Hg2+、Cd2+和Cu2+对菹草光合系统及保护酶系统的毒害作用

研究了Hg2 、Cd2 、Cu2 对高等水生沉水植物菹草光合系统及保护酶系统的毒害作用。结果表明 :3种离子均使菹草叶片叶绿体自发荧光强度、叶绿素含量、光合速率降低。Hg2 、Cd2 、Cu2 对菹草保护酶系统存在不同的影响 ,短时间低浓度条件下 ,诱导超氧化物歧化酶 (SOD )、过氧化氢酶 (CAT)、过氧化物酶(POD)活性上升 ,随着污染时间的延长、污染浓度的增加 ,酶活性下降 ,其中SOD活性上升持续时间最长 ,下降最慢。 3种离子均使菹草可溶性蛋白含量减少。Hg2 、Cu2 毒性较强 ,Cd2 毒性较弱。Hg2 、Cu2 对菹草的致死浓度为 0 .5～ 1mg/L ,Cd2 为 1～ 2 .5mg/L     

外源谷胱甘肽（GSH）对水鳖Zn2+毒害的缓解作用

研究在10 mg L-1 Zn2 毒害下外施10-50 mg L-1梯度浓度的还原型谷胱甘肽(GSH)对水鳖(Hydrocharis dubia)的保护酶(SOD、CAT、POD)活性、GSH、可溶性蛋白质、叶绿素、H2O2含量以及O2.-产生速率的影响。结果表明,相对单一的Zn2 毒害,施用外源GSH可明显减轻毒害症状,植物体内GSH含量增加了10.71%-35.71%,O2.-的产生速率最低降至78.2%,H2O2含量最低降至62.7%。植物体内可溶性蛋白含量和CAT、SOD、POD的活性最大分别增加了74.2%、108.2%、61.4%、19.5%。随GSH浓度增大,缓解能力下降,在培养液中最佳缓解浓度为20-40 mg L-1。     

Cd2+处理对菹草叶片保护酶活性和细胞超微结构的毒害影响

以不同浓度Cd^2 处理5d的菹草为实验材料,测定了叶片SOD,POD,CAT等生理生化指标的变化,并用透射电镜观察了Cd^2 对叶细胞超微结构,尤其是对叶绿体,线粒体和细胞核的损伤情况。结果表明：SOD活性,叶绿素含量随Cd^2 处理浓度的增加而下降,而CAT和POD活性都是在1mg／L浓度下达到峰值,而后降低。SOD对Cd^2 毒害最敏感,其次为POD和CAT。电镜观察发现：随Cd^2 浓度的增加,对细胞超微结构的损伤程度也加剧。表现为叶绿体膨大,被膜断裂、消失和叶绿体解体;线粒体变形,脊突膨大和空泡化;细胞核核仁分散,核膜断裂,核空泡化。并探讨了Cd^2 对植物的毒害机制。     

Effects of lanthanum on the active oxygenscavenging enzyme activities and ultrastructure in Potamogeton crispus leaves

在菹草培养液中施用LaCl3·8 H2O培养菹草,研究了稀土镧对菹草活性氧清除酶活性及叶细胞超微结构的影响.结果表明,菹草在含适宜浓度La3+的培养液中长势均好于对照.较低浓度La3+处理时,菹草叶绿素含量、叶片自发荧光强度、硝酸还原酶(NRase)活性、过氧化物酶(POD)活性、过氧化氢酶(CAT)活性及可溶性蛋白质含量均升高,而超氧化物歧化酶(SOD)活性、细胞膜透性、O2-产生速率及丙二醛(MDA)含量则呈降低趋势,电镜观察结果为La3+对菹草生长的影响提供了细胞学证据.实验认为促进菹草生长的最适La3+浓度为5～10 mg·L-1.     

木麻黄幼苗对模拟酸雨胁迫的响应和Ca2+的调节作用

随着酸雨pH值的下降,木麻黄幼苗中超氧化物歧化酶(SOD)活性、叶绿素含量和叶绿素a/b值逐渐下降,过氧化物酶(POD)活性、可溶性蛋白质含量、丙二醛(MDA)含量和超氧阴离子自由基(O2-·)含量逐渐增加,过氧化氢酶(CAT)活性和脯氨酸含量先升后降.在同一强度酸雨胁迫下,经0.1和1 mmol·L-1Ca(NO3)2处理的SOD活性、CAT活性、叶绿素含量和叶绿素a/b值相对较高,POD活性、蛋白质含量、MDA含量、O2-·含量和脯氨酸含量相对较低,Ca2 可缓解酸雨对木麻黄幼苗的伤害.     

