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1.
Hyperhomocysteinemia is associated with various pathologies including cardiovascular disease, stroke, and cognitive dysfunctions. Systemic administration of homocysteine can trigger seizures in animals, and patients with homocystinuria suffer from epileptic seizures. Available data suggest that homocysteine can be harmful to human cells because of its metabolic conversion to homocysteine thiolactone, a reactive thioester. A number of reports have demonstrated a reduction of Na+/K+-ATPase activity in cerebral ischemia, epilepsy and neurodegeneration possibly associated with excitotoxic mechanisms. The aim of this study was to examine the in vivo effects of d,l-homocysteine and d,l-homocysteine thiolactone on Na+/K+- and Mg2+-ATPase activities in erythrocyte (RBC), brain cortex, hippocampus, and brain stem of adult male rats. Our results demonstrate a moderate inhibition of rat hippocampal Na+/K+-ATPase activity by d,l-homocysteine, which however expressed no effect on the activity of this enzyme in the cortex and brain stem. In contrast,d,l-homocysteine thiolactone strongly inhibited Na+/K+-ATPase activity in cortex, hippocampus and brain stem of rats. RBC Na+/K+-ATPase and Mg2+-ATPase activities were not affected by d,l-homocysteine, while d,l-homocysteine thiolactone inhibited only Na+/K+-ATPase activity. This study results show that homocysteine thiolactone significantly inhibits Na+/K+-ATPase activity in the cortex, hippocampus, and brain stem, which may contribute at least in part to the understanding of excitotoxic and convulsive properties of this substance.  相似文献   

2.
3.

Background and aims

Saline soils limit plant production worldwide through osmotic stress, specific-ion toxicities, and nutritional imbalances.

Methods

The ability of Ca2+ and K+ to alleviate toxicities of Na+ and Mg2+ was examined using 89 treatments in short-term (48 h) solution culture studies for cowpea (Vigna unguiculata (L.) Walp.) roots. Root elongation was related to ionic activities at the outer surface of the root plasma membrane.

Results

The addition of K+ was found to alleviate the toxic effects of Na+, and supplemental Ca2+ improved growth further in these partially-alleviated solutions where K+ was present. Therefore, Na+ appears to interfere with K+ metabolism, and Ca2+ reduces this interference. Interestingly, the ability of Ca2+ to improve K-alleviation of Na+ toxicity is non-specific, with Mg2+ having a similar effect. In contrast, the addition of Ca2+ to Na-toxic solutions in the absence of K+ did not improve growth, suggesting that Ca2+ does not directly reduce Na+ toxicity in these short-term studies (for example, by reducing Na+ uptake) when supplied at non-deficient levels. Finally, K+ did not alleviate Mg2+ toxicity, suggesting that Mg2+ is toxic by a different mechanism to Na+.

Conclusions

Examination of how the toxic effects of salinity are alleviated provides clues as to the underlying mechanisms by which growth is reduced.  相似文献   

4.
5.
  • 1.1. The (Na+ + K+)- and Na+-ATPases, both present in kidney microsomes of Sparus auratus L., have different activities and optimal assay conditions as, in the first of the two stocks of fish used (A), the spec. act. of the former is 51.7 μmol Pi mg prot−1 hr−1 at pH 7.5, 100 mM Na+, 10 mM K+, 17.5 mM Mg2+, 7.5 mM ATP and that of the latter is 6.5 μmol Pi mg prot−1 hr−1 at pH 6.5, 40 mM Na+, 4.0 mM Mg2+, 2.5 mM ATP.
  • 2.2. Ouabain and vanadate specifically inhibit the (Na+ + K+)-ATPase but not the Na+-ATPase that is preferentially inhibited by ethacrynic acid.
  • 3.3. While the (Na+ + K+)-ATPase is strictly specific for ATP and Na+, Na+-ATPase can be activated by various monovalent cations and, apart from ATP, hydrolyses CTP, though less efficiently.
  • 4.4. The second stock B, subjected to higher salinity than A, shows an acidic shifted Na+-ATPase optimal pH, opposed to the stability of that of the (Na+ + K+)-ATPase, a decreased (Na+ + K+)-ATPase and a strikingly depressed Na+-ATPase.
  • 5.5. The results are compared with literature data and discussed on the basis of the presumptive different roles as well as functional prevalence in various salinities of the two ATPases.
  相似文献   

