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1.
Bang-Ping Jiann Yih-Chau Lu Hong-Tai Chang Jong-Khing Huang Chung-Ren Jan 《Life sciences》2002,70(26):269-3178
The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca2+ levels ([Ca2+]i) in populations of PC3 human prostate cancer cells was explored by using fura-2 as a Ca2+ indicator. Clomiphene at concentrations between 10-50 μM increased [Ca2+]i in a concentration-dependent manner. The [Ca2+]i signal was biphasic with an initial rise and a slow decay. Ca2+ removal inhibited the Ca2+ signal by 41%. Adding 3 mM Ca2+ increased [Ca2+]i in cells pretreated with clomiphene in Ca2+-free medium, confirming that clomiphene induced Ca2+ entry. In Ca2+-free medium, pretreatment with 50 μM brefeldin A (to permeabilize the Golgi complex), 1 μM thapsigargin (to inhibit the endoplasmic reticulum Ca2+ pump), and 2 μM carbonylcyanide m-chlorophenylhydrazone (to uncouple mitochondria) inhibited 25% of 50 μM clomiphene-induced store Ca2+ release. Conversely, pretreatment with 50 μM clomiphene in Ca2+-free medium abolished the [Ca2+]i increase induced by brefeldin A, thapsigargin or carbonylcyanide m-chlorophenylhydrazone. The 50 μM clomiphene-induced Ca2+release was unaltered by inhibiting phospholipase C with 2 μM 1-(6-((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). Trypan blue exclusion assay suggested that incubation with clomiphene (50 μM) for 2-15 min induced time-dependent decrease in cell viability by 10-50%. Collectively, the results suggest that clomiphene induced [Ca2+]i increases in PC3 cells by releasing store Ca2+ from multiple stores in an phospholipase C-independent manner, and by activating Ca2+ influx; and clomiphene was of mild cytotoxicity. 相似文献
2.
Chuen-Mao Yang 《Cellular signalling》1998,10(10):735-742
The relationship between the agonist-sensitive Ca2+ pool and those discharged by the Ca2+-ATPase inhibitor thapsigargin (TG) were investigated in canine tracheal smooth muscle cells (TSMCs). In fura-2-loaded TSMCs, 5-hydroxytryptamine (5-HT) stimulated a rapid increase in intracellular Ca2+ ([Ca2+]i), followed by a sustained plateau phase that was dependent on extracellular Ca2+. In such cells, TG produced a concentration-dependent increase in [Ca2+]i, which remained elevated over basal level for several minutes and was substantially attenuated in the absence of extracellular Ca2+. Application of 5-HT after TG demonstrated that the TG-sensitive compartment partly overlapped the 5-HT-sensitive stores. Pre-treatment of TSMCs with TG significantly inhibited the increase in [Ca2+]i induced by 5-HT in a time-dependent manner. Similar results were obtained with two other Ca2+-ATPase inhibitors, cyclopiazonic acid and 2,5-di-t-butylhydroquinone. Although these inhibitors had no effect on phosphoinositide hydrolysis, Ca2+-influx was stimulated by these agents. These results suggest that depletion of the agonist-sensitive Ca2+ stores is sufficient for activation of Ca2+ influx. Some characteristics of the Ca2+-influx activated by depletion of internal Ca2+ stores were compared with those of the agonist-activated pathway. 5-HT-stimulated Ca2+ influx was inhibited by La3+, membrane depolarisation, and the novel Ca2+-influx blocker 1-{β-[3-(4-methoxyphenyl) propoxy]-4-methoxyphenethyl}-1H-imidazole hydrochloride (SKF96365). Likewise, activation of Ca2+ influx by TG also was blocked by La3+, membrane depolarisation, and SKF96365. These results suggest that (1) in the absence of PI hydrolysis, depletion of the agonist-sensitive internal Ca2+ stores in TSMCs is sufficient for activation of Ca2+ influx, and (2) the agonist-activated Ca2+ influx pathway and the influx pathway activated by depletion of the inositol 1,4,5-trisphosphate-sensitive Ca2+ pool are indistinguishable. 相似文献
3.
