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1.
In previous studies, nonlethal CdCl 2 concentrations apparently inhibited basal Y-1 mouse adrenal tumor cell endogenous mitochondrial cholesterol conversion to pregnenolone. In addition, CdCl 2 inhibited all agents stimulating both plasma membrane-dependent cAMP synthesis and 20-hydroxy-4-pregnen-3-one (20DHP) secretion. Bypassing the plasma membrane using dibutyryl-cAMP (dbcAMP) stimulated cytoplasmic cholesterol metabolism and 20DHP secretion in the presence of CdCl 2. Since CdCl 2 competed at metabolic steps requiring Ca 2+ in other tissues, experiments were designed to examine Cd 2+ competition with Ca 2+ during steroidogenesis. Sets of cells incubated with either medium or adrenocorticotropin (ACTH) with or without CdCl 2 were also treated with 0, 1.0, 5.0 or 10.0 mmol/L CaCl 2 in the presence or absence of EGTA, a relatively specific Ca 2+, but not Cd 2+, chelating agent. Another experimental cell set incubated with either medium or ACTH, with or without CdCl 2, was treated with or without 1 mmol/L A23187, an ionophore specifically facilitating extracellular Ca 2+ transfer across plasma membranes. Besides determining Ca 2+ involvement in steroidogenesis using steroid secretion as an endpoint, we directly measured Ca 2+ concentrations using intracellular fura-2 fluorescence. Following loading with 2 mol/L fura-2, cells remained untreated or medium was infused with CdCl 2, ACTH, ACTH/CdCl 2 or ACTH followed after 50 s by CdCl 2. Using Ca 2+-supplemented media, we observed that Cd 2+ inhibition of ACTH-stimulated 20DHP secretion was completely reversed. Standard Ca 2+-containing medium supplemented with Ca 2+ also enhanced maximally stimulated 20DHP secretion by ACTH. 20DHP secretion by ACTH-treated and ACTH/Cd 2+-treated cells was only reduced by EGTA, when Ca 2+ was not supplemented. The ionophore A23187 increased basal and ACTH-stimulated 20DHP secretion by Cd 2+-treated cells, suggesting that extracellular Ca 2+ resources may compete against Cd 2+ effects on plasma membrane cAMP synthesis and on basal cholesterol metabolism by mitochondria. No time-dependent change in Ca 2+ concentrations occurred within untreated cell suspensions. ACTH stimulation caused a 25 s burst in Ca 2+ concentrations before returning to basal, steady-state levels. Cd 2+ also stimulated intracellular fura-2 fluorescence. Untreated cell suspensions infused with Cd 2+ exhibited a continuous rise in intracellular fluorescence. ACTH/CdCl 2-treated cells exhibited a hyperbolic rise in intracellular fluorescence over the 300 s study period. Cells treated with Cd 2+ 50 s after ACTH treatment initially exhibited the 25 s fluorescence burst followed by a Cd 2+-induced hyperbolic rise in intracellular Cd 2+. These fluorescence measurements suggested that cytoplasmic Ca 2+ changes do not appear to be necessary for basal 20DHP synthesis and secretion; only a 25 s burst in intracellular Ca 2+ is necessary to a slightly higher plateau level for stimulated 20DHP synthesis and secretion. Cd 2+ freely enters the cell under basal conditions and Cd 2+ entry is accelerated by ACTH stimulation. Data were consistent with Ca 2+ being required for optimal stimulated steroid production and Cd 2+ probably competing with Ca 2+ during basal mitochondrial cholesterol metabolism and plasma membrane ACTH-stimulated cAMP generation. 相似文献
3.
Cellular oxidative stress responses are caused in many ways, but especially by disease and environmental stress. After the initial burst of reactive oxygen species (ROS), the effective elimination of ROS is crucial for the survival of organisms and is mediated by antioxidant defense mechanisms. In this paper, we investigate the possible antioxidant function of Penaeus monodon Receptor for Activated C Kinase-1 (Pm-RACK1). When Pm-RACK1 was over-expressed in Escherichia coli cells or Spodoptera frugiperda ( Sf9) insect cells exposed to H 2O 2, it significantly protected the cells from oxidative damage induced by H 2O 2. When recombinant Pm-RACK1 protein was expressed as a histidine fusion protein in E. coli and purified with a Ni 2+-column it possessed antioxidant functions that protected DNA from metal-catalyzed oxidation. Shrimp ( Penaeus vannamei) held at an alkaline pH had a much higher hepatopancreatic expression of Pm-RACK1 than in those held at pH 7.4. The exposure of shrimp to alkaline pH is also known to increase ROS production. These results provide strong evidence that Pm-RACK1 can participate in the shrimp antioxidant response induced by the formation of ROS. 相似文献
5.