6.
7.
The affinity for K+ of silkworm nerve Na+/K+-ATPase is markedly lower than that of mammalian Na+/K+-ATPase (Homareda 2010). In order to obtain clues on the molecular basis of the difference in K+ affinities, we cloned cDNAs of silkworm (Bombyx mori) nerve Na+/K+-ATPase α and β subunits, and analyzed the deduced amino acid sequences. The molecular masses of the α and β subunits were presumed to be 111.5 kDa with ten transmembrane segments and 37.7 kDa with a single transmembrane segment, respectively. The α subunit showed 75% identity and 93% homology with the pig Na+/K+-ATPase α1 subunit. On the other hand, the amino acid identity of the β subunit with mammalian counterparts was as low as 30%. Cloned α and β cDNAs were co-expressed in cultured silkworm ovary-derived cells, BM-N cells, which lack endogenous Na+/K+-ATPase. Na+/K+-ATPase expressed in the cultured cells showed a low affinity for K+ and a high affinity for Na+, characteristic of the silkworm nerve Na+/K+-ATPase. These results suggest that the β subunit is responsible for the affinity for K+ of Na+/K+-ATPase.  相似文献   

8.

Aims

The objectives of this study were to evaluate salt tolerance level of rice genotypes using the well-established screening criteria; the salt injury score, survival percentage and ratio between Na+ and K+, as well as the contents of proline and chlorophyll, and to identify the relationship between salt tolerance and physiological characters.

Methods

One hundred and six rice genotypes were grown in hydroponic solutions subjected to salt stress and evaluated for salt tolerance ability and the physiological parameters. Multivariate cluster analysis was performed based on salinity tolerance scores (ST scores; score 1 being the most tolerant, score 9 the most sensitive), survival percentage and Na+/K+ ratio.

Results

ST scores based on salt injury symptoms were negatively correlated with survival percentage and chlorophyll concentration in the stressed seedlings but positively correlated with Na+/K+ ratio and proline content. Rice genotypes were classified into five salt tolerance groups: tolerant (T), moderately tolerant (MT), moderately sensitive (MS), sensitive (S) and highly sensitive (HS). The means of ST scores were significantly different among the five tolerance groups indicating that the ST score was the most reliable index for identifying salt tolerance. The means of Na+/K+ ratio and proline content in stressed seedlings were distinctively different between the extreme T and HS groups, but the means among the intermediate groups (MT, MS and S) were not significantly different. Chlorophyll content, on the other hand, was not related to the levels of salt tolerance.

Conclusions

In addition to the commonly used Na+/K+ ratio, proline content is suggested to be another useful criterion to differentiate salt-tolerant from salt-sensitive rice. This study also identified several Thai improved and local cultivars with the level of salt tolerance and physiological characters comparable to Pokkali, the standard salt-tolerant donor and may be utilized as alternative sources of salt tolerance alleles.  相似文献   

9.

Background and aims

Salinity is an increasing problem for agricultural production worldwide. Understanding how Na+ enters plants is important if reducing Na+ influx, a key component of the regulation of Na+ accumulation in plants and improving salt tolerance of crop plants, is to be achieved. Our previous work indicated that two distinct low-affinity Na+ uptake pathways exist in the halophyte Suaeda maritima. Here, we report the external NaCl concentration at which uptake switches from pathway 1 to pathway 2 and the kinetics of the interaction between external K+ concentration and Na+ uptake and accumulation in S. maritima in order to determine the roles of K+ transporters or channels in low-affinity Na+ uptake.

Methods

Na+ influx, Na+ and K+ accumulations in S. maritima exposed to various concentrations of NaCl (0–200 mM) were analyzed in the absence and presence of the inhibitors TEA and Ba+ (5 mM TEA or 3 mM Ba2+) or KCl (0, 10 or 50 mM).

Results

Our earlier proposal was confirmed and extended that there are two distinct low-affinity Na+ uptake pathways in S. maritima: pathway 1 might be mediated by a HKT-type transporter under low salinity conditions and pathway 2 by an AKT1-type channel or a KUP/HAK/KT type transporter under high salinity conditions. The external NaCl concentration at which two distinct low-affinity Na+ uptake switches from pathway 1 to pathway 2, the ‘turning point’, is between 90 and 95 mM. Over a short period (12 h) of Na+ and K+ treatments, a low concentration of K+ (10 mM) facilitated Na+ uptake by S. maritima under high salinity (100–200 mM NaCl), whether or not the plants had been subjected to a longer (3 d) period of K+ starvation. The kinetics suggests that low concentration of K+ (10 mM) might activate AKT1-type channels or KUP/HAK/KT-type transporters under high salinity (100–200 mM NaCl).