Gregory A. Moore George E. N. Kass Steven K. Duddy Geoffrey C. Farrell Juan Llopis Sten Orrenius 《Free radical research》1990,8(4):337-345
Isolated hepatocytes and the isolated perfused rat liver have been used to study the alterations of cytosolic free Ca2+ concentration ([Ca2+]i) produced by 2,5-di(tert-butyl)-l.4-benzohydroquinone (tBuBHQ), a potent inhibitor of hepatic microsomal Ca2+ sequestration (Moore. G.A., McConkey. D.J., Kass, G.E.N., OBrien, P.J. and Orrenius, S. FEBS Lett.,224, 331-336). (1987). Addition of tBuBHQ to isolated hepatocytes caused a rapid increase in [Ca2+]i which was similar in magnitude to the [Ca2+]i elevation induced by the Ca2+ mobilizing hormone, vasopressin. In contrast with vasopressin which caused a Ca2+ transient, tBuBHQ elevated [Ca2+]i to a new steady state that was maintained for up to 15-20min. When vasopressin was administered during the tBuBHQ-induced period of elevated [Ca2+]i. [Ca2+]i, rapidly returned to basal levels. Similarly, if vasopressin was administered just prior to tBuBHQ, the resultant tBuBHQ-dependent change in [Ca2+]i was transient. and not sustained. The hydroquinone mobilized the same intracellular Ca2+ pool as inositol 1,4,5-trisphosphate. but tBuBHQ did not produce any detectable inositol polyphosphate accumulation. IBuBHQ stimulated glucose release from perifused hepatocytes. mimicking the effect of vasopressin. In the perfused liver, tBuBHQ infusion produced a single, slow and prolonged release of Ca2+ into the perfusate and inhibition of subsequent vasopressin-induced Ca2+ effluxes. Inhibition of the response to vasopressin was reversed over time, and closely correlated with the extent of inhibition of both Ca2+ sequestration and (Ca2+-Mg2+)-ATPase activity in microsomes isolated from the isolated perfused liver. The present results are consistent with tBuBHQ inhibiting ATP-dependent Ca2+ sequestration by a direct effect on the endoplasmic reticular Ca2+ pump, which results in net Ca2+ release and elevation of [Ca2+]i. Furthermore. vasopressin appears to stimulate active removal of increased [Ca2+] from the hepatocyte cytosol by a mechanism which does not depend on reuptake of Ca2+ into the endoplasmic reticulum
2,5-Di(tert-butyl) -l,4-benmhydroquinone. calcium. hepatocytes. perfused liver, endoplasmic reticulum 相似文献
2,5-Di(tert-butyl) -l,4-benmhydroquinone. calcium. hepatocytes. perfused liver, endoplasmic reticulum 相似文献
4.
高Ca2+环境对许多植物的生长不利, 因此研究植物对高Ca2+环境的适应机制非常重要。研究发现, 拟南芥(Ara- bidopsis thaliana)镁转运体MGT7功能缺失突变体mgt7-1和mgt7-2具有高Ca2+敏感表型: 在高Ca2+培养基上, 相对于野生型Col-0, 突变体叶鲜重显著下降, 但根长无显著差异。高Ca2+对MGT7启动子活性和包括MGT7在内的镁转运体基因表达无显著调节作用。Col-0与mgt7突变体之间, 在外加Ca2+诱导细胞质Ca2+瞬时升高和Ca2+含量方面无显著差异; 但是, 在正常和高Ca2+培养基上, mgt7突变体的Mg含量均显著低于Col-0。高Ca2+显著抑制Col-0和mgt7突变体内Mg的积累。因此我们假设, mgt7突变体的高Ca2+敏感表型是由于其体内Mg含量下降导致的。进一步的研究证实, 只有增加培养基中Mg2+的含量, 而不是N、P、K和S, 才可以使突变体的高Ca2+敏感表型得到恢复。 相似文献
5.
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. 相似文献
6.
Chun-Hung Lin Makoto Shimazaki Chi-Huey Wong Mamoru Koketsu Lekh Raj Juneja Mujo Kim 《Bioorganic & medicinal chemistry》1995,3(12):1625-1630
A dimeric sialyl Lewis X (SLex) glycopeptide was synthesized enzymatically in three steps from an N-linked oligosaccharide prepared from egg yolk. Treatment of delipidated hen egg yolk with the protease Orientase and neuraminidase gave a dimeric N-acetyllactosamine-containing oligosaccharide linked to asparagine. Addition of sialic acid and fucose catalyzed by -2,3-sialyltransferase and -1,3-fucosyltransferase provided the dimeric SLex, which was shown to be as active as monomeric SLex as an inhibitor of E-selectin with IC50 0.75 mM. The synthetic dimeric SLex of the mucin type (i.e. SLex linked to the 3- and 6-OH groups of Gal) is, however, about five times as active as the monomer. It is suggested that dimeric SLex glycopeptides of the mucin type would be effective ligands for E-selectin. 相似文献
7.
