盐胁迫下不同的钙盐对小麦幼苗耐盐性的影响

利用Ｃａ（ＮＯ３）２和ＣａＣｌ２可以提高生长在盐渍条件下小麦幼苗的耐盐能力,增加幼苗的干、鲜重。其原因是由于两种钙盐均能防止膜脂过氧化,降低质膜透性,减少细胞内营养物质外渗,阻止Ｎａ＋进入细胞。实验结果证明,在降低小麦幼苗盐害方面,Ｃａ（ＮＯ３）２好于ＣａＣｌ２。讨论了两个钙盐在降低盐害机理方面的差异     

氯化钙浸种对玉米幼苗抗逆性的影响及其与谷胱甘肽还原酶的关系

两个抗逆性不同的玉米品种经过CaCl2 浸种处理后 ,能显著提高其幼苗在低温、高温、干旱和盐胁迫下的存活率 ;相反 ,Ca2 螯合剂EGTA浸种处理会降低玉米幼苗在上述逆境胁迫下的存活率 ,表明外源Ca2 处理能增强玉米幼苗对低温、高温、干旱和盐胁迫的多重抗逆性。此外 ,Ca2 浸种处理能使玉米幼苗在多种逆境胁迫下保持相对较高的谷胱甘肽还原酶 (GR)活性 ,而EGTA处理正好相反 ,表明GR可能参与了Ca2 提高的玉米幼苗多重抗逆性的调控     

Ca(NO3)2对NaCl胁迫下木麻黄扦插苗生理特征的调控

用不同浓度 Ca(NO3) 2 · 4 H2 O(0 .7、1.4、2 .1g Ca2 / kg土 )对 1年生的处在两种 Na Cl胁迫 (10和 2 0 g/ kg)处理下的木麻黄扦插苗进行化学调控 ,研究硝酸钙盐加氯化钠处理的木麻黄幼苗的生长量、木麻黄幼苗抗氧化酶系统活性和渗透调节物质的含量的变化 ,研究结果表明 :中度 Na Cl胁迫加硝酸钙处理下的木麻黄扦插苗的可溶性蛋白质含量增加 ,MDA含量降低说明膜脂过氧化作用减轻 ,而且抗氧化酶活性 (SOD、POD)之间协调变化有利于提高清除自由基的速率 ,中度盐胁迫下钙盐可以促进木麻黄体内脯氨酸的积累 ;但重度 Na Cl胁迫下钙盐对木麻黄的调控作用不显著 ,重度盐胁迫下钙盐反而降低木麻黄 SOD、POD活性和脯氨酸的含量 ,减弱了抗氧化酶系统对活性氧的清除作用 ,同时高浓度钙盐还会加重 Na Cl胁迫对木麻黄幼苗的损伤 ,这说明适量的钙盐有利于木麻黄幼苗抵抗盐胁迫能力的提高 ,而高浓度钙盐则可能会加重盐胁迫     

Ca~(2 )对盐胁迫下黄瓜幼苗中CaM、MDA含量和质膜透性的影响(简报)

添加CaCl2可提高黄瓜幼苗中CaM含量,降低MDA（丙二醛）和质膜透性,减轻盐害,添加CaM抑制剂CPZ（氯丙嗪）、TFP（三氟拉嗪）则取得相反效果。添加外源CaM可降低CaM在体内合成,起到降低盐害作用。     