镧对菹草活性氧清除酶活性及叶细胞超微结构的影响

在菹草培养液中施用LaCl3.8H2O培养菹草,研究了稀土镧对菹草活性氧清除酶活性及叶细胞超微结构的影响。结果表明,菹草在含适宜浓度La3+的培养液中长势均好于对照。较低浓度La3+处理时,菹草叶绿素含量、叶片自发荧光强度、硝酸还原酶(NRase)活性、过氧化物酶(POD)活性、过氧化氢酶(CAT)活性及可溶性蛋白质含量均升高,而超氧化物歧化酶(SOD)活性、细胞膜透性、O-2.产生速率及丙二醛(MDA)含量则呈降低趋势,电镜观察结果为La3+对菹草生长的影响提供了细胞学证据。实验认为促进菹草生长的最适La3+浓度为5～10mg.L-1。     

外源水杨酸对酸雨胁迫后龙眼幼苗生理特性恢复的影响

以龙眼幼苗为材料,研究酸雨胁迫(pH 3.0)后不同浓度外源水杨酸(0、0.1、0.5、1.0和2.0 mmol·L-1)对龙眼幼苗生理特性的影响.结果表明:酸雨胁迫后龙眼幼苗叶片中的超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)活性降低,叶绿素、蛋白质和可溶性糖含量下降,丙二醛含量升高,龙眼幼苗显示出毒害效应.0.1 ～1.0mmol·L-1外源水杨酸显著提高龙眼幼苗叶绿素、可溶性糖和蛋白质的含量,增强SOD、POD和CAT活性,降低丙二醛含量,减少幼苗所受氧化伤害的程度;其中0.5 mmol· L-1水杨酸处理效果最好,叶绿素、可溶性糖和蛋白质的含量分别比单独酸雨胁迫处理植株增加了62％、105％和177％,SOD、POD和CAT活性分别提高144％、440％和132％,丙二醛含量降低了35％;而2.0 mmol·L-1水杨酸却起到相反的作用.可见,低浓度水杨酸(0.1～1.0 mmol·L-1)能通过刺激龙眼抗氧化酶活性,减轻氧化胁迫,缓解酸雨胁迫后的毒害作用,而高浓度水杨酸(2.0 mmol·L-1)对龙眼幼苗的缓解作用下降.     

Cu胁迫对紫背萍的生长及活性氧清除系统的影响

通过水培实验研究了重金属铜(Cu)胁迫下的紫背萍的生理响应。结果表明:Cu对紫背萍的生长有低浓度(≤1.8mg.L-1)促进、高浓度(>1.8mg.L-1)抑制作用。紫背萍的植物体数(Y1)、叶绿素含量(Y2)均与Cu浓度(X)呈显著负相关,回归方程为:Y1=-0.53X 34.47、Y2=-0.035X 0.90;Cu对紫背萍的植物体净增殖量、叶绿素含量的4天半数抑制浓度(4d-IC50)分别为5.48mg.L-1和12.12mg.L-1。紫背萍体内的SOD活性(Y3)和CAT活性(Y4)与Cu浓度(X)之间均呈曲线相关,回归方程分别为:Y3=-5.367X2 140.56X-59.25、Y4=-7.146X2 123.65X 1101.03。POD活性在Cu浓度不超过10mg.L-1时,较之对照相差不大,但在18mg.L-1时则大幅度下降。     