Ca(2+) as second messenger in PTTH-stimulated prothoracic glands of the silkworm,Bombyx mori 总被引:1,自引:0,他引:1
Measurements of Ca2+ influx and [Ca2+]i changes in Fura-2/AM-loaded prothoracic glands (PGs) of the silkworm, Bombyx mori, were used to identify Ca2+ as the actual second messenger of the prothoracicotropic hormone (PTTH) of this insect. Dose-dependent increases of [Ca2+]i in PG cells were recorded in the presence of recombinant PTTH (rPTTH) within 5 minutes. The rPTTH-mediated increases of [Ca2+]i levels were dependent on extracellular Ca2+. They were not blocked by the dihydropyridine derivative, nitrendipine, an antagonist of high-voltage-activated (HVA) Ca2+ channels, and by bepridil, an antagonist of low-voltage-activated (LVA) Ca2+ channels. The trivalent cation La3+, a non-specific blocker of plasma membrane Ca2+ channels, eliminated the rPTTH-stimulated increase of [Ca2+]i levels in PG cells and so did amiloride, an inhibitor of T-type Ca2+ channels. Incubation of PG cells with thapsigargin resulted in an increase of [Ca2+]i levels, which was also dependent on extracellular Ca2+ and was quenched by amiloride, suggesting the existence of store-operated plasma membrane Ca2+ channels, which can also be inhibited by amiloride. Thapsigargin and rPTTH did not operate independently in stimulating increases of [Ca2+]i levels and one agent’s mediated increase of [Ca2+]i was eliminated in the presence of the other. TMB-8, an inhibitor of intracellular Ca2+ release from inositol 1,4,5 trisphosphate (IP3)-sensitive Ca2+ stores, blocked the rPTTH-stimulated increases of [Ca2+]i levels, suggesting an involvement of IP3 in the initiation of the rPTTH signaling cascade, whereas ryanodine did not influence the rPTTH-stimulated increases of [Ca2+]i levels. The combined results indicate the presence of a cross-talk mechanism between the [Ca2+]i levels, filling state of IP3-sensitive intracellular Ca2+ stores and the PTTH-receptor’s-mediated Ca2+ influx. 相似文献
8.
M. Wakui J. Wada N. Kamimura Y. Mio T. Sasaki Y. Fukushi A. Nishiyama 《Cellular signalling》1995,7(8):783-791
The store-mediated Ca2+ entry was detected in single and cluster of rat submandibular acinar cells by measuring the Ca2+ activated ionic membrane currents. In the cells where intracellular Ca2+ was partly depleted by stimulation with submaximal concentration of acetylcholine (ACh) under a Ca2+-free extracellular condition, an employment of external Ca2+ in the absence of ACh caused a sustained increase of the K+ current without affecting the Cl− current. A renewed ACh challenge without external Ca2+ caused repetitive spikes of both K+ and Cl− currents due to the Ca2+ release. SK & F 96365 inhibited the generation of the sustained K+ current and refilling of the Ca2+ store following the Ca2+ readmission. It is suggested that the Ca2+ enters the cell through the store-mediated pathway near the K+ channels and is taken up by the store. Thus, only Ca2+ released from the store can activate both the K+ and Cl− currents. 相似文献
9.
In a previous study in frog skin (Castro et al., J. Memb. Biol. 134:15-29, 1993), it was shown that TJs experimentally disrupted by a selective deposition of BaSO4 could be re-sealed upon addition of Ca2+to the apical solution; in the absence of apical Ca2+, the normal Ca2+ activity of the Na2SO4-Ringer's bathing the basolateral side was not able to induce TJ resealing. We now show that apical Ca2+also activates the TJ sealing mechanism in frog urinary bladders. Three known procedures were utilized to increase TJ permeability, all in the absence of apical Ca2+: (i) exposure to high positive transepithelial clamping potentials; (ii) exposure of the apical surface to hypertonic solutions; and (iii) selective deposition of BaSO4 in the TJs. The resealing of the TJs was promoted by raising the concentration of Ca2+ in the apical solution. This effect of Ca2+ is not impaired by the presence of Ca2+ channel blockers (nifedipine, verapamil, Mn2+ or Cd2+) in the apical solution, indicating that junction resealing does not depend on Ca2+ entering the cells through the apical membrane. TJ resealing that occurs in response to raised apical Ca2+ most likely results from a direct effect of Ca2+, entering the disrupted TJs from the apical solution and reaching the zonula adhaerens Ca2+ receptors (E-cadherins). Protein kinase C (PKC) must play a significant role in the control of TJ assembly in this tight epithelia since the PKC inhibitor (H7) and the activator (diC8) markedly affect TJ recovery after disruption by apical hypertonicity. H7 treated tissues show marked recuperation of conductance even in the absence of apical Ca2+. In contrast, diC8 prevents tissue recuperation which normally occurs after addition of Ca2+ to the apical solution. 相似文献
10.
