induced intracellular Ca²⁺ increases are currently debatable. Thus, in this study we investigated the exact source and mechanism of oxidant-induced liver cell damage using HepG2 human hepatoma cells as a model liver cellular system. Treatment with 200 μM of tert-butyl hydroperoxide (tBOOH) induced a sustained increase in the level of intracellular reactive oxygen intermediates (ROI) and apoptosis, assessed by 2',7'-dichlorofluorescein fluorescence and flow cytometry, respectively. Antioxidants, N-acetyl cysteine (NAC) or N,N'-diphenyl-p-phenylenediamine significantly inhibited both the ROI generation and apoptosis. In addition, tBOOH induced a slow and sustained increase in intracellular Ca²⁺ concentration, which was completely prevented by the antioxidants. An intracellular Ca²⁺ chelator, bis-(o-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid/cetoxymethyl ester significantly suppressed the tBOOH-induced apoptosis. These results imply that activation of an intracellular Ca²⁺ signal triggered by increased ROI may mediate the tBOOH-induced apoptosis. Both intracellular Ca²⁺ increase and induction of apoptosis were significantly inhibited by an extracellular Ca²⁺ chelator or Na⁺/Ca²⁺ exchanger blockers (bepridil and benzamil), whereas neither Ca²⁺ channel antagonists (verapamil and nifedipine) nor a nonselective cation channel blocker (flufenamic acid) had an effect. These results suggest that tBOOH may increase intracellular Ca²⁺ through the activation of reverse mode of Na⁺/Ca²⁺ exchanger. However, tBOOH decreased intracellular Na⁺ concentration, which was completely prevented by NAC. These results indicate that ROI generated by tBOOH may increase intracellular Ca²⁺ concentration by direct activation of the reverse mode of Na⁺/Ca>²⁺ exchanger, rather than indirect elevation of intracellular Na⁺ levels. Taken together, these results suggest that the oxidant, tBOOH induced apoptosis in human HepG2 cells and that intracellular Ca²⁺ may mediate this action of tBOOH. These results further suggest that Na⁺/Ca²⁺ exchanger may be a target for the management of oxidative hepatotoxicity.     

植物HKT蛋白耐盐机制研究进展

盐害是限制植物生长发育的重要环境因素, 对植物造成渗透胁迫和离子毒害。维持细胞及整株水平的Na⁺/K⁺平衡是植物重要的耐盐机制。目前, 已报道的高亲和性钾离子转运蛋白(HKT)具有钠、钾离子转运特性, 在植物体钠、钾离子长距离运输及分配过程中发挥重要作用。该文重点总结了淡土植物和盐土植物HKT蛋白的结构、功能及耐盐机理, 并对其在植物耐盐改良育种中的前景做出了展望。     

Ins(1,4,5)P3 induces Ca2+ release from brain microsomes loaded either by the Ca2+ ATPase or by the Na+/Ca2+ exchanger.

In this study we investigated the release of Ca²⁺ in brain microsomes after Ca²⁺ loading by the Ca²⁺-ATPase or by the Na⁺/Ca²⁺ exchanger. The results show that in microsomes loaded with Ca²⁺ by the Ca²⁺-ATPase, Ins(1,4,5)P₃ (5 μM) release 21±2% of the total Ca²⁺ accumulated, and that in the microsomes loaded with Ca²⁺ by the Na²⁺/Ca²⁺ exchanger, Ins(1,4,5)P₃ released 28±3% of the total Ca²⁺ accumulated. These results suggest that receptors of Ins(1,4,5)P₃ may be co-localized with the Na²⁺/Ca²⁺ exchanger in the endoplasmic reticulum membrane or that there are Ins(1,4,5)P₃ receptors in the plasma membrane where the Na²⁺/Ca²⁺ exchanger is normally present, or both. We also found that Ins(1,4,5)P₃ inhibited the Ca²⁺-ATPase by 33.7%, but that it had no significant effect on the Na²⁺/Ca²⁺ exchanger.     

Changes in water relation parameters under osmotic and salt stresses in maize and sorghum

A relatively drought tolerant cultivar of maize ( Zea mays L. cv. Pioneer 3950) and a drought tolerant line of sorghum ( Sorghum bicolor [L.] Moench cv. ICSV 112) were grown hydroponically for 11 days. Treatments for non-ionic osmotic and salt stresses were started at the 8th day by addition of polyethylene glycol 6000 and NaCl, respectively, at 200 mOsm equivalent concentrations in the presence or absence of 0. 1 μ M abscisic acid. Relative growth rate was depressed by both stress factors, more severely for maize than sorghum. Abscisic acid increased the growth rate and reverted the negative effect of NaCl in maize, while sorghum was only slightly affected. In general, sorghum had higher levels of K⁺ and lower levels of Na⁺ and the K⁺/Na⁺ ratio was further increased by abscisic acid treatment. From the pressure-volume curves, osmotic potential, the water potential at turgor loss point, bulk elastic modulus and the water saturation deficit at initial turgor loss were estimated. Most significantly, sorghum had a higher elastic modulus than maize and it decreased under osmotic treatment, while in maize it increased under NaCl stress. The results suggest that bulk tissue turgor was not limiting growth under these conditions and underscores the possible implications of changes in the elastic condition of the cell walls in stress responses.     