Conclusions

The turning-point of external NaCl concentrations for the two low-affinity Na+ uptake pathways in Suaeda maritima is between 90 and 95 mM. A low concentration of K+ (10 mM) might activate AKT1 or KUP/HAK/KT and facilitate Na+ uptake under high salinity (100–200 mM NaCl). The kinetics of K+ on Na+ uptake and accumulation in S maritima are also consistent with there being two low-affinity Na+ uptake pathways.  相似文献   

10.
Na+,K+-ATPase is an ubiquitous membrane enzyme that allows the extrusion of three sodium ions from the cell and two potassium ions from the extracellular fluid. Its activity is decreased in many tissues of streptozotocin-induced diabetic animals. This impairment could be at least partly responsible for the development of diabetic complications. Na+,K+-ATPase activity is decreased in the red blood cell membranes of type 1 diabetic individuals, irrespective of the degree of diabetic control. It is less impaired or even normal in those of type 2 diabetic patients. The authors have shown that in the red blood cells of type 2 diabetic patients, Na+,K+-ATPase activity was strongly related to blood C-peptide levels in non–insulin-treated patients (in whom C-peptide concentration reflects that of insulin) as well as in insulin-treated patients. Furthermore, a gene-environment relationship has been observed. The alpha-1 isoform of the enzyme predominant in red blood cells and nerve tissue is encoded by the ATP1A1 gene.Apolymorphism in the intron 1 of this gene is associated with lower enzyme activity in patients with C-peptide deficiency either with type 1 or type 2 diabetes, but not in normal individuals. There are several lines of evidence for a low C-peptide level being responsible for low Na+,K+-ATPase activity in the red blood cells. Short-term C-peptide infusion to type 1 diabetic patients restores normal Na+,K+-ATPase activity. Islet transplantation, which restores endogenous C-peptide secretion, enhances Na+,K+-ATPase activity proportionally to the rise in C-peptide. This C-peptide effect is not indirect. In fact, incubation of diabetic red blood cells with C-peptide at physiological concentration leads to an increase of Na+,K+-ATPase activity. In isolated proximal tubules of rats or in the medullary thick ascending limb of the kidney, C-peptide stimulates in a dose-dependent manner Na+,K+-ATPase activity. This impairment in Na+,K+-ATPase activity, mainly secondary to the lack of C-peptide, plays probably a role in the development of diabetic complications. Arguments have been developed showing that the diabetesinduced decrease in Na+,K+-ATPase activity compromises microvascular blood flow by two mechanisms: by affecting microvascular regulation and by decreasing red blood cell deformability, which leads to an increase in blood viscosity. C-peptide infusion restores red blood cell deformability and microvascular blood flow concomitantly with Na+,K+-ATPase activity. The defect in ATPase is strongly related to diabetic neuropathy. Patients with neuropathy have lower ATPase activity than those without. The diabetes-induced impairment in Na+,K+-ATPase activity is identical in red blood cells and neural tissue. Red blood cell ATPase activity is related to nerve conduction velocity in the peroneal and the tibial nerve of diabetic patients. C-peptide infusion to diabetic rats increases endoneural ATPase activity in rat. Because the defect in Na+,K+-ATPase activity is also probably involved in the development of diabetic nephropathy and cardiomyopathy, physiological C-peptide infusion could be beneficial for the prevention of diabetic complications.  相似文献   

11.
12.
13.

Aims

Peroxisomal biogenesis disorders (PBD) are inherited disorders clinically manifested by neurological symptoms and brain abnormalities, in which the cerebellum is usually involved. Biochemically, patients affected by these neurodegenerative diseases accumulate branched-chain fatty acids, including pristanic acid (Prist) in the brain and other tissues.

Main methods

In the present investigation we studied the in vitro influence of Prist, at doses found in PBD, on oxidative phosphorylation, by measuring the activities of the respiratory chain complexes I–IV and ATP production, as well as on creatine kinase and synaptic Na+, K+-ATPase activities in rat cerebellum.

Key findings

Prist significantly decreased complexes I–III (65%), II (40%) and especially II–III (90%) activities, without altering the activities of complex IV of the respiratory chain and creatine kinase. Furthermore, ATP formation and synaptic Na+, K+-ATPase activity were markedly inhibited (80–90%) by Prist. We also observed that this fatty acid altered mitochondrial and synaptic membrane fluidity that may have contributed to its inhibitory effects on the activities of the respiratory chain complexes and Na+, K+-ATPase.