等渗Ca（NO3）2和NaCl胁迫对黄瓜砧用南瓜幼苗生长和活性氧代谢的影响

以黄瓜砧用黑籽南瓜和白籽南瓜幼苗为材料,通过营养液栽培研究了等渗Ca(NO3)2和NaCl胁迫对南瓜幼苗生长和活性氧代谢的影响。结果表明,不同盐胁迫下两砧木幼苗生长和抗氧化系统活性均受到不同程度抑制;与黑籽南瓜相比,白籽南瓜‘青砧1号’植株的生物量和SOD、POD和CAT活性均较高,而盐害指数、膜相对透性、MDA含量及O2.-产生速率则明显降低。等渗Ca(NO3)2和NaCl对两砧木南瓜幼苗的盐胁迫效应不同,Ca(NO3)2胁迫对砧木生长的抑制作用及盐害指数、膜相对透性、MDA含量、O2.-产生速率均小于等渗的NaCl处理,而其SOD、POD、CAT活性高于NaCl处理。可见,白籽南瓜‘青砧1号’具有较强的生长势和有效清除体内活性氧能力,有效降低膜质过氧化伤害程度,这是其耐盐性高于黑籽南瓜的重要原因;Ca(NO3)2处理使两砧木幼苗细胞受氧化损伤程度较轻,对植株生长的抑制程度明显低于等渗的NaCl。     

Ca^2＋对小麦萌发及幼苗抗盐性的效应

以冬小麦（Triticum aestivum）临远077038为材料, 研究了施入外源Ca^2＋对150、200、250及350 mmol·L^-1NaCl胁迫下小麦种子萌发及幼苗生长发育的影响。结果表明： 20 mmol·L^-1CaCl2浸种能够提高小麦在150–250 mmol·L^-1盐胁迫下种子的发芽率, 并能增强其生长势; 当NaCl浓度为350 mmol·L^-1时, 小麦种子不能萌发, 且在以上浓度的NaCl胁迫下, 小麦种子均不能发育成苗。对NaCl胁迫下的小麦幼苗施入外源Ca^2＋后, 提高了幼苗膜稳定性, 降低了膜脂过氧化程度, 从而减轻了盐胁迫对幼苗膜的伤害, 表现为电导率降低、MDA含量降低及SOD和POD活性提高, 并且提高了幼苗的呼吸强度及叶绿素含量, 促进了幼苗生长及生物量的积累; Ca^2＋的缓解效应随着盐胁迫的加剧逐渐减弱, 在浓度为350 mmol·L^-1的盐胁迫下, 幼苗的生物量显著低于对照。以上结果表明, 与水处理相比, 20 mmol·L^-1CaCl2处理能够更大程度地促进小麦的生长发育。     

钙离子对盐胁迫小麦幼苗氮代谢的影响

为探讨增强小麦抗盐能力的调控途径,以普通小麦豫麦34为材料,研究了Ca2+对盐胁迫下小麦幼苗氮代谢及生长的影响.采用全营养液培养小麦幼苗至第一片叶完全展开,更换无钙营养液,并开始不同处理.处理分别为低盐胁迫(150 mmol · L-1 NaCl)、低盐胁迫+4 mmol · L-1 Ca2+、高盐胁迫(300 mmol · L-1 NaCl)、高盐胁迫+4mmol · L-1 Ca2+,以无NaCl胁迫的小麦为对照.5 d后取样,测定了氮同化酶活性、代谢物含量、积累量及幼苗生长状况.结果表明,Ca2+明显缓解了低盐胁迫对小麦幼苗的生长抑制,表现在鲜重、叶绿素及可溶性蛋白含量的增加,而对高盐胁迫下小麦幼苗的生长无明显改善效果;Ca2+改善了低盐胁迫下小麦幼苗的氮营养状况,表现在氮积累量的增加,这一效应主要是通过硝酸还原酶(NR)、谷氨酰胺合成酶(GS)以及异柠檬酸脱氢酶(NADP-ICDH)活性的增强而实现的.Ca2+未能改善高盐胁迫下小麦幼苗氮营养状况的主要限制因子在于NADP-ICDH活性未明显增加.     

