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1.
Summary The relative contributions of the Na+/Ca2+ exchange and the plasma membrane Ca2+ pump to active Ca2+ efflux from stimulated rat pancreatic acini were studied. Na+ gradients across the plasma membrane were manipulated by loading the cells with Na+ or suspending the cells in Na+-free media. The rates of Ca2+ efflux were estimated from measurements of [Ca2+] i using the Ca2+-sensitive fluorescent dye Fura 2 and45Ca efflux. During the first 3 min of cell stimulation, the pattern of Ca2+ efflux is described by a single exponential function under control, Na+-loaded, and Na+-depleted conditions. Manipulation of Na+ gradients had no effect on the hormone-induced increase in [Ca2+] i . The results indicate that Ca2+ efflux from stimulated pancreatic acinar cells is mediated by the plasma membrane Ca2+ pump. The effects of several cations, which were used to substitute for Na+, on cellular activity were also studied. Choline+ and tetramethylammonium+ (TMA+) released Ca2+ from intracellular stores of pancreatic acinar, gastric parietal and peptic cells. These cations also stimulated enzyme and acid secretion from the cells. All effects of these cations were blocked by atropine. Measurements of cholecystokinin-octapeptide (CCK-OP)-stimulated amylase release from pancreatic acini, suspended in Na+, TMA+, choline+, or N-methyl-d-glucamine+ (NMG+) media containing atropine, were used to evaluate the effect of the cations on cellular function. NMG+, choline+, and TMA+ inhibited amylase release by 55, 40 and 14%, respectively. NMG+ also increased the Ca2+ permeability of the plasma membrane. Thus, to study Na+ dependency of cellular function, TMA+ is the preferred cation to substitute for Na+. The stimulatory effect of TMA+ can be blocked by atropine.  相似文献   

2.
The mechanism of the protective effect of Ca2+ on cellular K+ content was studied by examination of the effect of Ca2+ on efflux of the K+ analog, 86Rb+, from preloaded cells with the use of compounds which interfere with monovalent cation movements. Ca2+ decreased 86Rb+ efflux to the same extent in the presence and absence of ouabain, suggesting that Ca2+ did not alter the activity of the (Na+ + K+)-adenosine triphosphatase pump. Ca2+ exerted a similar protective effect in the presence of furosemide, an inhibitor of K+-K+ exchange, indicative that Ca2+ was not inhibiting this pathway. Since Ca2+ did not influence these pathways, it is concluded that Ca2+ exerts its primary effect by slowing passive diffusion. In support of this, Ca2+ also slowed 22Na+ efflux. In addition, ethanol-induced leakage of 86Rb+ was reversed by extracellular Ca2+, suggestive of a Ca2+-membrane phospholipid interaction.  相似文献   

3.
Ouabain-blocked toad urinary bladders were maintained in Na+-free mucosal solutions, and a depolarizing solution of high K+ activity containing only 5 mM Na+ on the serosal side. Exposure to mucosal sodium (20 mM activity) evoked a transient amiloride-blockable inward current, which decayed to near zero within one hour. The apical sodium conductance increased in the initial phase of the current decay and decreased in the second phase. The conductance decrease required Ca2+ to be present on the serosal side and was more rapid when the mucosal Na+ activity was higher. At 20 mM mucosal Na+ and 3 mM serosal Ca2+ the initial (maximal) rate of inhibition amounted to 20% in 10 min. The conductance decrease could be accelerated by raising the serosal Ca2+ activity to 10 mM. The inhibition reversed on lowering the serosal Ca2+ to 3 μM and, in addition, the mucosal Na+ to zero. Exposure of the mucosal surface to the ionophore nystatin abolished the Ca2+ sensitivity of the transcellular conductance, showing that the Ca2+-sensitive conductance resides in the apical membrane. The data imply that in the K+-depolarized epithelia, cellular Ca2+, taken up from the serosal medium by means of a Na+-Ca2+ antiport, cause feedback inhibition by blockage of apical Na+ channels. However, the rate of inhibition is small, such that this regulatory mechanism will have little effect at 1 mM serosal Ca2+ and less than 20 mM cellular Na+.  相似文献   

