一氧化氮对不同耐旱性杨树幼苗抗旱性的影响

以乡土树种小青杨(Populus pseudo-simonii Kitag)和速生品种欧美杨107杨(Populus × euramericana cv."74/76")幼苗为试验材料,在水分胁迫条件下研究不同浓度的外源NO供体硝普纳(sodium nitroprusside, SNP)对2种杨树抗旱性的影响.结果表明,经不同浓度SNP处理后,2种杨树叶片水势对干旱胁迫的敏感程度下降,气孔导度降低,蒸腾作用减弱,叶片含水量升高,保水能力增强.同时,SNP处理能提高杨树叶片可溶性糖和可溶性蛋白含量,降低杨树叶片相对电导率,使杨树在干旱条件下的抗脱水能力提高,减轻了干旱胁迫对细胞膜的伤害.从品种间作用效果看,SNP对107杨的抗旱性提高的幅度高于小青杨,表明SNP更有利于提高速生杨的抗旱能力.     

外源一氧化氮对干旱胁迫下杨树光合作用的影响

NO是生物体中一种自由基分子,其NO对树木叶片光合作用的影响研究未见报道.本文研究了外源NO对杨树叶片水分状况、光合作用和抗氧化物酶活力的调节作用.不同浓度SNP处理对杨树叶片含水量具有显著影响,杨树叶片含水率随着SNP浓度的提高而增加.当SNP浓度增加到00μmol·L^-1后各处理杨树叶片含水率变化趋于稳定.外源NO能提高水分胁迫下杨树叶片的光合、原初光能转化率Fv/Fm、Fm/Fo和Fv/Fo等的比值.其效果随水分胁迫时间的延长而降低.与此对应的是,短时间水分处理(1 h)的杨树叶片SOD和POD抗氧化物酶的活性显著高于长时间(3h)水分胁迫处理.SNP能显著提高不同干旱时间处理组的POD活性,而对SOD活性影响不明显.同时,随SNP浓度的增加,POD和SOD活性呈现先升后降的趋势.因此,干旱胁迫可引起杨树叶片光合效率降低,出现氧化伤害症状,外源NO可诱导抗氧化物酶POD和SOD活性的升高,缓解原初光能转化率Fv/Fm、Fm/Fo和Fv/Fo等值的降低,从而延缓活性氧积累,减轻水分胁迫对杨树叶片光合作用的影响.     

外源一氧化氮对镉胁迫下玉米幼苗根生长及氧化伤害的影响

以玉米幼苗为材料,通过在镉处理的同时补充外源一氧化氮(NO)供体硝普钠(SNP)及其类似物[K3Fe(CN)6]、以及NO消除剂,分析NO对植物耐镉性的影响,探讨NO在植物逆境胁迫响应中的作用及其机理。结果显示:添加20μmol·L-1 SNP能显著降低镉引发的玉米幼苗根生长抑制及根尖内源镉的积累,减少电解质的渗漏以及超氧化物自由基(O2.-)和过氧化氢(H2O2)的上升幅度,抑制超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、抗坏血酸过氧化物酶(APX)活性的增加,进一步提高镉胁迫下谷胱甘肽还原酶(GR)的活性。SNP的上述效应可被NO消除剂2-(4-羧基-2-苯基)-4,4,5,5-四甲基咪唑-1-氧-3-氧化物(cPTIO)所逆转,而SNP类似物K3Fe(CN)6的应用对上述反应几乎无影响,说明该反应具有NO特异性。研究表明,外源NO能够显著缓解镉胁迫对玉米幼苗生长造成的伤害,该缓解作用主要是通过降低植株体内内源镉积累和减轻镉诱发的氧化伤害来实现的。     

水分亏缺对作物的伤害

全世界干旱、半干旱地区的总面积约占总陆地面积的1/3。中国是世界上主要的干旱国家之一,全国干旱、半干旱地区约占总国土面积的一半左右。干旱是制约我国西北和整个北方地区农业生产发展的基本自然因素,其他地区在作物生长季节也发生不同程度的干旱危害。研究作物水分胁迫及其伤害生理,不仅在理论上而且在实践中都有重要意义。     

丛枝菌根真菌对植物耐旱性的影响研究进展

丛枝菌根真菌(arbuscular mycorrhizal fungi,AMF)能与植物根系形成互惠共生体,对植物的生长发育和抗逆性有积极的影响,在改善植物水分代谢和提高植物耐旱性中发挥了重要作用.本文综述了近年来AMF与植物水分代谢关系的研究进展,从植物的光合作用、蒸腾与气孔导度、水分利用效率、水力导度、渗透调节、内源激素和抗氧化系统等方面说明AMF对植物水分代谢的影响.从4个方面介绍了AMF提高植物耐旱性的机理:1)菌丝网络增加植物根系吸收范围;2)增强植物保水能力和抗氧化能力;3)稳定和改善土壤团聚体;4)促进植物养分吸收.并提出今后研究需注意的问题和建议.     