不同盐胁迫下小麦叶片渗透性调节和叶绿素荧光特性

盐胁迫对植物伤害机理受到普遍关注。本试验以‘西旱3号’小麦幼苗为材料,通过比较钠盐(150 mmol·L^-1)、钙盐(5、30 mmol·L^-1)单独及其复合胁迫对叶片渗透调节和光合特性的影响,揭示不同盐胁迫对小麦的伤害机理。结果表明: 钠盐或钙盐单独胁迫显著抑制了小麦幼苗根、茎的生长,使叶片可溶性糖和脯氨酸含量、调节性能量耗散电子产量、非光化学猝灭及玉米黄质相对含量均显著增加,而叶绿素a和叶绿素b含量、最大光化学效率、PSⅡ实际光化学效率、光化学猝灭及光合电子传递效率均显著下降。此外,钙盐对小麦幼苗生长的抑制作用更强,钠盐处理下叶片叶绿素含量减少和叶绿素荧光参数降低更显著。除了可溶性蛋白、叶黄素和玉米黄质相对含量以外,低浓度钙盐有效缓解了钠盐诱导其他各指标的变化,而高浓度钙盐进一步增大了钠盐处理小麦幼苗各参数的变化幅度。总之,钠盐和钙盐显著抑制了小麦幼苗的生长,低浓度钙盐能有效缓解钠盐对小麦幼苗的伤害,而高浓度钙盐加剧了钠盐的毒害作用。这均与叶片光合色素含量、光能捕获及光合电子传递的改变有关。此外,渗透调节物质在增强钠盐或钙盐环境中小麦幼苗的抗性方面发挥着重要作用。     

钙对大麦幼苗盐胁迫的缓解效应

CaSO_4,Ca(NO_3)_2 ,CaCl_2三种钙盐缓解大麦幼苗的盐胁迫效应中,以Ca(NO_3)_2最为显著,Ca_(2 )/Na~ =1/10时最佳。钙提高盐胁迫下大麦种子α—淀粉酶活性是促进萌发的主要原因。     

钠盐和钙盐胁迫对草莓光合作用的影响

以草莓(Fragaria ananassaDuch.)达塞莱克特品种为试材,采用盆栽法研究了NaCl、CaCl2、Ca(AC)2和Ca(NO3)2胁迫对其生长及光合特性的影响.结果表明,4种盐胁迫下草莓的生物产量、叶绿素含量、净光合速率、蒸腾速率和气孔导度显著降低,且盐浓度越高,下降幅度越大.其中,净光合速率、蒸腾速率和气孔导度的降幅由大到小依次为:Ca(AC)2>Ca(NO3)2>CaCl2>NaCl.与对照相比,NaCl胁迫下草莓根冠比减小,而钙盐胁迫下草莓的根冠比增大,且各盐处理内均随盐浓度增加而增大.钙盐胁迫对草莓光合作用的影响大于钠盐,其中,NaCl胁迫对植株的伤害最小,Ca(AC)2处理的伤害最大.     

黄瓜砧用白籽南瓜对不同盐胁迫的耐性评价

采用营养液栽培,研究Ca(NO3)2和NaCl胁迫对黄瓜嫁接用砧木南瓜幼苗生长和抗氧化酶活性的影响,并用隶属函数法综合评价其耐盐性.结果表明:低浓度盐30 mmol·L-1Ca(NO3)2和等渗的45 mmol·L-1 NaCl处理促进砧木幼苗生长;高浓度盐60、120 mmol·L-1Ca(NO3)2和等渗的90、180 mmol·L-1NaCl胁迫下,各砧木幼苗的生长和抗氧化酶系统均受到不同程度的抑制,其中,‘青砧1号’的盐害指数最小,生物量及超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)活性的下降幅度以及相对电导率的上升幅度均小于其他砧木.高盐Ca(NO3)2胁迫下,各砧木SOD、POD和CAT酶活性均高于等渗的NaCl,而盐害指数和相对电导率低于NaCl,表明Ca(NO3)2对砧木南瓜幼苗生长的危害小于NaCl.4个砧木品种的耐盐性顺序为‘青砧1号’＞‘佐木南瓜’＞‘丰源铁甲’＞‘超霸南瓜’.     

