植物叶片脯氨酸的变化及其对亚硫酸伤害的防护作用

 在特定污染条件下,植物叶脯氨酸含量与K+渗出量(％)呈负相关变化,并因树种和叶片成熟度而异、脯氨酸含量为成叶>老叶,K+渗出量则是老叶>成叶,外施脯氨酸对植物亚硫酸伤害具有一定的防护作用。     

树木气孔浸润级与SO2伤害及ABA的防护作用

以常见绿化树种为材料,通过实地测定和熏烟实验,探讨了气孔浸润级与树木SO2伤害的关系及ABA的防护效应.结果表明,在特定环境下,相同树种的气孔浸润级较为稳定,不同树种的气孔浸润级差异较大;浸润级与叶绿素结合度呈负相关变化,但不明显;与K+渗出量呈正相关(r=0.92,α＜0.01),并按95%的置信度绘制了伤害预测图.不同SO2浓度条件下,对同一树种的气孔浸润级的影响甚小,不超过一个等级,K+渗出量则依大气SO2浓度和树木吸S量的增加而增多.气孔浸润级依ABA溶液处理浓度增大而降低,K+渗出量也相应减少,经2.5mol     

树木气孔浸润级与SO_2伤害及ABA的防护作用

以常见绿化树种为材料 ,通过实地测定和熏烟实验 ,探讨了气孔浸润级与树木SO2 伤害的关系及ABA的防护效应 .结果表明 ,在特定环境下 ,相同树种的气孔浸润级较为稳定 ,不同树种的气孔浸润级差异较大 ;浸润级与叶绿素结合度呈负相关变化 ,但不明显 ;与K 渗出量呈正相关 (r =0 .92 ,α <0 .0 1) ,并按 95 %的置信度绘制了伤害预测图 .不同SO2 浓度条件下 ,对同一树种的气孔浸润级的影响甚小 ,不超过一个等级 ,K 渗出量则依大气SO2 浓度和树木吸S量的增加而增多 .气孔浸润级依ABA溶液处理浓度增大而降低 ,K 渗出量也相应减少 ,经 2 .5mol·L-1× 4h剂量的SO2 熏烟 ,预涂 30mol·L-1ABA者 ,降低了 1.5～ 3个浸润级 ,K 渗出量减少 36 .5 %～ 5 4.8% ,其测定值与自然对照值相近 ,防护作用显著 .     

蚕豆叶片SOD活性监测大气SO2污染的可行性研究

 本文从实验室熏气和野外大气暴露两方面对利用蚕豆叶片SOD活性评价和监测大气SO2污染的可行性进行了研究。低浓度SO2(0.1312、0.2601mg·m-3)处理,引起叶片SOD活性升高,一定时间后,SOD活性趋于稳定,且0.2601mg·m-3SO2处理时,SOD活性较高,表现出SOD活性增量与SO2浓度相关,为利用SOD活性监测和评价SO2污染提供了可能性。大气暴露试验结果表明SOD活性与大气硫酸盐化速率存在极显著的相关性。利用SOD活性和大气硫酸盐化速率分别对大气SO2污染程度进行了评价,结果基本一致,并根据SOD活性估测了大气硫酸盐化速率,符合程度较高,置信分析表明估测结果可信。以上结果表明,利用蚕豆叶片SOD活性监测和评价大气SO2污染是可行的。     

湖南省大嵊山大气污染与杉木衰亡的关系

对湖南省大嵊山杉木衰亡现象进行了探讨。内容包括大气环境质量监测、杉木叶片叶绿素含量、钾离子外渗率、电解质外渗率、杉木叶片含硫量、杉木叶全N、P、K、Ca、Mg、杉木生长量的测定、树干解析。研究表明,大嵊山大气污染严重,研究地的大气综合污染指数对照区Site3为1,污染监测区Site 1和Site2分别为2.65和1.80。杉木叶片钾离子外渗率、电解质外渗率、全S含量、全N含量为大嵊山污染区>对照区;而P、K、Ca、Mg元素含量为对照区>污染区。而且杉木叶片含硫量与大气SO2之间存在较好的相关性,冬季二者的相关公式为：Y=1.3657+25.8146X(r=0.6319,P<0.05),分析认为： 大气污染是大嵊山杉木衰亡的重要原因之一。     