Richard S Perrier E Fauconnier J Perrier R Pereira L Gõmez AM Bénitah JP 《Progress in biophysics and molecular biology》2006,90(1-3):118-135
The adjustment of Ca2+ entry in cardiac cells is critical to the generation of the force necessary for the myocardium to meet the physiological needs of the body. In this review, we present the concept that Ca2+ can promote its own entry through Ca2+ channels by different mechanisms. We refer to it under the general term of ‘Ca2+-induced Ca2+ entry’ (CICE). We review short-term mechanisms (usually termed facilitation) that involve a stimulating effect of Ca2+ on the L-type Ca2+ current (ICa-L) amplitude (positive staircase) or a lessening of Ca2+-dependent inactivation of ICa-L. This latter effect is related to the amount of Ca2+ released by ryanodine receptors (RyR2) of the sarcoplasmic reticulum (SR). Both effects are involved in the control of action potential (AP) duration. We also describe a long-term mechanism based on Ca2+-dependent down-regulation of the Kv4.2 gene controlling functional expression of the repolarizing transient outward K+ current (Ito) and, thereby, AP duration. This mechanism, which might occur very early during the onset of hypertrophy, enhances Ca2+ entry by maintaining Ca2+ channel activation during prolonged AP. Both Ca2+-dependent facilitation and Ca2+-dependent down-regulation of Ito expression favour AP prolongation and, thereby, promote sustained voltage-gated Ca2+ entry used to enhance excitation–contraction (EC) coupling (with no change in the density of Ca2+ channels per se). These self-maintaining mechanisms of Ca2+ entry have significant functions in remodelling Ca2+ signalling during the cardiac AP. They might support a prominent role of Ca2+ channels in the establishment and progression of abnormal Ca2+ signalling during cardiac hypertrophy and congestive heart failure. 相似文献
11.
Light-dependent Ca2+ efflux via the Ca2+/H+ antiport in the photosynthetic purple sulfur bacterium Chromatium vinosum was inhibited by three phenothiazines: chlorpromazine; trifluoperazine and phenothiazine. The inhibitors had no effect on Ca2+ uptake by C. vinosum in the dark nor any effect on the light-dependent efflux of either Na+ or Tl+ catalyzed, respectively, by the C. vinosum Na+/H+ or K+/H+ antiports. Ruthenium red and LaCl3, neither of which inhibited light-dependent Ca2+ efflux in C. vinosum, markedly inhibited Ca2+ uptake in the dark by C. vinosum cells. Ruthenium red had no effect on the uptake of either Na+or the K+ analog T1+ by C. vinosum cells in the dark. These results have been interpreted in terms of two separate Ca2+ transport systems in C. vinosum: (i) a phenothiazine-sensitive and ruthenium red, La3+-insensitive Ca2+/H+ antiport responsible for Ca2+ efflux in the light; and (ii) a ruthenium red and La3+-sensitive but phenothiazine-insensitive Ca2+ uptake system. 相似文献
12.
Ca2+ mobilization elicited by simulation with brief pulses of high K + were monitored with confocal laser scanned microscopy in intact, guinea pig cardiac myocytes loaded with the calcium indicator fluo-3. Single wavelength ratioing of fluorescence images obtained after prolonged integration times revealed non-uniformities of intracellular Ca2+ changes across the cell, suggesting the presence of significant spatial Ca2+ gradients. Treatment with 20 μM ryanodine, an inhibitor of Ca2+ release from the SR, and 10 μM verapamil, a calcium channel blocker, reduced by 42% and 76% respectively the changes in [Ca2+]i elicited by membrane depolarization. The overall spatial distribution of [Ca2+]i changes appeared unchanged. Ca2+ transients recorded in the presence of verapamil and ryanodine (about 20% of the size of control responses), diminished in the presence of 50 μM 2-4 Dichlorbenzamil (DCB) or 5 mM nickel, two relatively specific inhibitors of the
exchange mechanism. Conversely, when the reversal potential of the
exchange was shifted to negative potentials by lowering [Na+]0 or by increasing [Na+]i by treatment with 20 μM monensin, the amplitude of these Ca2+ transients increased. Ca2+ transients elicited by membrane depolarization and largely mediated by reverse operation of Na+-Ca2+ exchange could be recorded in the presence of ryanodine, verapamil and monensin. These findings suggest that in intact guinea pig cardiac cells, Ca2+ influx through the
exchange mechanism activated by a membrane depolarization in the physiological range can be sufficient to play a significant role in excitation-contraction coupling. 相似文献
13.