Expression of Trp3 determines sensitivity of capacitative Ca2+ entry to nitric oxide and mitochondrial Ca2+ handling: evidence for a role of Trp3 as a subunit of capacitative Ca2+ entry channels

The role of Trp3 in cellular regulation of Ca(2+) entry by NO was studied in human embryonic kidney (HEK) 293 cells. In vector-transfected HEK293 cells (controls), thapsigargin (TG)-induced (capacitative Ca(2+) entry (CCE)-mediated) intracellular Ca(2+) signals and Mn(2+) entry were markedly suppressed by the NO donor 2-(N,N-diethylamino)diazenolate-2-oxide sodium salt (3 microm) or by authentic NO (100 microm). In cells overexpressing Trp3 (T3-9), TG-induced intracellular Ca(2+) signals exhibited an amplitude similar to that of controls but lacked sensitivity to inhibition by NO. Consistently, NO inhibited TG-induced Mn(2+) entry in controls but not in T3-9 cells. Moreover, CCE-mediated Mn(2+) entry into T3-9 cells exhibited a striking sensitivity to inhibition by extracellular Ca(2+), which was not detectable in controls. Suppression of mitochondrial Ca(2+) handling with the uncouplers carbonyl cyanide m-chlorophenyl hydrazone (300 nm) or antimycin A(1) (-AA(1)) mimicked the inhibitory effect of NO on CCE in controls but barely affected CCE in T3-9 cells. T3-9 cells exhibited enhanced carbachol-stimulated Ca(2+) entry and clearly detectable cation currents through Trp3 cation channels. NO as well as carbonyl cyanide m-chlorophenyl hydrazone slightly promoted carbachol-induced Ca(2+) entry into T3-9 cells. Simultaneous measurement of cytoplasmic Ca(2+) and membrane currents revealed that Trp3 cation currents are inhibited during Ca(2+) entry-induced elevation of cytoplasmic Ca(2+), and that this negative feedback regulation is blunted by NO. Our results demonstrate that overexpression of Trp3 generates phospholipase C-regulated cation channels, which exhibit regulatory properties different from those of endogenous CCE channels. Moreover, we show for the first time that Trp3 expression determines biophysical properties as well as regulation of CCE channels by NO and mitochondrial Ca(2+) handling. Thus, we propose Trp3 as a subunit of CCE channels.     

Ga3+ inhibits parathyroid hormone release without interacting with the Ca2+ receptor of the parathyroid cell.

Gallium nitrate is an antihypercalcemic agent with established actions on bone. The effects of Ga(NO3)3 on parathyroid hormone (PTH) release, cytoplasmic Ca2+ concentration ([Ca2+]i) and cAMP production of enzymatically dispersed parathyroid cells from bovine as well as normal and pathological human parathyroid glands have now been studied. Ga3+ at 200 microM inhibited PTH release whereas 600 microM NO3- had no effect. The inhibition was additive to that obtained by elevating extracellular Ca2+. Unlike Ca2+, Ga3+ failed to increase [Ca2+]i or reduce cAMP formation. The results indicate that Ga3+ inhibits PTH release by a mechanism other than activation of the cation receptor of the parathyroid cells. This mechanism may contribute also to inhibition by other cations.     

等渗盐胁迫对番茄抗氧化酶和ATP酶及焦磷酸酶活性的影响

用Ca(NO3)2 80 mmol/L和NaCl 120 mmol/L等渗溶液处理番茄幼苗后,细胞质和叶绿体中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、抗坏血酸过氧化物酶(APX)的活性升高,并且NaCl胁迫的作用明显高于Ca(NO3)2胁迫.Ca(NO3)2处理提高了线粒体中SOD、CAT、APX的活性,而NaCl处理降低了它们的活性.根系质膜H -ATPase、液泡膜H -ATPase、焦磷酸酶(H -PPase)的活性和叶片丙二醛(MDA)及脯氨酸含量在两种盐胁迫后明显增加.NaCl处理对植株生长的抑制程度明显高于Ca(NO3)2处理.     