外源NO对酸雨胁迫下龙眼幼苗生理特性的影响

研究了外源NO供体硝普钠(SNP)对pH3.0酸雨胁迫下龙眼幼苗叶绿素含量、抗氧化酶活性和渗透调节物质含量的影响.结果表明:酸雨胁迫下,龙眼幼苗叶片中的超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)活性降低,叶绿素、蛋白质和可溶性糖含量下降,丙二醛含量升高,呈现出一定的毒害效应.外源NO对酸雨胁迫下龙眼幼苗的生理代谢的作用具有双重性,0.1 ～0.5.mmol·L-1SNP显著提高叶绿素、可溶性糖和蛋白质含量,增强SOD、POD和CAT活性,降低丙二醛含量;其中0.5 mmol·L-1 SNP处理效果最好,叶绿素、可溶性糖和蛋白质含量分别比单独酸雨胁迫处理增加了76.0％、107.0％和216.1％,SOD、POD和CAT活性分别提高150.0％、350.9％和97.1％,丙二醛含量降低了46.4％.低浓度外源NO能通过刺激抗氧化酶活性来清除活性氧,减轻氧化胁迫,缓解酸雨胁迫对龙眼幼苗的毒害作用;而高浓度外源NO对酸雨胁迫的缓解作用减弱.     

Cu2+、Pb2+胁迫对秋茄幼苗可溶性蛋白和抗氧化酶活性的影响

【摘要】为研究重金属胁迫对秋茄幼苗抗氧化系统的影响, 砂培红树植物秋茄幼苗一个月,研究不同重金属浓度(Cu2+: 0、3、15、30、45 mg·L–1, Pb2+: 0、1、5、10、15 mg·L–1)和不同实验时间(0、3、7、14、28 d)对叶片的影响。测量的生理指标包括: 可溶性蛋白、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和过氧化物酶(POD), 实验条件下两种重金属对各项参数的影响一致。结果表明: 在特定浓度重金属处理下(Cu2+: 0、3、15、30、45 mg·L–1, Pb2+: 0、1、5、10、15 mg·L–1), 可溶性蛋白含量随着时间的增加基本呈先升后降趋势; SOD活性呈降低趋势; CAT活性最初受到明显促进, 后促进作用减弱; POD活性变化规律并不一致。在相同处理时间下, 可溶性蛋白含量随Cu2+浓度的增加而降低, 在Pb2+处理下有所波动; SOD活性在各浓度条件下均降低; CAT活性基本呈降低趋势; POD活性呈先升后降的趋势。通过Pearson相关性分析和PCA分析表明, 可溶性蛋白含量与SOD、POD、CAT三种酶活性呈显著负相关关系, 相关系数分别为–0.401, –0.722, –0.521; 而SOD、POD和CAT活性则表现为显著正相关关系, SOD与POD的相关系数为0.359, SOD与CAT的相关系数为0.384, POD与CAT的相关系数为0.485, 说明三种抗氧化酶协同作用形成一条抗氧化链抵御重金属胁迫。     

Intracellular Na+ Regulates Epithelial Na+ Channel Maturation

Epithelial Na⁺ channel (ENaC) function is regulated by the intracellular Na⁺ concentration ([Na⁺]_i) through a process known as Na⁺ feedback inhibition. Although this process is known to decrease the expression of proteolytically processed active channels on the cell surface, it is unknown how [Na⁺]_i alters ENaC cleavage. We show here that [Na⁺]_i regulates the posttranslational processing of ENaC subunits during channel biogenesis. At times when [Na⁺]_i is low, ENaC subunits develop mature N-glycans and are processed by proteases. Conversely, glycan maturation and sensitivity to proteolysis are reduced when [Na⁺]_i is relatively high. Surface channels with immature N-glycans were not processed by endogenous channel activating proteases, nor were they sensitive to cleavage by exogenous trypsin. Biotin chase experiments revealed that the immature surface channels were not converted into mature cleaved channels following a reduction in [Na⁺]_i. The hypothesis that [Na⁺]_i regulates ENaC maturation within the biosynthetic pathways is further supported by the finding that Brefeldin A prevented the accumulation of processed surface channels following a reduction in [Na⁺]_i. Therefore, increased [Na⁺]_i interferes with ENaC N-glycan maturation and prevents the channel from entering a state that allows proteolytic processing.     