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. 相似文献
14.
Using a new fluorescence imaging technique, LAMP, we recently reported that Ca2+ influx through store operated Ca2+ channels (SOCs) strongly inhibits cell coupling in primary human fibroblasts (HF) expressing Cx43. To understand the mechanism of inhibition, we studied the involvement of cytosolic pH (pHi) and Ca2+([Ca2+]i) in the process by using fluorescence imaging and ion clamping techniques. During the capacitative Ca2+ influx, there was a modest decline of pHi measured by BCECF. Decreasing pHi below neutral using thioacetate had little effect by itself on cell coupling, and concomitant pHi drop with thioacetate and bulk [Ca2+i rise with ionomycin was much less effective in inhibiting cell coupling than Ca2+ influx. Moreover, clamping pHi with a weak acid and a weak base during Ca2+ influx largely suppressed bulk pHi drop, yet the inhibition of cell coupling was not affected. In contrast, buffering [Ca2+i with BAPTA, but not EGTA, efficiently prevented cell uncoupling by Ca2+ influx. We concluded that local Ca2+ elevation subjacent to the plasma membrane is the primary cause for closing Cx43 channels during capacitative Ca2+ influx. To assess how Ca2+ influx affects junctional coupling mediated by other types of connexins, we applied the LAMP assay to Hela cells expressing Cx26. Capacitative Ca2+ influx also caused a strong reduction of cell coupling, suggesting that the inhibitory effect by Ca2+ influx may be a more general phenomenon. 相似文献
15.
A wasp venom, mastoparan, rapidly increased the cytosolic free Ca2+ concentration ([Ca2+]i) and activated phosphorylase in rat hepatocytes in a concentration-dependent manner. Mastoparan could increase [Ca2+]i even in the absence of extracellular Ca2+, but a larger increase was observed in the presence of extracellular Ca2+. Thus, mastoparan mobilized Ca2+ from intracellular and extracellular Ca2+ stores. It also activated inositol triphosphate (IP3) accumulation, but did not stimulate cAMP production. From these results, we conclude that mastoparan activates rat hepatic glycogenolysis mediated by the accumulation of IP3, which causes an increase of [Ca2+]i but not that mediated by cAMP. 相似文献
16.
Marsha A. Black Geoffrey A. R. Mealing James F. Whitfield Jean-Louis Schwartz Nicole B gin-heick 《Cellular signalling》1994,6(8):897-904
Glucose-induced insuline release, glucose-induced rises in intracellular free Ca2+ concentration ([Ca2+]i), and voltage-dependent Ca2+ channel activity were assessed in monolayer cultures of β-vells 3–5 day-old rats. The glucose-stimulated insulin secretory responses and [Ca2+]i rises were like those in adult rat β-cells rather than fetal rat β-cells. Voltage-dependent Ca2+ channel antagonists decreased glucose-induced insulin secretion, aborted the [Ca2+]2 rise and, like deprivation of extracellular Ca2+, prevented the glucose-induced rise in [Ca2+]i when added before the glucose challenge. The presence of nifedipine-sensitive, voltage-dependent Ca2+ channels was demonstrated directly by measuring Ca2+ currents using the whole-cell configuration of the patch-clamp technique and indirectly by measuring [Ca2+]1 after membrane depolarization by 45 mMm K+ or 200 μM tolbutamide. Thus, in cultured β-cells of 3–5 day-old rats the coupling of glucose stimulation to Ca2+ influx is essentially mature, in contrast to what has been reported for fetal or very early neonatal cells. 相似文献
17.
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. 相似文献
18.