This study was aimed at investigating the toxicity mechanism of lipopolysaccharide (LPS) on Penaeus monodon haemocytes at a cellular level. Reactive oxygen species (ROS) production, nitric oxide (NO) production, non-specific esterase activity, cytoplasmic free-Ca 2 + (CF-Ca 2 +) concentration, DNA damaged cell ratio and apoptotic cell ratio of in vitro LPS-treated haemocytes were measured by flow cytometry. Two concentrations of Escherichia coli LPS (5 and 10 μg mL ? 1) were used. Results showed that ROS production, NO production and CF-Ca 2 + concentration were significantly induced in the LPS-treated haemocytes. Ratio of DNA damaged cell and apoptotic cell increased caused by LPS, while esterase activity increased at the initial 60 min and dropped later. The initial increase in esterase activity suggested that LPS activated the release of esterase, and the later decrease might result from apoptosis. These results indicated that LPS would induce oxidative stress on shrimp haemocytes, and cause Ca 2 + release, DNA damage and subsequently cell apoptosis. This process of ROS/RNS-induced Ca 2 +-mediated apoptosis might be one of the toxicity mechanisms of LPS on shrimp haemocytes. 相似文献
6.
Prolactin (PRL) release and intracellular free calcium concentration [Ca 2+] i were measured in two populations of normal rat lactotrophs (light and heavy fractions) in culture. Spontaneous PRL release of heavy fraction cells was more sensitive to dihydropyridines (DHPs; Bay K 8644 and nifedipine) when compared to the light fraction lactotrophs. The stimulatory effect of thyrotropin-releasing hormone (TRH) on PRL release from heavy fraction cells was inhibited by Cd 2+ and mimicked by Bay K 8644. Indo-1 experiments revealed that TRH-increased [Ca 2+] i was reversibly inhibited by Cd 2+. In a Ca 2+-free EGTA-containing medium, TRH did not modify [Ca 2+] i.Abbreviations [Ca 2+] i
intracellular free calcium concentration
- DA
dopamine
- DHP
dihydropyridine(s)
- DMEM
Dulbecco's Modified Eagle's Medium
- Ins(1,4,5)P 3
inositol 1,4,5-trisphosphate
- PRL
prolactin
- RIA
radioimmunoassay
- TRH
thyrotropin-releasing hormone
- VGCC
voltage-gated calcium channel 相似文献
7.
Recent studies have shown that Cd 2+ can damage the Ca 2+-dependent junctions between renal epithelial cells in culture, and preliminary evidence suggests that this effect may involve the interaction of Cd 2+ with E-cadherin, a Ca 2+-dependent cell adhesion molecule that is localized at the adhering junctions of epithelial cells. To determine whether or not Cd 2+ might bind directly to the E-cadherin molecule, we studied the binding of Cd 2+ to E-CAD1, a recombinant, 145-residue polypeptide that corresponds to one of the extracellular Ca 2+-binding regions of mouse E-cadherin. By using an equilibrium microdialysis technique, we were able to show that Cd 2+ could, in fact, bind to E-CAD1. The binding was saturable, with a maximum of one Cd 2+ binding site per E-CAD1 molecule. The apparent dissociation constant (K D) for the binding was about 20 μM, a concentration similar to that which has been shown to disrupt the junctions between epithelial cells. Other results showed that the binding of Cd 2+ was greatly reduced when excess Ca 2+ was included in the dialysis solution. These results suggest that Cd 2+ can interact with the Ca 2+ binding regions on the E-CAD1 molecule, and they provide additional support for the hypothesis that E-cadherin might be a molecular target for Cd 2+ toxicity. 相似文献
8.