披针叶黄华试管苗适应盐胁迫的渗透调节机制

以披针叶黄华(Thermopsis lanceolata)试管苗为材料,通过组培方法研究其在0、0.2%、0.4%、0.6%、0.8%和1.0%NaCl和Na2SO4胁迫30d后的生长、有机渗透调节物质和无机渗透调节物质(Na+、K+和Ca2+)含量的变化,以探讨其耐盐性机制。结果显示:(1)随NaCl和Na2SO4胁迫浓度的增加,披针叶黄华试管苗叶片脯氨酸和可溶性糖含量均显著持续增加,且NaCl胁迫下脯氨酸上升的幅度均大于相同浓度Na2SO4胁迫下的增幅,而可溶性糖上升的幅度却小于相同浓度Na2SO4胁迫下的幅度;可溶性蛋白含量随NaCl浓度的增大呈先升高后降低的趋势,但随Na2SO4浓度的增加呈持续上升的趋势。(2)随NaCl和Na2SO4浓度的增加,披针叶黄华试管苗Na+含量呈增加趋势且各处理均显著高于对照,Ca2+含量和叶片K+含量却呈逐渐减少趋势且各处理均显著低于对照,而根系K+含量呈先降后升的趋势;Na2SO4胁迫下披针叶黄华试管苗叶片Na+含量上升幅度以及K+和Ca2+含量下降幅度均明显低于相同浓度NaCl胁迫组;而Na+/K+和Na+/Ca2+比值随NaCl和Na2SO4浓度增加而升高;NaCl胁迫下,叶片Na+/K+和Na+/Ca2+高于相同浓度Na2SO4胁迫下的比值,而根系Na+/K+和Na+/Ca2+却低于相同浓度Na2SO4胁迫下的比值。研究表明,盐胁迫下,披针叶黄华试管苗通过抑制叶片中Na+积累并增加可溶性糖和可溶性蛋白含量,在根系中维持较高K+和Ca2+含量以及较低水平Na+/K+和Na+/Ca2+比,以降低披针叶黄华细胞渗透势来适应盐渍环境;披针叶黄华对NaCl胁迫的调节能力弱于Na2SO4。     

桂花叶片含硫量分析在监测大气中SO2污染的作用

<正> 利用植物监测大气污染早已为人们所发现,但目前多从植物(如紫花苜蓿、向日葵,地衣等)叶片出现的伤害症状来估测大气受污染的程度。植物能吸收大气中的污染物质,使叶片含污染物质的量增加。并且污染物质在植物体内的含量有一定的稳定性,能比较准确地反映大气的污染程度。利用分析叶片污染物质含量来估测大气的污染状况是切实可行的。 几年来我们研究了植物对大气污染的净化能力,对桂林市内和市郊十多种主要绿化植物叶片污染物质含量进行了分析。并为了利用分析叶片污染物质含量来监测环境。对桂花树叶片含硫量分析监测大气的SO_2污染作了一些工作,现将结果进行整理如下,供参考。     

大气CO_2浓度升高对红三叶和高丹草Cs、K竞争吸收与转运的影响

水培条件下,研究了大气C02浓度升高对红三叶(Trifolium Pratene L.)和高丹草(Sorhum vulgare x Sorghum.vulgare va r.sudanense hybrids)在不同铯(Cs)浓度(0、200、500、1 000μmol·L~(-1))下生物量、铯和钾的竞争吸收及转运的影响。结果表明,大气CO_2浓度升高显著提高了2种植物叶、茎和根各部位的生物量,其中,红三叶各部生物量分别提高了42.6%、66.2%和45.0%,高丹草分别提高了17.4%、18.9%和22.3%。大气CO:浓度升高提高了红三叶和高丹草叶片及茎中的Cs含量,提升比例最大的为红三叶的茎(达9.7%),同时显著提高了2种植物对Cs的转运系数及红三叶的茎和根中Cs/K的区别系数。对于红三叶,大气CO_2浓度升高引起叶片K含量略微增加,而茎和根系中K含量显著降低;对于高丹草,大气CO_2浓度升高引起叶片和茎中K含量增加,而根系中K含量降低。2种植物对Cs的吸收都与介质中Cs浓度呈显著的线性相关,溶液中Cs浓度的增加提高了红三叶和高丹草的Cs/K区别系数,并且Cs的添加不仅对红三叶和高丹草的生物量都起到了一定的抑制作用,同时还降低了2种植物对钾的吸收。在正常的CO_2浓度下,1000μmol·L~(-1)Cs处理可使2种植物叶、茎和根中的K含量分别降低10.4%、13.3%、32.5%(红三叶)和18.3%、42.1%和38.9%(高丹草);在大气C02浓度升高的条件下,分别降低12.2%、22.0%、35.0%(红三叶)和17.9%、38.7%、34.6%(高丹草)。     