铜、镉及其复合作用下中华大蟾蜍蝌蚪Na+-K+-ATPase酶的变化

采用动物毒理实验法,研究了铜、镉及其复合污染对中华大蟾蜍(Bufo gargarizans)蝌蚪Na -K -ATPase酶活性的影响。结果表明,在0.0298mg/LCu2 和1.14mg/LCd2 作用下,蝌蚪Na -K -ATPase酶活性极显著高于对照组(P<0.01)。随着Cu2 、Cd2 暴露浓度的增加,蝌蚪Na -K -ATPase酶活性又逐渐降低,甚至被抑制。铜、镉复合污染在Na -K -ATPase酶水平上表现出一定的协同作用。     

Na+-Ca2+ exchange activity in rabbit lymphocyte plasma membranes

Plasma membranes of rabbit thymus lymphocytes accumulated Ca²⁺ when a Na⁺ gradient (intravesicular > extravesicular) was formed across the membranes. Dissipation of the Na⁺ gradient by the addition of Na⁺ to the external medium decreased Ca²⁺ uptake. Ca²⁺ preloaded into the lymphocytes was extruded when Na⁺ was added to the external medium. The Ca²⁺ uptake decreased at acidic pH but increased at alkaline pH (above 8) and the activity was saturable for Ca²⁺ (apparent K_m for Ca²⁺ was 61 μM and apparent V_max was 11.5 nmol/mg protein per min). Na⁺-dependent uptake of Ca²⁺ was inhibited by tetracaine and verapamil, and partially inhibited by La³⁺. The uptake was not influenced by orthovanadate.     

Kinetics of high-affinity K+ uptake in plants, derived from K+-induced changes in current-voltage relationships

To investigate coupled, charge-translocating transport, it is imperative that the specific transporter current-voltage (IV ) relationship of the transporter is separated from the overall membrane IV relationship. We report here a case study in which the currents mediated by the K⁺-H⁺ symporter, responsible for high-affinity K⁺ uptake in Arabidopsis thaliana (L.) Heynh. cv. Columbia roots, are analyzed with an enzyme kinetic reaction scheme. The model explicitly incorporates changes in membrane voltage and external substrate, and enables the derivation of the underlying symport IV relationships from the experimentally obtained difference IV data. Data obtained for high-affinity K⁺ transport in A. thaliana root protoplasts were best described by a 1:1 coupled K⁺-H⁺ symport-mediated current with a parallel, outward non-linear K⁺ pathway. Furthermore, the large predictive value of the model was used to describe symport behaviour as a function of the external K⁺ concentration and the cytoplasmic K⁺ concentration. Symport activity is a complex function of the external K⁺ concentration, with first-order saturating kinetics in the micromolar range and a strong activity reduction when external K⁺ is in the millimolar range and the membrane depolarises. High cytoplasmic K⁺ levels inhibit symport activity. These responses are suggested to be part of the feedback mechanisms to maintain cellular K⁺ homeostasis. The general suitability of the model for analysis of carrier-mediated transport is discussed. Received: 23 November 1996 / Accepted: 22 April 1997     

Removal of Cr6+ from groundwater using zero-valence iron in the laboratory

Abstract

In this paper, we describe a series of laboratory experiments which quantify the rate of Cr⁶⁺ reduction by Fe⁰. The main goal of these experiments was to determine the removal efficiency of Cr⁶⁺ by iron. The results indicate that Fe⁰ reduces Cr⁶⁺ to Cr³⁺ under alkaline and slightly acidic conditions. The removal efficiency rises with an increase of the initial concentration of Cr⁶⁺ (1 mg/L to 10 mg/L) when the quantity of Fe⁰ is stable. The removal efficiency increases as the quantity of Fe⁰ is raised when other conditions are constant. The removal efficiency would not be affected by other inorganic ions unless they were present at very high concentrations. When the initial concentration Cr⁶⁺ is 10mg/L and pH is 6.5–7.7, the final concentration of Cr⁶⁺ in effluent is less than 0.05 mg/L and the total Fe is less than 0.3 mg/L in effluent.     