Cadmium is a highly toxic metal entering cells by a variety of mechanisms. Its toxic action is far from being completely understood, although specific interaction with the cellular calcium metabolism has been indicated. Metal ions that influence intracellular Ca 2+ concentrations or compete with Ca 2+ for protein binding sites may exert an effect on actin filaments, whose assembly and disassembly are both regulated by a number of calcium-dependent factors. Cadmium is such a metal. Much evidence demonstrates that cadmium interferes with the dynamics of actin filaments in various types of cells. Here we show that, at high (0.8–1.0 mM) concentrations, CdCl 2 causes actin denaturation. At such Cd 2+ concentrations, actin precipitates (really actin, as shown by SDS-PAGE, see Fig. 1B) in the form of irregular, disordered clots, clearly appreciable by electron microscopy. Denaturation seems to be reversible since, after Cd 2+ removal by dialysis, the polymerizability of sedimented actin is restored almost completely. On the other hand, at concentrations ranging from 0.25 to 0.6 mM, CdCl 2 is more effective as an actin polymerizing agent than both MgCl 2 and CaCl 2. The Cd-related increase in the actin assembly rate is ascribable to an enhanced nucleation rather than to an increased monomer addition to filament growing ends. The latter, in contrast, appears quite slow. Critical concentration measurements revealed that the extent of polymerization of both Mg- and Cd-assembled actin are very close ( Cc ranges from 0.25 to 0.5 μM), while Ca-polymerized actin shows a polymerization extent markedly lower ( Cc=4.0 μM). By both the fluorescent Ca 2+ chelator Quin-2 assay and limited proteolysis of actin by trypsin and α-chymotrypsin, the real substitution of G-actin-bound Ca 2+ by Cd 2+ has been appreciated. The increase in Quin-2 fluorescence after addition of excess CdCl 2 indicates that, in our experimental conditions, Ca 2+ tightly-bound to actin is partially (60–70%) replaced by Cd 2+, forming Cd-actin. Electrophoretic patterns after limited proteolysis reveal that the trypsin cleavage sites in the segment 61–69 of the actin polypeptide chain are less accessible in Cd-actin than in Ca-actin, although the cation-dependent effect is less pronounced in Cd-actin than in Mg-actin. Our results are consistent with some of the consequences on microfilament organization observed in Cd 2+-treated cells; however, considering the positive effect of Cd 2+ on actin polymerization in solution we have noticed that this was never observed in vivo. A different indirect effect of Cd 2+ on some cellular event(s) influencing cytoplasmic actin polymerization appears to be reasonable. © 1997 Elsevier Science B.V. All rights reserved. 相似文献
9.
The effects of heavy metals Cd 2+, Pb 2+ and Zn 2+ at 0.05, 0.5 and 5.0 mg/L level and their interactions at 0.5 mg/L level on DNA damage in hepatopancreas of loach Misgurnus anguillicaudatus for 1–35 days exposure were examined by single cell gel electrophoresis (SCGE). For each test group, 20 loaches with similar
body size (5.17–7.99 g; 11.79–13.21 cm) were selected and kept in aquaria with dechlorinated water at (22±1)°C and fed a commercial
diet every 48 h. According to the percentage of damaged DNA with tail and its TL/D (tail length to diameter of nucleus) value,
the relationship between DNA damage degree and heavy metal dose and exposure time was determined. Results showed that the
percentage of damaged DNA and the TL/D value were increased with the prolonged exposure time. The highest percentage (84.85%)
of damaged DNA was shown in 5.0 mg/L Zn 2+ group after 28 days exposure and the biggest TL/D value (2.50) in all treated groups after 35 days exposure. During the first
treated week, the damnification of DNA was mainly recognized as the first level, after that time, the third damaged level
was mostly observed and the percentage of damaged DNA was beyond 80%. The joint toxic effects among Cd 2+, Pb 2+ or Zn 2+ revealed much complexity, but it generally displayed that the presence of Cd 2+ could enhance the genotoxicity of Pb 2+ or Zn 2+. In conclusion, the results suggested that there was a significant time-and dose-depended relationship between the heavy
metal and DNA damage in hepatopancreas of loach, and SCGE could represent a useful means to evaluate the genotoxicity of environmental
contamination on aquatic organisms.
__________
Translated from Acta Hydrobiologica Sinica, 2006, 30(4): 399–403 [译自: 水生生物学报] 相似文献
10.