大气SO2、氟化物对植物生理生态指标的影响

运用多元回归分析方法研究不同污染区生长的植物叶片的生理生态指标的变化与大气硫酸盐化速率及氟化物浓度的关系.结果表明,植物的叶面积(LA)、叶绿素总量(Chl)、细胞液pH值(pH)和细胞质膜透性(CML电导率)等生理生态指标的变化幅度与大气污染物含量呈显著相关.与大气硫酸盐化速率关系式为Ys=0.034XLA-0.011XChl+0.017XpH+40.0003XCML+0.034(r=0.99,p＜0.001);与大气氟化物含量的关系式为YF=0.362XLA+0.329XChl+0.814XpH+0.024XCML-4.596(r=0.947,p＜0.03).利用这些生理生态指标的变化幅度作为生物监测的指标来评价不同污染区的大气硫氧化物、氟化物的污染状况,与大气监测结果有很高的一致性,并且与实际环境污染状况相符.     

园林绿化植物对大气二氧化硫和氟化物污染的净化能力及修复功能

研究32种盆栽于佛山市污染区的城市园林绿化植物对大气二氧化硫(SO2)和氟化物的净化能力及其对大气污染的修复功能。结果显示,竹节树、傅园榕等14种植物对SO2、氟化物等污染气体不但具有较强的抗性,而且具有较高的吸收净化能力,叶片平均含硫量达17442(11754—27658mg kg^-1 DW),是清洁区(5988mg kg^-1 DW)的2．9倍;平均含氟量达3725．9(1954．9—5331.7mg kg^-1 DW),是清洁区(1703：mg kg^-1DW)的21倍。表明这些植物对大气SO2、HF复合污染具有很好的净化能力和修复功能。是值得推广的城市园林绿化树种。     

树木气孔浸润级与SO2伤害及ABA的防护作用

以常见绿化树种为材料,通过实地测定和熏烟实验,探讨了气孔浸润级与树木SO₂伤害的关系及ABA的防护效应.结果表明,在特定环境下,相同树种的气孔浸润级较为稳定,不同树种的气孔浸润级差异较大;浸润级与叶绿素结合度呈负相关变化,但不明显;与K⁺渗出量呈正相关(r=0.92,α＜0.01),并按95%的置信度绘制了伤害预测图.不同SO₂浓度条件下,对同一树种的气孔浸润级的影响甚小,不超过一个等级,K⁺渗出量则依大气SO₂浓度和树木吸S量的增加而增多.气孔浸润级依ABA溶液处理浓度增大而降低,K⁺渗出量也相应减少,经2.5mol·L^-1×4h剂量的SO₂熏烟,预涂30mol·L^-1ABA者,降低了1.5～3个浸润级,K⁺渗出量减少36.5%～54.8%,其测定值与自然对照值相近,防护作用显著.     