Light-induced pH and K+ changes in the apoplast of intact leaves

The K⁺-sensitive fluorescent dye benzofuran isophthalate (PBFI) and the pH-sensitive fluorescein isothiocyanate dextran (FITC-Dextran) were used to investigate the influence of light/dark transitions on apoplastic pH and K⁺ concentration in intact leaves of Vicia faba L. with fluorescence ratio imaging microscopy. Illumination by red light led to an acidification in the leaf apoplast due to light-induced H⁺ extrusion. Similar apoplastic pH responses were found on adaxial and abaxial sides of leaves after light/dark transition. Stomatal opening resulted only in a slight pH decrease (0.2 units) in the leaf apoplast. Gradients of apoplastic pH exist in the leaf apoplast, being about 0.5–1.0 units lower in the center of the xylem veins as compared with surrounding cells. The apoplastic K⁺ concentration in intact leaves declined during the light period. A steeper light-induced decrease in apoplastic K⁺, possibly caused by higher apoplastic K⁺, was found on the abaxial side of leaves concentration. Simultaneous measurements of apoplastic pH and K⁺ demonstrated that a light-induced decline in apoplastic K⁺ concentration indicative of net K⁺ uptake into leaf cells occurs independent of apoplastic pH changes. It is suggested that the driving force that is generated by H⁺ extrusion into the leaf apoplast due to H⁺-ATPase activity is sufficient for passive K⁺ influx into the leaf cells. Received: 7 March 2000 / Accepted: 12 May 2000     

CD8+ cytotoxic T lymphocytes in cancer immunotherapy: A review

CD8⁺ cytotoxic T lymphocytes (CTLs) are preferred immune cells for targeting cancer. During cancer progression, CTLs encounter dysfunction and exhaustion due to immunerelated tolerance and immunosuppression within the tumor microenvironment (TME), with all favor adaptive immune-resistance. Cancer-associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and regulatory T cells (Tregs) could make immunologic barriers against CD8 ⁺ T cell-mediated antitumor immune responses. Thus, CD8 ⁺ T cells are needed to be primed and activated toward effector CTLs in a process called tumor immunity cycle for making durable and efficient antitumor immune responses. The CD8 ⁺ T cell priming is directed essentially as a corroboration work between cells of innate immunity including dendritic cells (DCs) and natural killer (NK) cells with CD4 ⁺ T cells in adoptive immunity. Upon activation, effector CTLs infiltrate to the core or invading site of the tumor (so-called infiltrated–inflamed [I–I] TME) and take essential roles for killing cancer cells. Exogenous reactivation and/or priming of CD8 ⁺ T cells can be possible using rational immunotherapy strategies. The increase of the ratio for costimulatory to coinhibitory mediators using immune checkpoint blockade (ICB) approach. Programmed death-1 receptor (PD-1)–ligand (PD-L1) and CTL-associated antigen 4 (CTLA-4) are checkpoint receptors that can be targeted for relieving exhaustion of CD8 ⁺ T cells and renewing their priming, respectively, and thereby eliminating antigen-expressing cancer cells. Due to a diverse relation between CTLs with Tregs, the Treg activity could be dampened for increasing the number and rescuing the functional potential of CTLs to induce immunosensitivity of cancer cells.     

Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP) and Ca2+ Mobilization

Many physiological processes are controlled by a great diversity of Ca^{2 +} signals that depend on Ca^{2 +} entry into the cell and/or Ca^{2 +} release from internal Ca^{2 +} stores. Ca^{2 +} mobilization from intracellular stores is gated by a family of messengers including inositol-1,4,5-trisphosphate (InsP₃), cyclic ADP-ribose (cADPR), and nicotinic acid adenine dinucleotide phosphate (NAADP). There is increasing evidence for a novel intracellular Ca^{2 +} release channel that may be targeted by NAADP and that displays properties distinctly different from the well-characterized InsP₃ and ryanodine receptors. These channels appear to localize on a wider range of intracellular organelles, including the acidic Ca^{2 +} stores. Activation of the NAADP-sensitive Ca^{2 +} channels evokes complex changes in cytoplasmic Ca^{2 +} levels by means of channel chatter with other intracellular Ca^{2 +} channels. The recent demonstration of changes in intracellular NAADP levels in response to physiologically relevant extracellular stimuli highlights the significance of NAADP as an important regulator of intracellular Ca^{2 +} signaling.     

Examples of non-trivial efficiency-balanced designs with b=v+1

This note provides examples of binary efficiency-balanced block designs with b=v+1, having no complete blocks, which are unequal-replicated and unequal-blocksized from a biometrical and agricultural standpoint.