外源EBR和NO信号对低温胁迫下玉米种胚抗氧化系统和低温响应基因表达的影响

以玉米主栽品种先玉335为试材,研究24-表油菜素内酯(EBR)对低温胁迫下玉米种胚抗氧化能力和低温响应基因表达的影响.结果表明:EBR浸种处理后,玉米种子活力指数和早期幼苗生长显著提高,种胚中超氧自由基(O2(-))含量明显降低,抗氧化酶(包括超氧化物歧化酶SOD、过氧化物酶POD、过氧化氢酶CAT和谷胱甘肽还原酶GR等)活性和非酶类抗氧化物质谷胱甘肽GSH及脯氨酸含量升高,同时促进一氧化氮(NO)的累积,而使用NO清除剂c-PTIO和NO合成酶抑制剂L-NAME处理后,种胚中CAT、POD和脯氨酸含量有所下降,但是外源NO可提高种胚中CAT、POD和脯氨酸的含量,表明EBR诱导的玉米种胚抗氧化能力增加是通过NO介导的.低温胁迫诱导玉米幼胚中P5CS1、CBF1、CBF3和COR15a等基因的表达,EBR处理基因表达进一步提高,而c-PTIO和L-NAME处理基因表达降低;NO供体SNP则提高了这些基因的表达,这表明EBR可能通过NO途径调控低温响应基因的表达.可见,外源EBR可通过NO途径增强玉米种胚抗氧化能力和调控低温响应基因的表达,进而提高低温胁迫的耐受性.     

不同耐旱性水稻幼苗对氧化胁迫的应用

干旱条件下水稻（Ｏｒｙｚａ ｓａｔｉｖａ Ｌ．）耐旱性较强的“湘中籼２号”比耐旱性较弱的“湘早籼１２号”Ｏ＾７２的产生速率低。百草枯（０．０１ｍｍｏｌ／Ｌ）和Ｈ２Ｏ２（１０ ｍｍｏｌ／Ｌ）处理进干旱对水稻幼苗的伤害,但耐早性较强的品种伤害较轻。单独用百草枯处理后,耐旱性较强的品种比耐旱性较弱的品种能更大幅度地提高超氧化经酶的过氧化物酶的活性;而Ｈ２Ｏ２处理后耐旱性较强的品种能提高过氧化氯酶活性。这     

盐分胁迫对杨树苗期生长和土壤酶活性的影响

通过盐分胁迫下杨树2个无性系的盆栽试验,发现盐分对苗木的生长有一定的抑制作用.随着盐分浓度的提高,苗高、地上与地下部分生物量都呈下降趋势;当盐分浓度为0.2%、0.4%、0.6%和0.8%时,P₁、P₂的新稍生长量分别比对照下降23.24%、48.56%、70.76%、83.33%和71.77%、83.25%、86.28%、91.39%;P₂地上生物量分别比对照下降72.44%、82.92%、92.82%和94.41%.回归分析发现,盐分浓度与叶片叶绿素含量之间存在线性相关关系,与脯氨酸含量之间存在抛物线形相关关系.土壤中盐分的增加不仅影响到植物的生长发育,而且对土壤自身的物理、化学性状也产生不良效应.同时测定了盆栽土壤中葡萄糖苷酶和左旋天门冬酰胺酶活性的变化.结果表明,两种酶活性都随土壤中盐分浓度的提高而下降.当盐分浓度为0.2%、0.4%、0.6%和0.8%时,P₁土壤中葡萄糖苷酶活性分别比对照下降了10.96%、20.07%、30.96%和37.44%;而P₂土壤中葡萄糖苷酶活性分别比对照下降11.21%、18.94%、34.89%和41.31%,说明盐分对土壤的理化性状和肥力状况都产生了不良影响.参试的2个无性系中,P₁的耐盐能力强于P₂.     