4.
Mitochondrial calcium channels   总被引:1,自引:0,他引:1  
Uta C. Hoppe 《FEBS letters》2010,584(10):1975-1981
Mitochondrial Ca2+ handling plays an important role in energy production and various cellular signaling processes. Mitochondrial Ca2+ uptake is regulated by the mitochondrial Ca2+ uniporter (MCU), at least one non-MCU Ca2+ channel and possibly a mitochondrial ryanodine receptor. Two distinct mechanisms mediate Ca2+ outward transport, the Na+-dependent (mNCX) and the Na+-independent Ca2+ efflux. In recent years we gained more insight into the regulation and function of these different Ca2+ transport mechanisms. However, the precise physiological role and the molecular structure of all mitochondrial Ca2+ transporters and channels still has to be determined.  相似文献   

5.
The cellular mechanisms that regulate potassium (K+) channels in guard cells have been the subject of recent research, as K+ channel modulation has been suggested to contribute to stomatal movements. Patch clamp studies have been pursued on guard cell protoplasts of Vicia faba to analyze the effects of physiological cytosolic free Ca2+ concentrations, Ca2+ buffers and GTP-binding protein modulators on inward-rectifying K+ channels. Ca2+ inhibition of inward-rectifying K+ currents depended strongly on the concentration and effectiveness of the Ca2+ buffer used, indicating a large Ca2+ buffering capacity and pH increases in guard calls. When the cytosolic Ca2+ concentration was buffered to micromolar levels using BAPTA, inward-rectifying K+ channels were strongly inhibited. However, when EGTA was used as the Ca2+ buffer, much less inhibition was observed, even when pipette solutions contained 1 µM free Ca2+. Under the imposed conditions, GTPγS did not significantly inhibit inward-rectifying K+ channel currents when cytosolic Ca2+ was buffered to low levels or when using EGTA as the Ca2+ buffer. Furthermore, GDPβS reduced inward K+ currents at low cytosolic Ca2+, indicating a novel mode of inward K+ channel regulation by G-protein modulators, which is opposite in effect to that from previous reports. On the other hand, when Ca2+ was effectively elevated in the cytosol to 1 µM using BAPTA, GTPγS produced an additional inhibition of the inward-rectifying K+ channel currents in a population of cells, indicating possible Ca2+-dependent action of GTP-binding protein modulators in K+ channel inhibition. Assays of stomatal opening show that 90% inhibition of inward K+ currents does not prohibit, but slows, stomatal opening and reduces stomatal apertures by only 34% after 2 h light exposure. These data suggest that limited K+ channel down-regulation alone may not be rate-limiting, and it is proposed that the concerted action of proton-pump inhibition and additional anion channel activation is likely required for inhibition of stomatal opening. Furthermore, G-protein modulators regulate inward K+ channels in a more complex and limited, possibly Ca2+-dependent, manner than previously proposed.  相似文献   

6.
Although the role of Na+ in several aspects of Ca2+ regulation has already been shown, the exact mechanism of intracellular Ca2+ concentration ([Ca2+]i) increase resulting from an enhancement in the persistent, non‐inactivating Na+ current (INa,P), a decisive factor in certain forms of epilepsy, has yet to be resolved. Persistent Na+ current, evoked by veratridine, induced bursts of action potentials and sustained membrane depolarization with monophasic intracellular Na+ concentration ([Na+]i) and biphasic [Ca2+]i increase in CA1 pyramidal cells in acute hippocampal slices. The Ca2+ response was tetrodotoxin‐ and extracellular Ca2+‐dependent and ionotropic glutamate receptor‐independent. The first phase of [Ca2+]i rise was the net result of Ca2+ influx through voltage‐gated Ca2+ channels and mitochondrial Ca2+ sequestration. The robust second phase in addition involved reverse operation of the Na+–Ca2+ exchanger and mitochondrial Ca2+ release. We excluded contribution of the endoplasmic reticulum. These results demonstrate a complex interaction between persistent, non‐inactivating Na+ current and [Ca2+]i regulation in CA1 pyramidal cells. The described cellular mechanisms are most likely part of the pathomechanism of certain forms of epilepsy that are associated with INa,P. Describing the magnitude, temporal pattern and sources of Ca2+ increase induced by INa,P may provide novel targets for antiepileptic drug therapy.  相似文献   