The electromagnetic field (EMF) is newly considered as an exogenous environmental stimulus that is closely related to ion transportation on the cellular membrane, maintaining the internal ionic homeostasis. Cation transports of Ca 2+ and other metal ions, Cd 2+, Zn 2+, and Mn 2+were studied in terms of the external Ca 2+ stress, [Ca 2+] ext, and exposure to the physical EMF. A specific yeast strain K667 was used for controlling CAX5 (cation/H + exchanger) expression. Culture samples were exposed to 60 Hz, 0.1 mT sinusoidal or square magnetics waves, and intracellular cations of each sample were measured and analyzed. AtCAX5 transformant yeast grew normally under the metallic stress. However, the growth of the control group was significantly inhibited under the same cation concentration; 60 Hz and 0.1 mT magnetic field enhanced intracellular cation concentrations significantly as exposure time increased both in the AtCAX5 transformed yeast and in the control group. However, the AtCAX5-transformed yeast showed higher concentration of the intracellular cations than the control group under the same exposure EMF. AtCAX5-transformed yeasts displayed an increment in [Ca 2+] int, [K +] int, [Na +] int, and [Zn 2+] int concentration under the presence of both sinusoidal and square-waved EMF stresses compared to the control group, which shows that AtCAX5 expressed in the vacuole play an important role in maintaining the homeostasis of intracellular cations. These findings could be utilized in the cultivation of the crops which were resistant to excessive exogenous ions or in the production of biomass containing a large proportion of ions for nutritional food or in the bioremediation process in metal-polluted environments. 相似文献
11.
During the conversion of newt iris epithelial cells into lens cells, melanosomes disappear from the cytoplasm. In this “depigmentation,” exocytosis of melanosomes is involved. The role of Ca 2+ in this process has been the subject of this work. The intracellular Ca 2+ concentration of cultured iris epithelial cells was increased by three methods: microinjection of 10 ?3, M CaCl 2 into the cytoplasm, fusion of phospholipid vesicles containing 10 ?3, M CaCl 2 with the cell membrane, and exposure to the calcium ionophore A23187. Each of these treatments caused an increase in the release of melanosomes. Further experiments suggest that cAMP stimulates exocytosis probably by liberating Ca 2+ from intracellular stores. 相似文献
12.
We report that a localized intracellular and extracellular Ca 2+ mobilization occurs at the site of microscopic epithelial damage in vivo and is required to mediate tissue repair. Intravital confocal/two-photon microscopy continuously imaged the surgically exposed stomach mucosa of anesthetized mice while photodamage of gastric epithelial surface cells created a microscopic lesion that healed within 15 min. Transgenic mice with an intracellular Ca 2+-sensitive protein (yellow cameleon 3.0) report that intracellular Ca 2+ selectively increases in restituting gastric epithelial cells adjacent to the damaged cells. Pretreatment with U-73122, indomethacin, 2-aminoethoxydiphenylborane, or verapamil inhibits repair of the damage and also inhibits the intracellular Ca 2+ increase. Confocal imaging of Fura-Red dye in luminal superfusate shows a localized extracellular Ca 2+ increase at the gastric surface adjacent to the damage that temporally follows intracellular Ca 2+ mobilization. Indomethacin and verapamil also inhibit the luminal Ca 2+ increase. Intracellular Ca 2+ chelation (1,2- bis( o-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid/acetoxymethyl ester, BAPTA/AM) fully inhibits intracellular and luminal Ca 2+ increases, whereas luminal calcium chelation ( N-(2-hydroxyetheyl)-ethylendiamin- N, N, N′-triacetic acid trisodium, HEDTA) blocks the increase of luminal Ca 2+ and unevenly inhibits late-phase intracellular Ca 2+ mobilization. Both modes of Ca 2+ chelation slow gastric repair. In plasma membrane Ca-ATPase 1 +/− mice, but not plasma membrane Ca-ATPase 4 −/− mice, there is slowed epithelial repair and a diminished gastric surface Ca 2+ increase. We conclude that endogenous Ca 2+, mobilized by signaling pathways and transmembrane Ca 2+ transport, causes increased Ca 2+ levels at the epithelial damage site that are essential to gastric epithelial cell restitution in vivo. 相似文献
13.