不同土壤水分状况对杨树、沙棘水分关系及生长的影响

在盆栽条件下对杨树、沙棘进行了3种土壤水分处理,研究结果表明：沙棘的叶含水率在同一土壤水分下比杨树高、而水势低,说明沙棘叶的抗旱保水能力强于杨树;沙棘单叶的光合速率能够长时间维持在较高的水平,蒸腾速率却并非如此。杨树无论在生长初期,还是生长中期其单叶WUE均高于沙棘。以新生枝生物量／耗水总量计算的整体WUE在3种土壤水分条件下,杨树的WUE分别是沙棘的2．4倍、2．3倍、2倍,其差异达极显著水平,但在3种土壤水分条件下2个树种都以中度亏缺下的水分利用率最高。整个生长季节处在严重干旱下的杨树和沙棘的生长均受到显著影响,沙棘生长受干旱影响程度小于杨树,从整个生长趋势上看杨树适宜于良好水分下的生长,沙棘在适宜水分和中度亏缺下均可良好生长。     

水分胁迫对小麦根细胞质膜氧化还原系统的影响

水分胁迫使小麦根质膜ＮＡＤＨ和ＮＡＤＰＨ的氧化速率及Ｆｅ（ＣＮ）６＾３－和ＥＤＴＡ－Ｆｅ＾３＋的还原速率明显降低。对照与胁迫处理的质膜氧化还原系统活性均不受鱼藤酮、抗霉素Ａ和ＤＣＮ等呼吸链抑制剂的影响。在不加Ｆｅ（ＣＮ）６＾－３作为电子受体时,水杨基羟肟酸（ＳＨＡＭ）可明显刺激质膜ＮＡＤＨ的氧化和Ｏ２吸收速率。水分胁迫促使ＳＨＡＭ刺激的ＮＡＤＨ氧化明显降低,但却使Ｏ２吸收略有上升。     

南京市城市化过程中聚落动态的热点分析

利用南京市1988、1998、2003和2006年的Landsat TM遥感影像,采用邻域分析方法,提取1988—2006年间3个时段南京地区聚落占地率变化速率最快的5%区域作为聚落动态的热点,并对其空间分布格局的变化规律进行了研究。结果表明：聚落增长热点和萎缩热点总体上随城市的扩张而外移,其中,增长热点主要发生于建成区边缘外侧6 km以内的区域,而萎缩热点的高发区位于建成区边缘外侧1 km以内,在城乡梯度上二者都随离建成区边缘距离的增加而减少。在不同方向上,热点发生的频度、幅度具显著的差异性,且表现出易受短期城市发展决策的影响,阶段性重点开发地区往往成为聚落变化的热点,并导致热点集中分布区位的阶段性差异。某一时期萎缩热点在空间上集中分布的区位往往是前一时期增长热点集中发生的区位,反映了城市化过程中聚落快速增长后可能伴随着相对较大规模的重组、整合过程。     

外源NO对铜胁迫下番茄幼苗根系抗坏血酸谷胱甘肽循环的影响

采用营养液培养方法,研究外源NO对铜胁迫下番茄(Lycopersicon esculentum Mill.)幼苗根系抗坏血酸(AsA)-谷胱甘肽(GSH)循环中抗氧化物质和抗氧化酶系的影响.结果表明：外施适量NO(硝普钠)可提高铜胁迫下番茄幼苗根系AsA、GSH含量和AsA/DHA(氧化型抗坏血酸)、GSH/GSSG(氧化型谷胱甘肽),降低DHA和GSSG含量.添加100 μmol·L^-1 BSO(谷胱甘肽合成酶抑制剂)处理下,外源NO可提高铜胁迫下番茄幼苗根系的AsA含量、AsA/DHA及抗坏血酸酶(AAO)、单脱氢抗坏血酸还原酶(MDHAR)和脱氢抗坏血酸还原酶(DHAR)比活性,降低DHA、GSH、GSSG含量及抗坏血酸过氧化物酶(APX)、谷胱甘肽还原酶(GR)比活性;添加250 μmol·L^-1 BSO处理下,外源NO提高了铜胁迫下番茄幼苗根系的AsA、GSH、GSSG含量、AsA/DHA及APX和GR比活性,降低了DHA含量及AAO、DHAR和MDHAR比活性.说明外源NO影响了铜胁迫下番茄根系的AsA-GSH代谢循环,并通过调节AsA/DHA、GSH/GSSG的变化来减轻氧化胁迫,从而缓解铜胁迫对番茄根系的伤害.     