7.
Abstract: Bovine chromaffin secretory vesicle ghosts loaded with Na+ were found to take up Ca2+ when incubated in K+ media or in sucrose media containing micromolar concentrations of free Ca2+. Li+- or choline+loaded ghosts did not take up Ca2+. The Ca2+ accumulated by Na+-loaded ghosts could be released by the Ca2+ ionophore A23187, but not by EGTA. Ca2+ uptake was inhibited by external Sr2+, Na +, Li +, or choline +. All the 45Ca2+ accumulated by Na+-dependent Ca2+ uptake could be released by external Na +, indicating that both Ca2+ influx and efflux occur in a Na+-dependent manner. Na + -dependent Ca2+ uptake and release were only slightly inhibited by Mg2+. In the presence of the Na+ ionophore Monensin the Ca2+ uptake by Na +-loaded ghosts was reduced. Ca2+ sequestered by the Na+-dependent mechanism could also be released by external Ca2+ or Sr2+ but not by Mg2+, indicating the presence of a Ca2+/Ca2+ exchange activity in secretory membrane vesicles. This Ca2+/Ca2+ exchange system is inhibited by Mg2+, but not by Sr2+. The Na + -dependent Ca2+ uptake system in the presence of Mg2+ is a saturable process with an apparent Km of 0.28 μM and a Vmax= 14.5 nmol min?1 mg protein?1. Ruthenium red inhibited neither the Na+/Ca2+ nor the Ca2+/Ca2+ exchange, even at high concentrations.  相似文献   

8.
The major players in the processes of cellular mechanotransduction are considered to be mechanosensitive (MS) or mechano-gated ion channels. Non-selective Ca2+-permeable channels, whose activity is directly controlled by membrane stretch (stretch-activated channels, SACs) are ubiquitously present in mammalian cells of different origin. Ca2+ entry mediated by SACs presumably has a significant impact on various Ca2+-dependent intracellular and membrane processes. It was proposed that SACs could play a crucial role in the different cellular reactions and pathologies, including oncotransformation, increased metastatic activity and invasion of malignant cells. In the present work, coupling of ion channels in transformed fibroblasts in course of stretch activation was explored with the use of patch-clamp technique. The combination of cell-attached and inside-out single-current experiments showed that Ca2+ influx via SACs triggered the activity of Ca2+-sensitive K+ channels indicating functional compartmentalization of different channel types in plasma membrane. Importantly, the analysis of single channel behavior demonstrated that K+ currents could be activated by the rise of intracellular calcium but displayed no direct mechanosensitivity. Taken together, our data imply that local changes in Ca2+ concentration due to SAC activity may provide a functional link between various Ca2+-dependent molecules in the processes of cellular mechanotransduction.  相似文献   

9.
Modulation of calcium signalling by mitochondria   总被引:1,自引:0,他引:1  
Ciara Walsh 《BBA》2009,1787(11):1374-1382
In this review we will attempt to summarise the complex and sometimes contradictory effects that mitochondria have on different forms of calcium signalling. Mitochondria can influence Ca2+ signalling indirectly by changing the concentration of ATP, NAD(P)H, pyruvate and reactive oxygen species — which in turn modulate components of the Ca2+ signalling machinery i.e. buffering, release from internal stores, influx from the extracellular solution, uptake into cellular organelles and extrusion by plasma membrane Ca2+ pumps. Mitochondria can directly influence the calcium concentration in the cytosol of the cell by importing Ca2+ via the mitochondrial Ca2+ uniporter or transporting Ca2+ from the interior of the organelle into the cytosol by means of Na+/Ca2+ or H+/Ca2+ exchangers. Considerable progress in understanding the relationship between Ca2+ signalling cascades and mitochondrial physiology has been accumulated over the last few years due to the development of more advanced optical techniques and electrophysiological approaches.  相似文献   