Significance

Considering the importance of oxidative phosphorylation for mitochondrial homeostasis and of Na+, K+-ATPase for the maintenance of cell membrane potential, the present data indicate that Prist compromises brain bioenergetics and neurotransmission in cerebellum. We postulate that these pathomechanisms may contribute to the cerebellar alterations observed in patients affected by PBD in which Prist is accumulated.  相似文献   

14.

Background

Acute renal failure is a serious complication of human envenoming by Bothrops snakes. The ion pump Na+/K+-ATPase has an important role in renal tubule function, where it modulates sodium reabsorption and homeostasis of the extracellular compartment. Here, we investigated the morphological and functional renal alterations and changes in Na+/K+-ATPase expression and activity in rats injected with Bothrops alternatus snake venom.

Methods

Male Wistar rats were injected with venom (0.8 mg/kg, i.v.) and renal function was assessed 6, 24, 48 and 72 h and 7 days post-venom. The rats were then killed and renal Na+/K+-ATPase activity was assayed based on phosphate release from ATP; gene and protein expressions were assessed by real time PCR and immunofluorescence microscopy, respectively.

Results

Venom caused lobulation of the capillary tufts, dilation of Bowman's capsular space, F-actin disruption in Bowman's capsule and renal tubule brush border, and deposition of collagen around glomeruli and proximal tubules that persisted seven days after envenoming. Enhanced sodium and potassium excretion, reduced proximal sodium reabsorption, and proteinuria were observed 6 h post-venom, followed by a transient decrease in the glomerular filtration rate. Gene and protein expressions of the Na+/K+-ATPase α1 subunit were increased 6 h post-venom, whereas Na+/K+-ATPase activity increased 6 h and 24 h post-venom.

Conclusions

Bothrops alternatus venom caused marked morphological and functional renal alterations with enhanced Na+/K+-ATPase expression and activity in the early phase of renal damage.

General significance

Enhanced Na+/K+-ATPase activity in the early hours after envenoming may attenuate the renal dysfunction associated with venom-induced damage.  相似文献   

15.
Na+, K+-ATPase is ubiquitously expressed in the plasma membrane ofall animal cells where it serves as the principal regulator of intracellularion homeostasis. Na+, K+-ATPase is responsible for generating andmaintaining transmembrane ionic gradients that are of vital importance forcellular function and subservient activities such as volume regulation, pHmaintenance, and generation of action potentials and secondary activetransport. The diversity of Na+, K+-ATPase subunit isoforms andtheir complex spatial and temporal patterns of cellular expression suggestthat Na+, K+-ATPase isozymes perform specialized physiologicalfunctions. Recent studies have shown that the subunit isoformspossess considerably different kinetic properties and modes of regulationand the subunit isoforms modulate the activity, expression and plasmamembrane targeting of Na+, K+-ATPase isozymes. This review focuseson recent developments in Na+, K+-ATPase research, and in particular reportsof expression of isoforms in various tissues and experiments aimed atelucidating the intrinsic structural features of isoforms important forNa+, K+-ATPase function.  相似文献   

16.
17.
  • 1.1. Na+,K+-ATPase, which mediates the active transport of Na+ and K+ across the plasma membrane, is found in equivalent amounts in both plasma membranes of the electrocyte, the anterior, non-innervated (fraction P2) and the posterior, innervated (fraction P3) obtained by differential centrifu gation of Electrophorus electricus (L.) electric organ.
  • 2.2. The kinetic effects of Hg2+ and A13+, described as neurotoxic metals, on the Na+,K+-ATPase activity of the two membrane fractions (P2 and P3) were analysed with respect to Na+ and K+ ions, after the I50 estimation of each metal.
  • 3.3. Mercury is a potent Na+,K+-ATPase inhibitor in the nanomolar range. In all cases, it behaved as a mixed partial hyperbolic inhibitor.
  • 4.4. Aluminum was shown to be a poor enzyme inhibitor. Changing the K+ concentration, it behaved as a mixed linear inhibitor (P2 fraction) and as a non-essential mixed activator (fraction P3). Aluminum behaved as a partial hyperbolic inhibitor for both P2 and P3 fractions with respect to Na+ concentration.
  • 5.5. The observation of the variable kinetic behaviour of P2 and P3 led us to attribute these differences to the Na+,K+-ATPase electrocyte isoenzymes which occur in different proportions in these fractions (Gomes-Quintana et al., 1992 Comp. biochem. Physiol.103B/3 623–628).
  相似文献   

18.