Effect of exogenous nitric oxide on sperm motility in vitro

Background

Nitric oxide (NO) has been shown to be important in sperm function, and the concentration of NO appears to determine these effects. Studies have demonstrated both positive and negative effects of NO on sperm function, but have not been able to provide a clear link between NO concentration and the extent of exposure to NO. To study the relationship between nitric oxide and sperm capacitation in vitro, and to provide a theoretical basis for the use of NO-related preparations in improving sperm motility for in vitro fertilization, we investigated the effects of NO concentration and time duration at these concentrations on in vitro sperm capacitation in both normal and abnormal sperm groups. We manipulated NO concentrations and the time duration of these concentrations using sodium nitroprusside (an NO donor) and NG-monomethyl-L-argenine (an NO synthase inhibitor).

Results

Compared to the normal sperm group, the abnormal sperm group had a longer basal time to reach the appropriate concentration of NO (p < 0.001), and the duration of time at this concentration was longer for the abnormal sperm group (p < 0.001). Both the basal time and the duration of time were significantly correlated with sperm viability and percentage of progressive sperm (p < 0.001). The experimental group had a significantly higher percentage of progressive sperm than the control group (p < 0.001).

Conclusions

We hypothesize that there is a certain regularity to both NO concentration and its duration of time in regards to sperm capacitation, and that an adequate duration of time at the appropriate NO concentration is beneficial to sperm motility.     

Involvement of nitric oxide in water stress-induced responses of cucumber roots

The effect of water deficit on nitric oxide (NO) generation was investigated in cucumber (Cucumis sativus cv. Dar) seedling roots using bio-imaging with an NO-selective fluorophor, diaminofluorescein-2-diacetate (DAF-2DA). Roots subjected to mild (5 and 10 h) water deficit showed slightly enhanced NO synthesis in cells of root tips and in the surrounding elongation zone. However, severe (17 h) stress resulted in an intensive NO production localized mainly in and above the elongation zone. Water stress-induced NO generation was blocked by a specific NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) as well as nitrate reductase (NR) and partially by nitric oxide synthase (NOS-like) inhibitors.A pharmacological approach was used in order to verify the capacity of NO to induce adaptive responses of cucumber roots to water deficit. A positive correlation was found between NO donor (SNP 100 μM and GSNO 100 μM) pretreatment and plant hydration status, measured as relative water content (RWC) during progressive dehydration. At an early stage (5 h) of stress duration NO caused a periodical increase in lipoxygenase (LOX) activity, correlated with time-dependent enhancement of lipid peroxidation. Beginning from 10 h up to severe stress (17 h) exogenous NO was able to diminish LOX activity and alleviate water deficit-induced membrane permeability and lipid peroxidation, measured as TBARS content and visualised by histochemical staining in situ. Observed changes via NO were accompanied by a significant reduction of proline level, suggesting that the accumulation of this osmolyte might not be essential in water stress tolerance. Obtained results clearly indicate that NO augmentation is likely to help the plant at the initial stage of tissue dehydration to trigger efficient mechanisms, mitigating severe water deficit effects in roots of cucumber seedlings.     

一氧化氮对增强的UV_B胁迫下螺旋藻生物损伤的减缓作用

为了探讨一氧化氮对增强的UV-B胁迫下螺旋藻生物学特性的影响,通过色素含量、蛋白质含量和生物量3个方面的变化证实了0.5mmol/L的一氧化氮(Nitric oxide,NO)供体硝普钠(Sodium nitroprusside,SNP)对增强UV-B胁迫下的螺旋藻(Spirulina platensis)794细胞生物损伤有明显的减缓作用。实验结果显示,NO能够显著诱导增强的UV-B胁迫下螺旋藻细胞内蛋白质含量、脯氨酸含量的提高,促进正常生长条件下螺旋藻(Spirulina platensis)794细胞内抗氧化物质GSH含量的增多,但外源NO又可以降低增强UV-B胁迫下螺旋藻细胞中GSH含量的增加。说明NO对增强UV-B胁迫下的螺旋藻794细胞有保护作用,可以减轻UV-B胁迫对螺旋藻(S.platensis)细胞引起的生物损伤。首次研究报道了增强UV-B胁迫下NO信号分子对蓝细菌———螺旋藻细胞生物损伤调节能力的影响,为进一步探讨NO信号及其与其它信号分子之间相互作用、相互关联来调节细胞的生理生化过程,以减缓UV-B胁迫下的生物损伤机理奠定了基础。     