Sulfate-chloride exchange transport in a glioma cell line

Transport of SO4(2-) was studied in the glioma cell line LRM55 to determine whether it is mediated by the Cl-/HCO3- exchanger or the K+/Cl- cotransporter previously described in these cells (Wolpaw, E.W. and Martin, D.L. (1984) Brain Res. 297, 317-327). 35SO4(2-) influx was saturable with SO4(2-). External SO4(2-) stimulated 35SO4(2-) efflux, indicating an exchange mechanism. External Cl- was a competitive inhibitor of 35SO4(2-) influx. Internal Cl- stimulated 35SO4(2-) influx and external Cl- stimulated 35SO4(2-) efflux, indicating that Cl- is an exchange substrate for the SO4(2-) carrier. Also, SO4(2-) flux was sensitive to SITS, DIDS and furosemide. However, saturating external SO4(2-) did not inhibit 36Cl- influx and did not inhibit 36Cl- efflux via the Cl-/HCO3- exchanger. Moreover, K+ did not stimulate 36Cl- efflux via the Cl-/HCO3- exchanger. Moreover, K+ did not stimulate 35SO4(2-) influx as it does Cl- influx. These findings indicate that SO4(2-) transport into these cells is mediated by an exchange carrier distinct from both the Cl-/HCO3- exchanger and the K+/Cl- cotransporter. While Cl- is an alternative substrate for the SO4(2-) porter, this carrier is responsible for only a minor fraction of total Cl- flux in these cells.     

The Protective Effect of Phosphate Buffer on SO2 Harmed Wheat Seedling

When 1/15 mol/L of phosphate buffer at pH 6. 4, was used to spray wheat seedling three times, the plasmolemma structure become stabilized and k+ efflux was decreased. After fumigation with SO2 the K+ efflux of wheat seedling ,sprayed with phosphate buffer, decreased markedly. At SO2 dosage of 1.54 ppm × 4h, the decreasing rate of K+ efflux was 54. 11%–81.29% and the decrease rate was in concert with the increase of SO2 dosage. Therefore, the authors consider that the phosphate buffer, at pH 6.4, has a good protective effect against SO2 insult.     

Anion-coupled Na efflux mediated by the human red blood cell Na/K pump

The red cell Na/K pump is known to continue to extrude Na when both Na and K are removed from the external medium. Because this ouabain-sensitive flux occurs in the absence of an exchangeable cation, it is referred to as uncoupled Na efflux. This flux is also known to be inhibited by 5 mM Nao but to a lesser extent than that inhibitable by ouabain. Uncoupled Na efflux via the Na/K pump therefore can be divided into a Nao-sensitive and Nao-insensitive component. We used DIDS-treated, SO4-equilibrated human red blood cells suspended in HEPES-buffered (pHo 7.4) MgSO4 or (Tris)2SO4, in which we measured 22Na efflux, 35SO4 efflux, and changes in the membrane potential with the fluorescent dye, diS-C3 (5). A principal finding is that uncoupled Na efflux occurs electroneurally, in contrast to the pump's normal electrogenic operation when exchanging Nai for Ko. This electroneutral uncoupled efflux of Na was found to be balanced by an efflux of cellular anions. (We were unable to detect any ouabain-sensitive uptake of protons, measured in an unbuffered medium at pH 7.4 with a Radiometer pH-STAT.) The Nao-sensitive efflux of Nai was found to be 1.95 +/- 0.10 times the Nao-sensitive efflux of (SO4)i, indicating that the stoichiometry of this cotransport is two Na+ per SO4=, accounting for 60-80% of the electroneutral Na efflux. The remainder portion, that is, the ouabain-sensitive Nao-insensitive component, has been identified as PO4-coupled Na transport and is the subject of a separate paper. That uncoupled Na efflux occurs as a cotransport with anions is supported by the result, obtained with resealed ghosts, that when internal and external SO4 was substituted by the impermeant anion, tartrate i,o, the efflux of Na was inhibited 60-80%. This inhibition could be relieved by the inclusion, before DIDS treatment, of 5 mM Cli,o. Addition of 10 mM Ko to tartrate i,o ghosts, with or without Cli,o, resulted in full activation of Na/K exchange and the pump's electrogenicity. Although it can be concluded that Na efflux in the uncoupled mode occurs by means of a cotransport with cellular anions, the molecular basis for this change in the internal charge structure of the pump and its change in ion selectivity is at present unknown.     