10.
Isolated hepatocytes release 2–3 nmol Mg2+/mg protein or ~10% of the total cellular Mg2+ content within 2 minutes from the addition of agonists that increase cellular cAMP, for example, isoproterenol (ISO). During Mg2+ release, a quantitatively similar amount of Ca2+ enters the hepatocyte, thus suggesting a stoichiometric exchange ratio of 1 Mg2+:1Ca2+. Calcium induced Mg2+ extrusion is also observed in apical liver plasma membranes (aLPM), in which the process presents the same 1 Mg2+:1Ca2+ exchange ratio. The uptake of Ca2+ for the release of Mg2+ occurs in the absence of significant changes in Δψ as evidenced by electroneutral exchange measurements with a tetraphenylphosphonium (TPP+) electrode or 3H-TPP+. Collapsing the Δψ by high concentrations of TPP+ or protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) does not inhibit the Ca2+-induced Mg2+ extrusion in cells or aLPM. Further, the process is strictly unidirectional, serving only in Ca2+ uptake and Mg2+ release. These data demonstrate the operation of an electroneutral Ca2+/Mg2+ exchanger which represents a novel pathway for Ca2+ accumulation in liver cells following adrenergic receptor stimulation. This work was supported by National Institutes of Health Grant HL 18708.  相似文献   

11.
Calcium uptake by microsomal membranes from the cellular slime mould Dictyostelium discoideum was measured using Calcium Green-2 as a fluorescent probe of external free Ca2+ concentration. High-affinity Ca2+ uptake was found to be completely inhibited by low concentrations of vanadate, but not by thapsigargin, suggesting that the activity is mediated by a Ca2+-ATPase distinct from sarco(endo)plasmic reticulum type of higher animal cells. On sucrose density gradients, Ca2+ uptake distributes with vacuolar proton pump activity and part of the observed Ca2+ uptake is dependent on the pH gradient generated by the vacuolar-type H+-ATPase, indicating that the Ca2+ pump is located on both acidic and non-acidic vesicles, possibly derived from the H+-ATPase-rich contractile vacuole complex.  相似文献   

12.
Targets of oxidative stress in cardiovascular system   总被引:4,自引:0,他引:4  
Although oxidants such as superoxide (O2.-) and hydrogen peroxide (H2O2) play a role in host-mediated destruction of foreign pathogens yet excessive generation of oxidants may lead to a variety of pathological complications in the cardiovascular system. An important mechanism by which oxidants cause dysfunction of the cardiovascular system appears to be due to the increase in intracellular free Ca2+ concentration. Oxidants cause cellular Ca2+ mobilization by modulating activities of a variety of regulators such as Na+/H+ and Na+/Ca2+ exchangers, Na+/K+ ATPase and Ca2+ ATPase and Ca2+ channels that are associated with Ca2+ transport in the plasma membrane and the sarco(endo)plasmic reticular membrane of myocardial cells. Recent research have suggested that the increase in Ca2+ level by oxidants plays a pivotal role in indicing several protein kinases such as protein kinase C, tyrosine kinase and mitogen activated protein kinases. Oxindant-mediated alteration of different signal transduction systems and their interations eventually regulate a variety of pathological conditoins such as atherosclerosis, apoptosis and necrosis in the myocardium  相似文献   