Analysis of the effects of nitric oxide and oxygen on nitric oxide production by macrophages

The interactions between NO and O(2) in activated macrophages were analysed by incorporating previous cell culture and enzyme kinetic results into a novel reaction-diffusion model for plate cultures. The kinetic factors considered were: (i) the effect of O(2) on NO production by inducible NO synthase (iNOS); (ii) the effect of NO on NO synthesis by iNOS; (iii) the effect of NO on respiratory and other O(2) consumption; and (iv) the effects of NO and O(2) on NO consumption by a possible NO dioxygenase (NOD). Published data obtained by varying the liquid depth in macrophage cultures provided a revealing test of the model, because varying the depth should perturb both the O(2) and the NO concentrations at the level of the cells. The model predicted that the rate of NO(2)(-) production should be nearly constant, and that the net rate of NO production should decline sharply with increases in liquid depth, in excellent agreement with the experimental findings. In further agreement with available results for macrophage cultures, the model predicted that net NO synthesis should be more sensitive to liquid depth than to the O(2) concentration in the headspace. The main reason for the decrease in NO production with increasing liquid depth was the modulation of NO synthesis by NO, with O(2) availability playing only a minor role. The model suggests that it is the ability of iNOS to consume NO, as well as to synthesize it, that creates very sensitive feedback control, setting an upper bound on the NO concentration of approximately 1 microM. The effect of NO consumption by other possible pathways (e.g., NOD) would be similar to that of iNOS, in that it would help limit net NO production. The O(2) utilized during enzymatic NO consumption is predicted to make the O(2) demands of activated macrophages much larger than those of unactivated ones (where iNOS is absent); this remains to be tested experimentally.     

Effects of cold exposure and shear stress on endothelial nitric oxide synthase activation

Endothelial nitric oxide synthase (eNOS) is the primary enzyme that produces nitric oxide (NO), which plays an important role in blood vessel relaxation. eNOS activation is stimulated by various mechanical forces, such as shear stress. Several studies have shown that local cooling of the human finger causes strong vasoconstriction, followed after several minutes by cold-induced vasodilation (CIVD). However, the role played by endothelial cells (ECs) in blood vessel regulation in respond to cold temperatures is not fully understood. In this study, we found that low temperature alone does not significantly increase or decrease eNOS activation in ECs. We further found that the combination of shear stress with temperature change leads to a significant increase in eNOS activation at 37 °C and 28 °C, and a decrease at 4 °C. These results show that ECs play an important role in blood vessel regulation under shear stress and low temperature.     

Glyceryl trinitrate,a nitric oxide donor,abrogates ferric nitrilotriacetate-induced oxidative stress and renal damage

Ferric nitrilotriacetate (Fe-NTA), a common water pollutant and a known renal carcinogen, acts through the generation of oxidative stress and hyperproliferative response. In the present study, we show that the nitric oxide (NO) generated by the administration of glyceryl trinitrate (GTN) affords protection against Fe-NTA-induced oxidative stress and proliferative response. Administration of Fe-NTA resulted in a significant (P<0.001) depletion of renal glutathione (GSH) content with concomitant increase in lipid peroxidation and elevated tissue damage marker release in serum. Parallel to these changes, Fe-NTA also caused down-regulation of GSH metabolizing enzymes including glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione-S-transferase and several fold induction in ornithine decarboxylase (ODC) activity and rate of DNA synthesis. Subsequent exogenous administration of GTN at doses of 3 and 6mg/kg body weight resulted in significant (P<0.001) recovery of GSH metabolizing enzymes and amelioration of tissue GSH content, in a dose-dependent manner. GTN administration also inhibited malondialdehyde (MDA) formation, induction of ODC activity, enhanced rate of DNA synthesis, and pathological deterioration in a dose-dependent fashion. Further, administration of NO inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), exacerbated Fe-NTA-induced oxidative tissue injury, hyperproliferative response, and pathological damage. Overall, the study suggests that NO administration subsequent to Fe-NTA affords protection against ROS-mediated damage induced by Fe-NTA.