Na+- and K+-dependent uridine transport in rat renal brush-border membrane vesicles

The transport of uridine into rat renal brush-border membrane vesicles was investigated using an inhibitor-stop filtration method. Uridine was not metabolized under these conditions. The rapid efflux of intravesicular uridine was prevented by adding 1 mM phloridzin to the ice-cold stop solution. In the presence of inwardly directed gradients of either Na+ or K+, zero-trans uridine uptake exhibited a transient overshoot phenomenon indicating active transport. The overshoot was much more pronounced with Na+ than K+ and it was not observed when either Na+ or K+ was at equilibrium across the membrane. The K+-induced overshoot was not due to the presence of a membrane potential alone, as an inwardly directed gradient of choline chloride failed to produce it. The amplitude of the overshoot was increased by raising either the Na+ or K+ concentration outside the membrane or by using more lipophilic anions (reactive order was NO3- greater than SCN- greater than Cl- greater than SO4(2-). Zero-trans efflux studies showed that the uridine transport is bidirectional. Li+ could substitute poorly for Na+ but not at all for K+. Stoichiometries of 1:1 and greater than 1:1 were observed for Na+: uridine and K+: uridine coupling, respectively. A preliminary analysis of the interactions between Na+ and K+ for uridine uptake showed complex interactions which can best be explained by the involvement of two different systems for nucleoside transport in the rat renal brush-border membrane, one requiring Na+ and the other K+ as transport coupler.     

Phosphate from the phosphointermediate (EP) of the human red blood cell Na/K pump is coeffluxed with Na, in the absence of external K

This study is concerned with Na/K pump-mediated phosphate efflux that occurs during uncoupled Na efflux in human red blood cells. Uncoupled Na efflux is known to be a ouabain-sensitive mode of the Na/K pump that occurs in the absence of external Nao and Ko. Because this efflux (measured with 22Na) is also inhibited by 5 mM Nao, the efflux can be separated into a Nao-sensitive and a Nao-insensitive component. Previous work established that the Nao-sensitive efflux is actually comprised of an electroneutral coefflux of Na with cellular anions, such as SO4 (as 35SO4). The present work focuses on the Nao-insensitive component in which the principal finding is that orthophosphate (P(i)) is coeffluxed with Na in a ouabain-sensitive manner. This P(i) efflux can be seen to occur, in the absence of Ko, in both DIDS-treated intact cells and resealed red cell ghosts. This efflux of P(i) was shown to be derived directly from the pump's substrate, ATP, by the use of resealed ghosts made to contain both ATP and P(i) in which either the ATP or the P(i) were labeled with, respectively, [gamma-32P]ATP or [32P]H3PO4. (These resealed ghosts also contained Na, Mg, P(i), SO4, Ap5A, as well as an arginine kinase/creatine kinase nucleotide regenerating system for the control of ATP and ADP concentrations, and were suspended usually in (NMG)2SO4 at pH 7.4.) It was found that 32P was only coeffluxed with Na when the 32P was contained in [gamma-32P]ATP and not in [32P]H3PO4. This result implies that the 32P that is released comes from ATP via the pump's phosphointermediate (EP) without commingling with the cellular pool of P(i). Ko (as K2SO4) inhibits this 32P efflux as well as the Nao-sensitive 35SO4 efflux, with a K0.5 of 0.3-0.4 mM. The K0.5 for inhibition of P(i) efflux by Ko is not influenced by Nao, nor can Nao act as a congenor for Ko in any of the flux reactions involving Ko. The stoichiometry of Na to SO4 and Na to P(i) efflux is approximately 2:1 under circumstances where the stoichiometry of Na effluxed to ATP utilized is 3:1. From these and other results reported, it is suggested that there are two types of uncoupled Na efflux that differ from each other on the basis of their sensitivity to Nao, the source (cellular vs substrate) and kind of anion (SO4 vs P(i)) transported.(ABSTRACT TRUNCATED AT 400 WORDS)     

几种抗血吸虫药物对日本血吸虫雄虫体表膜液内K~+,Na~+,H~+转递的影响

本文采用Oak＇s脱膜方法与火焰光度测定经吡喹酮,吐酒石和敌百虫作用后的日本血吸虫体表膜液内的K~+,Na~+的含量实验结果,吡喹酮和吐酒石能刺激K~+从虫体表膜内向外流,分别降低K~+浓度约50%和20%,但对Na~+转运无显著影响.敌百虫的作用是减少膜内K~+外流,导致了膜内K~+浓度升高.这些结果是与体外~(86)Rb渗入虫膜实验一致的.我们也测定了药物作用后虫体表膜液内的H~+,其结果是K~+的外流与H~+的内流有关.