The aim of this study was to characterize the role of CFTR during Cd 2+-induced apoptosis. For this purpose primary cultures and cell lines originated from proximal tubules (PCT) of wild-type cftr+/+ and cftr?/? mice were used. In cftr+/+ cells, the application of Cd 2+ (5 μM) stimulated within 8 min an ERK1/2-activated CFTR-like Cl ? conductance sensitive to CFTR inh-172. Thereafter Cd 2+ induced an apoptotic volume decrease (AVD) within 6 h followed by caspase-3 activation and apoptosis. The early increase in CFTR conductance was followed by the activation of volume-sensitive outwardly rectifying (VSOR) Cl ? and TASK2 K + conductances. By contrast, cftr?/? cells exposed to Cd 2+ were unable to develop VSOR currents, caspase-3 activity, and AVD process and underwent necrosis. Moreover in cftr+/+ cells, Cd 2+ enhanced reactive oxygen species (ROS) production and induced a 50% decrease in total glutathione content (major ROS scavenger in PCT). ROS generation and glutathione decrease depended on the presence of CFTR, since they did not occur in the presence of CFTR inh-172 or in cftr?/? cells. Additionally, Cd 2+ exposure accelerates effluxes of fluorescent glutathione S-conjugate in cftr+/+ cells. Our data suggest that CFTR could modulate ROS levels to ensure apoptosis during Cd 2+ exposure by modulating the intracellular content of glutathione. 相似文献
15.
Classic calcium hypothesis states that depolarization-induced increase in intracellular Ca 2+ concentration ([Ca 2+] i) triggers vesicle exocytosis by increasing vesicle release probability in neurons and neuroendocrine cells. The extracellular Ca 2+, in this calcium hypothesis, serves as a reservoir of Ca 2+ source. Recently we find that extracellular Ca 2+per se inhibits the [Ca 2+] i dependent vesicle exocytosis, but it remains unclear whether quantal size is regulated by extracellular, or intracellular Ca 2+ or both [1]. In this work we showed that, in physiological condition, extracellular Ca 2+per se specifically inhibited the quantal size of single vesicle release in rat adrenal slice chromaffin cells. The extracellular Ca 2+ in physiological concentration (2.5 mM) directly regulated fusion pore kinetics of spontaneous quantal release of catecholamine. In addition, removal of extracellular Ca 2+ directly triggered vesicle exocytosis without eliciting intracellular Ca 2+. We propose that intracellular Ca 2+ and extracellular Ca 2+per se cooperately regulate single vesicle exocytosis. The vesicle release probability was jointly modulated by both intracellular and extracellular Ca 2+, while the vesicle quantal size was mainly determined by extracellular Ca 2+ in chromaffin cells physiologically. 相似文献
16.
Application of fluid pressure (FP) using pressurized fluid flow suppresses the L-type Ca 2+ current through both enhancement of Ca 2+ release and intracellular acidosis in ventricular myocytes. As FP-induced intracellular acidosis is more severe during the inhibition of Na +–H + exchange (NHE), we examined the possible role of NHE in the regulation of ICa during FP exposure using HOE642 (cariporide), a specific NHE inhibitor. A flow of pressurized (∼16 dyn/cm 2) fluid was applied onto single rat ventricular myocytes, and the ICa was monitored using a whole-cell patch-clamp under HEPES-buffered conditions. In cells pre-exposed to FP, additional treatment with HOE642 dose-dependently suppressed the ICa (IC 50 = 0.97 ± 0.12 μM) without altering current–voltage relationships and inactivation time constants. In contrast, the ICa in control cells was not altered by HOE642. The HOE642 induced a left shift in the steady-state inactivation curve. The suppressive effect of HOE642 on the ICa under FP was not altered by intracellular high Ca 2+ buffering. Replacement of external Cl − with aspartate to inhibit the Cl −-dependent acid loader eliminated the inhibitory effect of HOE642 on ICa. These results suggest that NHE may attenuate FP-induced ICa suppression by preventing intracellular H + accumulation in rat ventricular myocytes and that NHE activity may not be involved in the Ca 2+-dependent inhibition of the ICa during FP exposure. 相似文献
17.