一氧化氮调节盐胁迫下小麦幼苗根部质膜H^＋-ATPase和焦磷酸酶活性提高耐盐性

采用外源一氧化氮(NO)供体硝普钠(SNP)研究了NO对盐胁迫下小麦(Triticum aestivum L.)幼苗耐盐性的影响。结果表明,0.1 mmol/L SNP处理显著缓解了150 mmol/L NaCl 胁迫对小麦幼苗生长的抑制效应,包括水分丧失以及叶绿素降解,从而提高了小麦幼苗的耐盐性。进一步结合1 mg/mL血红蛋白处理则显著逆转了SNP诱导的上述效应;利用亚硝酸钠和铁氰化钾作为对照也证实了NO对小麦幼苗耐盐性的专一性调节作用,并可能与NO对小麦幼苗根部质膜 H -ATPase和焦磷酸酶活性诱导有关。此外,尽管NO显著提高了盐胁迫下小麦幼苗根部细胞质膜H -ATPase和焦磷酸酶的ATP水解活性,但是对跨膜H 转运则没有明显影响。应用外源CaSO4 和 EGTA 处理也证实,Ca2 可能在NO诱导的质膜 H -ATPase和焦磷酸酶活性的提高过程中起信号作用。另外,分析盐胁迫下小麦幼苗根部 Na 和K 含量的变化也发现,NO对Na 含量没有明显影响,但是却显著提高了K 水平和K /Na 比,这可能也是NO提高小麦幼苗耐盐性的原因之一。     

组培条件下不同番茄品种及砧木自交系幼苗期硝酸盐耐性的比较

采用组培的方法,对15个番茄普通栽培品种的幼苗进行系列浓度Ca(NO₃)₂胁迫处理,10 d后调查不同品种单株幼苗的生长情况和盐害程度。结果表明,15个供试品种幼苗期硝酸盐耐性存在显著差异。上海903、苏红2003、阳光906、大禹中蔬4号、三星L402、番茄大红、中蔬4号、宝大903、霞粉、毛粉 802为硝酸盐敏感品种;早丰番茄、江蔬14号、宝粉和三星906为中等耐硝酸盐品种;日本大粉皇后为耐硝酸盐品种。同时对7个番茄砧木自交系（TR-1、TR-2、TR-3、TR-4、TR-5、TR-7、TR-8）进行了幼苗期高浓度Ca(NO₃)₂的耐盐分析。结果表明,砧木自交系的平均侧根数均显著高于同浓度下供试的普通番茄栽培品种,盐胁迫指数均显著低于普通栽培品种,具有较强的耐盐性;其中TR-8耐盐性最强。     

Autocrine action and its underlying mechanism of nitric oxide on intracellular Ca2+ homeostasis in vascular endothelial cells