Ion transport in heart mitochondria. XIII. The effect of ethylenediaminetetraacetate on monovalent ion uptake

1. Ethylenediaminetetraacetate (EDTA) markedly activates the accumulation of Na⁺ and Li⁺ and the swelling which accompanies the ion uptake by isolated heart mitochondria. This activation is reflected in the removal of limited amounts of endogenous Mg²⁺ and extensive loss of K⁺. The removal of these cations requires the presence of Na⁺, a source of energy, and a permeant anion as well as EDTA. The effects of EDTA on the activation of Na⁺ uptake and cation removal are duplicated by chelators with a high affinity for Mg²⁺, but not by ethyleneglycol-bis-(β-aminoethylether)-N, N′-tetraacetic acid. Mg²⁺ at concentrations 5 to 6 times less than EDTA prevents both activation of Na⁺ uptake and cation removal.

2. EDTA does not appear to be bound by heart mitochondria. At neutral pH the chelator penetrates into the mitochondrial water volume to the same extent as sucrose and mannitol. At pH 8.1 where the removal of mitochondrial Mg²⁺ by EDTA is more effective, EDTA penetrates virtually the entire water volume. This penetration requires the presence of a source of energy, a transported cation such as Na⁺, and a permeant anion. It appears possible that the oscillations in ion uptake and swelling observed in the presence of EDTA at pH 8.1 may be related to the presence of the chelator in the interior compartment under these conditions.     

NaK ATPase activity in the rat hippocampus: A study in the pilocarpine model of epilepsy

Biochemical abnormalities have been implicated in possible mechanisms underlying the epileptic phenomena. Some of these alterations include changes in the activity of several enzymes present in epileptic tissues. Systemic administration of pilocarpine in rats induces electrographic and behavioral limbic seizures and status epilepticus, that is followed by a transient seizure-free period (silent period). Finally a chronic phase ensues, characterized by spontaneous and recurrent seizures (chronic period), that last for the rest of the animal's life. The present work aimed to study the activity of the enzyme Na⁺ K⁺ ATPase, in rat hippocampus, during the three phases of this epilepsy model. The enzyme activity was determined at different time points from pilocarpine administration (1 and 24 h of status epilepticus, during the silent and chronic period) using a spectrophotometric assay previously described by Mishra and Delivoria-Papadopoulos [Neurochem. Res. (1988) 13, 765–770]. The results showed decreased enzyme activities during the acute and silent periods and increased Na⁺K⁺ ATPase activity during the chronic phase. These data show that changes in Na⁺K⁺ ATPase activity could be involved in the appearance of spontaneous and recurrent seizures following brain damage induced by pilocarpine injection.     

Docosahexaenoic acid (omega-3) blocks voltage-gated sodium channel activity and migration of MDA-MB-231 human breast cancer cells

Omega − 3 polyunsaturated fatty acids have been suggested to play an important role in cancer prevention/progression, on the one hand, and in modulation of membrane ion channels on the other. We investigated whether docosahexaenoic acid would influence the in vitro migration of MDA-MB-231 human breast cancer cells. An important follow-up question was whether any effect would involve voltage-gated Na⁺ channels, shown previously to occur in human breast cancer in vitro and in vivo and to correlate with metastatic potential. Short-term (acute) and long-term (24–72 h) application of docosahexaenoic acid suppressed the activity of the channel activity in a dose-dependent manner. At the working concentrations of docosahexaenoic acid used (0.05–0.5 μM), there was no effect on proliferation. Long-term treatment with docosahexaenoic acid down-regulated mRNA and protein (total and plasma membrane) levels of neonatal Nav1.5 voltage-gated Na⁺ channel, known to be predominant in these cells. Docosahexaenoic acid suppressed migration of the MDA-MB-231 cells to the same extent as tetrodotoxin, a highly specific blocker of voltage-gated Na⁺ channels, but the two effects were not additive. It was concluded that the docosahexaenoic acid-induced suppression of cellular migration occurred primarily via down-regulation of voltage-gated Na⁺ channel (neonatal Nav1.5) mRNA and functional protein expression.     

外生菌根真菌通过调节离子平衡提高蒙古栎耐盐性

为探究盐胁迫对蒙古栎生长的影响以及外生菌根真菌(ECMF)对蒙古栎离子平衡的调节作用,对蒙古栎幼苗接种4种ECMF(铆钉菇、褐环乳牛肝菌、厚环粘盖牛肝菌和美味牛肝菌)后,以1年生非菌根化与菌根化幼苗为试验材料,进行36 d的NaCl胁迫(0、100、200、300 mmol·L^-1)处理,分析幼苗的菌根特征、生长量、叶伤害症状、叶片电解质渗透率及含水量、根茎叶离子含量的变化特征。结果表明: 4种ECMF均能与蒙古栎建立共生体系,菌根化幼苗的根系较非菌根化幼苗粗壮。盐胁迫下,蒙古栎幼苗的生长受到抑制并出现焦叶症状,其叶片质膜损伤和失水程度随盐胁迫浓度升高而加重。低盐胁迫时(100 mmol·L^-1),蒙古栎优先将Na⁺积累在根和茎中,中高浓度盐胁迫下(200～300 mmol·L^-1),根成为积累Na⁺的首要器官。ECMF通过增加根部的Na⁺水平和减少茎、叶的Na⁺积累,加强对K⁺和Ca²⁺的吸收以提高K⁺/Na⁺和Ca²⁺/Na⁺,进而调节蒙古栎的离子平衡。4种ECMF对蒙古栎盐毒害的缓解作用存在差异,铆钉菇作用效果最好,褐环乳牛肝菌次之,厚环粘盖牛肝菌和美味牛肝菌的作用相对较小。