13.
Summary Intracellular Ca2+ has been suggested to play an important role in the regulation of epithelial Na+ transport. Previous studies showed that preincubation of toad urinary bladder, a tight epithelium, in Ca2+-free medium enhanced Na+ uptake by the subsequently isolated apical membrane vesicles, suggesting the downregulation of Na+ entry across the apical membrane by intracellular Ca2+. In the present study, we have examined the effect of Ca2+-free preincubation on apical membrane Na+ transport in a leaky epithelium, i.e., brush border membrane (BBM) of rabbit renal proximal tubule. In contrast to toad urinary bladder, it was found that BBM vesicles derived from proximal tubules incubated in 1mm Ca2+ medium exhibited higher Na+ uptake than those derived from proximal tubules incubated in Ca2+-free EGTA medium. Such effect of Ca2+ in the preincubation medium was temperature dependent and could not be replaced by another divalent cation, Ba2+ (1mm). Ca2+ in the preincubation medium did not affect Na+-dependent BBM glucose uptake, and its effect on BBM Na+ uptake was pH gradient dependent and amiloride (10–3 m) sensitive, suggesting the involvement of Na+/H+ antiport system. Addition of verapamil (10–4 m) to 1mm Ca2+ preincubation medium abolished while ionomycin (10–6 m) potentiated the effect of Ca2+ to increase BBM Na+ uptake, suggesting that the effect of Ca2+ in the preincubation medium is likely to be mediated by Ca2+-dependent cellular pathways and not due to a direct effect of extracellular Ca2+ on BBM. Neither the proximal tubule content of cAMP nor the inhibitory effect of 8, bromo-cAMP (0.1mm) on BBM Na+ uptake was affected by the presence of Ca2+ in the preincubation medium, suggesting that Ca2+ in the preincubation medium did not increase BBM Na+ uptake by removing the inhibitory effect of cAMP. Addition of calmodulin inhibitor, trifluoperazine (10–4 m) to 1mm Ca2+ preincubation medium did not prevent the increase in BBM Na+ uptake. The effect of Ca2+ was, however, abolished when protein kinase C in the proximal tubule was downregulated by prolonged (24 hr) incubation with phorbol 12-myristate 13-acetate (10–6 m). In summary, these results show the Ca2+ dependency of Na+ transport by renal BBM, possibly through stimulation of Na+/H+ exchanger by protein kinase C.  相似文献   

14.
The ability of mitochondria to capture Ca2+ ions has important functional implications for cells, because mitochondria shape cellular Ca2+ signals by acting as a Ca2+ buffer and respond to Ca2+ elevations either by increasing the cell energy supply or by triggering the cell death program of apoptosis. A mitochondrial Ca2+ channel known as the uniporter drives the rapid and massive entry of Ca2+ ions into mitochondria. The uniporter operates at high, micromolar cytosolic Ca2+ concentrations that are only reached transiently in cells, near Ca2+ release channels. Mitochondria can also take up Ca2+ at low, nanomolar concentrations, but this high affinity mode of Ca2+ uptake is not well characterized. Recently, leucine-zipper-EF hand-containing transmembrane region (Letm1) was proposed to be an electrogenic 1:1 mitochondrial Ca2+/H+ antiporter that drives the uptake of Ca2+ into mitochondria at nanomolar cytosolic Ca2+ concentrations. In this article, we will review the properties of the Ca2+ import systems of mitochondria and discuss how Ca2+ uptake via an electrogenic 1:1 Ca2+/H+ antiport challenges our current thinking of the mitochondrial Ca2+ uptake mechanism.  相似文献   