The rise in cytosolic Ca(2+) concentration (Ca(2+)(i)) in vascular endothelial cells (ECs) activates the production and release of nitric oxide (NO). NO modifies Ca(2+)(i) homeostasis in many types of nonendothelial cells. However, its effect on endothelial Ca(2+)(i) homeostasis at basal and excited states remains unclear. In the present study, to elucidate the effect of NO on basal Ca(2+)(i), inositol 1,4,5-trisphosphate-induced Ca(2+)(i) release (IICR) was blocked by expressing an antisense against type-1 inositol 1,4,5-trisphosphate receptors or by microinjecting heparin to individual ECs, and the effects of NO that was released by and diffused from adjacent IICR-intact ECs were recorded. After ATP or bradykinin stimulation, IICR-inhibited ECs showed a marked reduction of basal Ca(2+)(i), which was abolished by N(G)-monomethyl-l-arginine monoacetate pretreatment. The reduction disappeared in sparsely seeded ECs. Exogenous NO gas mimicked the effect of ATP or bradykinin to reduce basal Ca(2+)(i). Blocking plasma membrane Ca(2+)-ATPase (PMCA), but not Na(+)-Ca(2+) exchange or sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase, suppressed the reduction, indicating that the reduction resulted from a NO-dependent potentiation of PMCA. To elucidate the effect of NO on elevated Ca(2+)(i), ATP-, bradykinin-, or thapsigargin-evoked Ca(2+)(i) response in the presence and absence of NO production was compared in adjacent IICR-intact ECs. NO was found to potentiate PMCA, which, in turn, greatly attenuated agonist-evoked Ca(2+)(i) elevation. NO also potentiated Ca(2+) influx, which markedly increased the sustained phase of Ca(2+)(i) elevation and possibly NO production. NO did not affect other Ca(2+)(i)-elevating and Ca(2+)(i)-sequestrating components. Thus, NO-dependent potentiation of PMCA is crucial for Ca(2+)(i) homeostasis over a wide Ca(2+)(i) range.     

Bcl-2 and Bcl-X(L) block thapsigargin-induced nitric oxide generation, c-Jun NH(2)-terminal kinase activity, and apoptosis.

The proteins Bcl-2 and Bcl-X(L) prevent apoptosis, but their mechanism of action is unclear. We examined the role of Bcl-2 and Bcl-X(L) in the regulation of cytosolic Ca(2+), nitric oxide production (NO), c-Jun NH(2)-terminal kinase (JNK) activation, and apoptosis in Jurkat T cells. Thapsigargin (TG), an inhibitor of the endoplasmic reticulum-associated Ca(2+) ATPase, was used to disrupt Ca(2+) homeostasis. TG acutely elevated intracellular free Ca(2+) and mitochondrial Ca(2+) levels and induced NO production and apoptosis in Jurkat cells transfected with vector (JT/Neo). Buffering of this Ca(2+) response with 1, 2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM) or inhibiting NO synthase activity with N(G)-nitro-L-arginine methyl ester hydrochloride (L-NAME) blocked TG-induced NO production and apoptosis in JT/Neo cells. By contrast, while TG produced comparable early changes in the Ca(2+) level (i.e., within 3 h) in Jurkat cells overexpressing Bcl-2 and Bcl-X(L) (JT/Bcl-2 or JT/Bcl-X(L)), NO production, late (36-h) Ca(2+) accumulation, and apoptosis were dramatically reduced compared to those in JT/Neo cells. Exposure of JT/Bcl-2 and JT/Bcl-X(L) cells to the NO donor, S-nitroso-N-acetylpenacillamine (SNAP) resulted in apoptosis comparable to that seen in JT/Neo cells. TG also activated the JNK pathway, which was blocked by L-NAME. Transient expression of a dominant negative mutant SEK1 (Lys-->Arg), an upstream kinase of JNK, prevented both TG-induced JNK activation and apoptosis. A dominant negative c-Jun mutant also reduced TG-induced apoptosis. Overexpression of Bcl-2 or Bcl-X(L) inhibited TG-induced loss in mitochondrial membrane potential, release of cytochrome c, and activation of caspase-3 and JNK. Inhibition of caspase-3 activation blocked TG-induced JNK activation, suggesting that JNK activation occurred downstream of caspase-3. Thus, TG-induced Ca(2+) release leads to NO generation followed by mitochondrial changes including cytochrome c release and caspase-3 activation. Caspase-3 activation leads to activation of the JNK pathway and apoptosis. In summary, Ca(2+)-dependent activation of NO production mediates apoptosis after TG exposure in JT/Neo cells. JT/Bcl-2 and JT/Bcl-X(L) cells are susceptible to NO-mediated apoptosis, but Bcl-2 and Bcl-X(L) protect the cells against TG-induced apoptosis by negatively regulating Ca(2+)-sensitive NO synthase activity or expression.