Introduction

CD4+ T cells express K2P5.1 (TWIK-related acid-sensitive potassium channel 2 (TASK2); KCNK5), a member of the two-pore domain potassium channel family, which has been shown to influence T cell effector functions. Recently, it was shown that K2P5.1 is upregulated upon (autoimmune) T cell stimulation. The aim of this study was to correlate expression levels of K2P5.1 on T cells from patients with rheumatoid arthritis (RA) to disease activity in these patients.

Methods

Expression levels of K2P5.1 were measured by RT-PCR in the peripheral blood of 58 patients with RA and correlated with disease activity parameters (C-reactive protein levels, erythrocyte sedimentation rates, disease activity score (DAS28) scores). Twenty patients undergoing therapy change were followed-up for six months. Additionally, synovial fluid and synovial biopsies were investigated for T lymphocytes expressing K2P5.1.

Results

K2P5.1 expression levels in CD4+ T cells show a strong correlation to DAS28 scores in RA patients. Similar correlations were found for serological inflammatory parameters (erythrocyte sedimentation rate, C-reactive protein). In addition, K2P5.1 expression levels of synovial fluid-derived T cells are higher compared to peripheral blood T cells. Prospective data in individual patients show a parallel behaviour of K2P5.1 expression to disease activity parameters during a longitudinal follow-up for six months.

Conclusions

Disease activity in RA patients correlates strongly with K2P5.1 expression levels in CD4+ T lymphocytes in the peripheral blood in cross-sectional as well as in longitudinal observations. Further studies are needed to investigate the exact pathophysiological mechanisms and to evaluate the possible use of K2P5.1 as a potential biomarker for disease activity and differential diagnosis.  相似文献   

19.

Aims and background

The ability to suppress soil nitrification through the release of nitrification inhibitors from plant roots is termed ‘biological nitrification inhibition’ (BNI). Earlier, we reported that sorghum roots release higher BNI-activity when grown with NH 4 + , but not with NO 3 - as N source. Also for BNI release, rhizosphere pH of <5.0 is needed; beyond this, a negative effect on BNI release was observed with nearly 80% loss of BNI activity at pH >7.0. This study is aimed at understanding the inter-functional relationships associated with NH 4 + uptake, rhizosphere-pH and plasma membrane H+-ATPase (PM H+-ATPase) activity in regulating the release of BNIs (biological nitrification inhibitors) from sorghum roots.

Methods

Sorghum was grown hydroponically and root exudates were collected from intact plants using a pH-stat system to separate the secondary acidification effects by NH 4 + uptake on BNIs release. A recombinant luminescent Nitrosomonas europaea bioassay was used to determine BNI-activity. Root plasma membrane was isolated using a two-phase partitioning system. Hydrolytic H+-ATPase activity was determined. Split-root system setup was deployed to understand the localized responses to NH 4 + , H+-ATPase-stimulator (fusicoccin) or H+-ATPase-inhibitor (vanadates) on BNI release by sorghum.

Results

Presence of NH 4 + in the rhizosphere stimulated the expression of H+-ATPase activity and enhanced the release of BNIs from sorghum roots. Fusicoccin, which stimulates H+-ATPase activity, also stimulated BNIs release in the absence of NH 4 + ; vanadate, which suppresses H+-ATPase activity, also suppressed the release of BNIs. NH 4 + levels (in rhizosphere) positively influenced BNIs release and root H+-ATPase activity in the concentration range of 0-1.0 mM, indicating a close relationship between BNI release and root H+-ATPase activity with a possible involvement of carrier-mediated transport for the release of BNIs in sorghum.

Conclusion

Our results suggest that NH 4 + uptake, PM H+-ATPase activity, and rhizosphere acidification are functionally inter-connected with BNI release in sorghum. Such knowledge is critical to gain insights into why BNI function is more effective in light-textured, mildly acidic soils compared to other soil types.  相似文献   

20.
Summary Sodium- and potassium-dependent adenosine triphosphatase (Na+–K+-ATPase) is demonstrated in the branchial heart of Sepia officinalis L. by biochemical, cytochemical and autoradiographical methods. The biochemical data indicate the presence of Na+–K+-ATPase, shown by potassium and magnesium dependency and inhibition by ouabain. Cytochemically and autoradiographically, the enzyme is localized in the sarcolemma of the muscle cells. The positive reaction of the transparent cells (type I cells) is due to activity of alkaline phosphatases. The dark cells (type II cells) react negatively. In addition to the Na+–K+-ATPase, a magnesium-activated adenosine triphosphatase (Mg2+-ATPase) and a bicarbonate-stimulated ATPase (HCO 3 - -ATPase) are localized in the mitochondria.This study was supported by the Deutsche Forschungsgemeinschaft and is part of the doctoral dissertation  相似文献   

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