Stanko S. Stojilkovi Antonio Torsello Toshihiko Iida Eduardo Rojas Kevin J. Catt 《The Journal of steroid biochemistry and molecular biology》1992,41(3-8):453-467
In cultured pituatary gonadotrophs, gonadotropin-releasing hormone (GnRH) caused dose-dependent and biphasic increases in cytoplasmic calcium concentration ([Ca2+]i) and LH release. Both extra- and intracellular calcium pools participate in GnRH-induced elevation of [Ca2+]i and LH secretion. The spike phase of the [Ca2+]i response represents the primary signal derived predominantly from the rapid mobilization of intracellular Ca2+. In contrast, the prolonged phase of the Ca2+ signal depends exclusively on Ca2+ entry from the extracellular pool. The influx of Ca2+ occurs partially through dihydropyridine-sensitive calcium channels. Both [Ca2+]i and LH responses to increasing concentrations of GnRH occur over very similar time scales, suggesting that increasing degrees of receptor occupancy are transduced into amplitude-modulated Ca2+ responses, which in turn activate exocytosis in a linear manner. However, several lines of evidence indicated the complexity over the relationship between Ca2+ signaling and LH exocytosis. In contrast to [Ca2+]i measurements in cell suspension, single cell Ca2+ measurements revealed the existence of a more complicated pattern of Ca2+ response to GnRH, with a biphasic response to high agonist doses and prominent oscillatory responses to lower GnRH concentrations, with a log-linear correlation between GnRH dose and the frequency of Ca2+ spiking. In addition, analysis of the magnitudes of the magnitudes of the [Ca2+]i and LH responses of gonadotrophs to a wide range of GnRH concentrations in the presence and absence of extracellular Ca2+, and to K+ and phorbol ester stimulation, showed non-linearity between these parameters with amplification of [Ca2+]i-mediated exocytosis. Studies on cell depleted of protein kinase C under conditions that did not change the LH pool suggested the participation of protein kinase C in this amplication, especially during the plateau phase of the secretory response to GnRH. 相似文献
19.
Hans W. M. Niessen Taco W. Kuijpers Dirk Roos Arthur J. Verhoeven 《Cellular signalling》1991,3(6):625-633
We have used a continuous spectrofluorimetric method to analyse the role of cytosolic free Ca2+ ([Ca2+]i) in the lysosomal enzyme release from the azurophilic granules in human neutrophils stimulated with f-Met-Leu-Phe (fMLP) in the presence of cytochalasin B. Measurements were performed with the β-glucuronidase substrate 4-methylumbelliferyl-β-
-glucuronide. We found that the transient rise in [Ca2+]i induced by fMLP is a necessary signal to obtain to obtain maximal degranulation. When this Ca2+ transient is prevented by the Ca2+ chelator BAPTA, degranulation can still be induced by a stimulated Ca2+ influx, albeit to a lower extent. We also studied the degranulation process in the neutrophils of a patient with a generalized chemotactic defect. Release of β-glucuronidase from the patient's neutrophils could not be induced despite the occurrence of a normal Ca2+ response and normal degranulation of specific granules. We conclude that, besides an increase in [Ca2+]i], an additional signal is required for the fusion of azurophilic granules with the plasma membrane in human neutrophils. 相似文献
20.
Chao YY Jan CR Ko YC Chen JJ Jiann BP Lu YC Chen WC Su W Chen IS 《Life sciences》2002,70(26):4367-3121
The effect of five lignans isolated from Hernandia nymphaeifolia on estrogenic compounds (17β-estradiol, tamoxifen and clomiphene)-induced Ca2+ mobilization in human neutrophils was investigated. The five lignans were epi-yangambin, epi-magnolin, epi-aschantin, deoxypodophyllotoxin and yatein. In Ca2+–containing medium, the lignans (50–100 μM) inhibited 10 μM 17β-estradiol- and 5 μM tamoxifen-induced increases in intracellular free Ca2+ levels ([Ca2+]i) without changing 25 μM clomiphene-induced [Ca2+]i increase. 17β-estradiol and tamoxifen increased [Ca2+]i by causing Ca2+ influx and Ca2+ release because their responses were partly reduced by removing extracellular Ca2+. In contrast, clomiphene solely induced Ca2+ release. The effect of the lignans on these two Ca2+ movement pathways underlying 17β-estradiol- and tamoxifen-induced [Ca2+]i increases was explored. All the lignans (50–100 μM) inhibited 10 μM 17β-estradiol-and 5 μM tamoxifen-induced Ca2+ release, and 17β-estradiol-induced Ca2+ influx. However, only 100 μM epi-aschantin was able to reduce tamoxifen-induced Ca2+ influx while the other lignans had no effect. Collectively, this study shows that the lignans altered estrogenic compounds-induced Ca2+ signaling in human neutrophils in a multiple manner. 相似文献