15.
Summary The influence of Ca2+ and other cations on electrolyte permeability has been studied in isolated membrane vesicles from cat pancreas.Ca2+ in the micromolar to millimolar concentration range, as well as Mg2+, Sr2+, Mn2+ and La3+ at a tested concentration of 10–4 m, increased Na+ permeability when applied at the vesicle inside. When added to the vesicle outside, however, they decreased Na+ permeability. Ba2+ was effective from the outside but not from the vesicle inside.When Ca2+ was present at both sides of the membrane, Na+ efflux was not affected as compared to that in the absence of Ca2+. Monovalent cations such as Rb+, Cs+, K+, Tris+ and choline+ decreased Na+ permeability when present at the vesicle outside at a concentration range of 10 to 100mm. Increasing Na+ concentrations from 10 to 100mm at the vesicle inside increased Na+ permeability.The temperature dependence of Na+ efflux revealed that the activation energy increased in the lower temperature range (0 to 10°C) when Ca2+ was present at the outside or at both sides, but not when present at the vesicle inside only or in the absence of Ca2+.The results suggest that the Ca2+ outside effect is due to binding of calcium to negatively charged phospholipids with a consequent reduction of both fluidity and Na+ permeability of the membrane. The Ca2+-inside effect most likely involves interaction with proteins with consequent increase in Na+ permeability.The data are consistent with current hypotheses on secretagogue-induced fluid secretion in acinar cells of the pancreas according to which secretagogues elicit NaCl and fluid secretion by liberating Ca2+ from cellular membranes and by stimulating Ca2+ influx into the cell. The increased intracellular Ca2+ concentration in turn increases the contraluminal Na+ permeability which leads to NaCl influx. The luminal sodium pump finally transports Na+ ions into the lumen.  相似文献   

16.
Abstract: The role of voltage-sensitive Ca2+ channels in mediating Ca2+ influx during ischemia was investigated in NG108-15 cells, a neuronal cell line that does not express glutamate-sensitive receptor-mediated Ca2+ channels. Concurrent 31P/19F and 23Na double-quantum filtered (DQF) NMR spectra were used to monitor cellular energy status, intracellular [Ca2+] ([Ca2+]i), and intracellular Na+ content in cells loaded with the calcium indicator 1,2-bis-(2-amino-5-fluorophenoxy)ethane-N,N,N′,N′-tetraacetic acid (5FBAPTA) during ischemia and reperfusion. Cells loaded with 5FBAPTA were indistinguishable from unloaded cells except for small immediate decreases in levels of phosphocreatine (PCr) and ATP. Ischemia induced a steady decrease in intracellular pH and PCr and ATP levels, and a steady increase in intracellular Na+ content; however, a substantial increase in [Ca2+]i (about threefold) was seen only following marked impairment of cellular energy status, when PCr was undetectable and ATP content was reduced to 55% of control levels. A depolarization-induced increase in [Ca2+]i could be completely blocked by 1 µM nifedipine, whereas up to 20 µM nifedipine had no effect on the increase in [Ca2+]i seen during ischemia. These data demonstrate that voltage-gated Ca2+ channels do not mediate significant Ca2+ flux during ischemia in this cell line and suggest an important role for Ca2+i stores, the Na+/Ca2+ antiporter, or other processes linked to cellular energy status in the increase in cytosolic Ca2+ level during ischemia.  相似文献   

17.
《Cell calcium》2015,58(5-6):348-365
High environmental salt elicits an increase in cytosolic Ca2+ ([Ca2+]cyt) in plants, which is generated by extracellular Ca2+ influx and Ca2+ release from intracellular stores, such as vacuole and endoplasmic reticulum. This study aimed to determine the physiological mechanisms underlying Ca2+ release from vacuoles and its role in ionic homeostasis in Populus euphratica. In vivo Ca2+ imaging showed that NaCl treatment induced a rapid elevation in [Ca2+]cyt, which was accompanied by a subsequent release of vacuolar Ca2+. In cell cultures, NaCl-altered intracellular Ca2+ mobilization was abolished by antagonists of inositol (1, 4, 5) trisphosphate (IP3) and cyclic adenosine diphosphate ribose (cADPR) signaling pathways, but not by slow vacuolar (SV) channel blockers. Furthermore, the NaCl-induced vacuolar Ca2+ release was dependent on extracellular ATP, extracellular Ca2+ influx, H2O2, and NO. In vitro Ca2+ flux recordings confirmed that IP3, cADPR, and Ca2+ induced substantial Ca2+ efflux from intact vacuoles, but this vacuolar Ca2+ flux did not directly respond to ATP, H2O2, or NO. Moreover, the IP3/cADPR-mediated vacuolar Ca2+ release enhanced the expression of salt-responsive genes that regulated a wide range of cellular processes required for ion homeostasis, including cytosolic K+ maintenance, Na+ and Cl exclusion across the plasma membrane, and Na+/H+ and Cl/H+ exchanges across the vacuolar membrane.  相似文献   