Abscisic acid (ABA), a widely known phytohormone involved in the plant response to abiotic stress, plays a vital role in mitigating Cd2+ toxicity in herbaceous species. However, the role of ABA in ameliorating Cd2+ toxicity in woody species is largely unknown. In the present study, we investigated ABA restriction on Cd2+ uptake and the relevance to Cd2+ stress alleviation in Cd2+-hypersensitive Populus euphratica. ABA (5 μM) markedly improved cell viability and growth but reduced membrane permeability in CdCl2 (100 μM)-stressed P. euphratica cells. Moreover, ABA significantly increased the activity of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and ascorbate peroxidase (APX), contributing to the scavenging of Cd2+-elicited H2O2 within P. euphratica cells during the period of CdCl2 exposure (100 μM, 24–72 h). ABA alleviation of Cd2+ toxicity was mainly the result of ABA restriction of Cd2+ uptake under Cd2+ stress. Steady-state and transient flux recordings showed that ABA inhibited Cd2+ entry into Cd2+-shocked (100 μM, 30 min) and short-term-stressed P. euphratica cells (100 μM, 24–72 h). Non-invasive micro-test technique data showed that H2O2 (3 mM) stimulated the Cd2+-elicited Cd2+ influx but that the plasma membrane (PM) Ca2+ channel inhibitor LaCl3 blocked it, suggesting that the Cd2+ influx was through PM Ca2+-permeable channels. These results suggested that ABA up-regulated antioxidant enzyme activity in Cd2+-stressed P. euphratica and that these enzymes scavenged the Cd2+-elicited H2O2 within cells. The entry of Cd2+ through the H2O2-mediated Ca2+-permeable channels was subsequently restricted; thus, Cd2+ buildup and toxicity were reduced in the Cd2+-hypersensitive species, P. euphratica. 相似文献
18.
In a transgenic strain of Caenorhabditis elegans carrying a stress-inducible lacZ reporter gene, short-term sublethal exposure to heavy metals activates transgene expression. The transgene response to Cd 2+ is strongly inhibited by Ca 2+ ions; furthermore, Ca 2+ reduces the net accumulation of Cd 2+ by worms. Both Ca 2+ and a variety of calcium uptake inhibitors (nifedipine, La 3+, verapamil) depress the dose response of the transgene to Cd 2+. Calcium ionophore (A23187) slightly increases transgene activity in control and Cd 2+ treated worms, but has a much larger effect in the case of Mn 2+, reflecting its much greater affinity for this ion. 相似文献
19.
Recent studies have shown that ionic cadmium (Cd 2+) can selectively damage the tight junctions between LLC-PK 1 cells. The objective of the present studies was to determine if cadmium that is bound to metallothionein (Cd-Mt) can also damage the junctions between these cells. Cells on Falcon Cell Culture Inserts were exposed to Cd 2+ or Cd-Mt from the apical and basolateral compartments. The integrity of cell junctions was assessed by monitoring the transepithelial electrical resistance, and cell viability was evaluated by monitoring the release of lactate dehydrogenase into the medium. Exposure to Cd 2+ for 1–4 hours caused a pronounced decrease in the transepithelial resistance without affecting cell viability. By contrast, exposure to Cd-Mt had little effect on the electrical resistance until the cells began to die, which did not occur until 24–48 hours of exposure. Additional results showed that the cells accumulated Cd 2+ more rapidly than Cd-Mt. These results indicate that Cd-Mt does not damage the junctions between LLC-PK 1 cells, but that it can kill the cells after prolonged exposure. 相似文献
20.
The uptake of K + and Ca 2+ in Dunaliella salina is mediated by two distinct carriers: a K + carrier with a high selectivity against Na +, Li +, and choline + but not towards Rb +, K +, Cs +, or NH 4+, and a Ca 2+ carrier with a high selectivity against Mg 2+. The latter is specifically blocked by La 3+ and by Cd 2+. Apparent Km values for K + and Ca 2+ uptake are 2.5 and 0.8 millimolar, respectively, and their maximal calculated fluxes are 22 and 0.8 nanomoles per square meter per second, respectively. Effects of permeable ions and ionophores on K + and Ca 2+ uptake suggest that the driving force for their uptake is the transmembrane electrical potential. Inhibitors of ATP production, typical inhibitors of plasma membrane H +-ATPases and protonionophores inhibit K + and Ca 2+ uptake and accelerate K + efflux. The results suggest that an H +-ATPase in the cell membrane provides the driving force for K + and Ca 2+ uptake. Efflux measurements from 86Rb + and 45Ca 2+ loaded cells suggest that part of the intracellular K + and most of the intracellular Ca 2+ is nonexchangeable with the extracellular pool. Correlations between phosphate and K + contents and the effect of phosphate on K + efflux suggest intracellular associations between K + and polyphosphates. On the basis of these results, it is suggested that: (a) K + and Ca 2+ uptake in D. salina is driven by the transmembrane electrical potential which is generated by the action of an H +-ATPase of the plasma membrane. (b) Part of the intracellular K + is associated with polyphosphate bodies, while most of the intracellular Ca 2+ is accumulated in intracellular organelles in the algal cells. 相似文献
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