18.
We examined the effects of pH, internal ionized Ca (Ca2+ i ), cellular ATP, external divalent cations and quinine on Cl-independent ouabain-resistant K+ efflux in volume-clamped sheep red blood cells (SRBCs) of normal high (HK) and low (LK) intracellular K+ phenotypes. In LK SRBCs the K+ efflux was higher at pH 9.0 (350%) than at pHs 7.4 and 6.5, and was inhibited by external divalent cations, quinine, and cellular ATP depletion. The above findings suggest that the increased K+ efflux at alkaline pH is due to the opening of ion channels or specific transporters in the cell membrane. In addition, K+ efflux was activated (100%) when Ca2+ i was increased (+A23187, +Ca2+ o ) into the μm range. However, in comparison to human red blood cells, the Ca2+ i -induced increase in K+ efflux in LK SRBCs was fourfold smaller and insensitive to quinine and charybdotoxin. The Na+ efflux was also higher at pH 9.0 than at pH 7.4, and activated (about 40%) by increasing Ca2+ i . In contrast, in HK SRBCs the K+ efflux at pH 9.0 was neither inhibited by quinine nor activated by Ca2+ i . These studies suggest the presence in LK SRBCs, of at least two pathways for Cl-independent K+ and Na+ transport, of which one is unmasked by alkalinization, and the other by a rise in Ca2+ i . Received: 23 May 1996/Revised: 6 December 1996  相似文献   

19.
Mitochondria, the major source of cellular ATP, display high vulnerability to metabolic stress, in particular to excessive Ca2+ loading. Here, we show that Ca2+-inhibited mitochondrial ATP generation could be restored through stimulated Ca2+ discharge from mitochondrial matrix. This was demonstrated using a Ca2+ ionophore or through Na+/Ca2+ exchange-mediated decrease of mitochondrial Ca2+ load. Furthermore, diazoxide, a mitochondrial potassium channel opener, which maintained mitochondrial Ca2+ homeostasis, also restored Ca2+-inhibited ATP synthesis and preserved the structural integrity of Ca2+-challenged mitochondria. Thus, under conditions of excessive mitochondrial Ca2+ overload targeting mitochondrial Ca2+ transport pathways restores oxidative phosphorylation required for vital cellular processes. This study, therefore, identifies an effective strategy capable to rescue Ca2+-disrupted mitochondrial energetics.  相似文献   

20.
Cadmium (Cd2+) interferes with the uptake, transport and utilization of several macro‐ and micronutrients, which accounts, at least in part, for Cd2+ toxicity in plants. However, the mechanisms underlying Cd2+ interference of ionic homeostasis is not understood. Using biophysical techniques including membrane potential measurements, scanning ion‐selective electrode technique for non‐invasive ion flux assays and patch clamp, we monitored the effect of Cd2+ on calcium (Ca2+) and potassium (K+) transport in root hair cells of rice. Our results showed that K+ and Ca2+ contents in both roots and shoots were significantly reduced when treated with exogenous Cd2+. Further studies revealed that three cellular processes may be affected by Cd2+, leading to changes in ionic homeostasis. First, Cd2+‐induced depolarization of the membrane potential was observed in root hair cells, attenuating the driving force for cation uptake. Second, the inward conductance of Ca2+ and K+ was partially blocked by Cd2+, decreasing uptake of K+ and Ca2+. Third, the outward K+ conductance was Cd2+‐inducible, decreasing the net content of K+ in roots. These results provide direct evidence that Cd2+ impairs uptake of Ca2+ and K+, thereby disturbing ion homeostasis in plants.  相似文献   

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