酸沉降影响下庐山森林生态系统水相硫的分布与动态研究

从1997年7月到1999年8月,在庐山植物园选取针叶林和阔叶林各一片样地,对降雨、透冠水、干流水、渗漏水和地表径流进行了监测.结果表明庐山降雨SO2-4浓度有升高趋势,1998年降雨中SO2-4浓度为4.21±3.48mg/L.林冠对干沉降硫有吸收和截获作用,透冠水和干流水中SO2-4明显高于雨水,针叶林中分别为13.68±17.40mg/L和15.50±25.20mg/L,阔叶林分别为6.18±6.37mg/L和7.35±7.73mg/L,是森林中硫沉降的重要组成部分.针叶林地下水中SO2-4含量与雨水的显著正相关(R2=0.758,n=6),与透冠水和树干流中SO2-4含量之和极显著正相关(R2=0.880,n=8),说明日本柳杉针叶林加重了硫沉降,对土壤中SO2-4有较大影响;阔叶林的相关性都不显著,说明阔叶林虽然对SO2-4在土壤中的输入有所贡献,但相对作用较小.针叶林SO2-4输入高而输出低;阔叶林输入低而输出高,可能处于稳态平衡.针叶林地表径流中SO2-4含量受雨水影响较大,阔叶林中的则可能主要是土壤溶液中保存的SO2-4持续淋洗的结果.     

二氧化硫代谢衍生物对大鼠海马CA1区神经元钠电流的影响

实验采用全细胞膜片钳技术 ,研究了SO2 代谢衍生物亚硫酸钠和亚硫酸氢钠 (两者分子比为 3∶1)对大鼠海马CA1区神经元钠电流的影响。结果表明 ,SO2 代谢衍生物可剂量依赖性地增大钠电流 ,剂量为 10和 10 0μmol/L时 ,钠电流分别增大 5 0 .5 9± 19.0 8%和 82 .0 6± 18.5 1%(n =15 ) ;此外还与电压呈依赖性关系 ,但不具有频率依赖性 ;10 μmol/LSO2 代谢衍生物不影响钠电流的激活过程 ,却非常显著地影响其失活过程 ,作用前后的半数失活电压分别为 - 6 9.71± 4.6 7和 - 5 3.2 7± 4.95mV (n =10 ,P <0 .0 1) ,但不改变失活曲线的斜率因子。实验结果提示 ,SO2 衍生物具有类似神经毒物的作用 ,大气SO2 污染可能与一些中枢神经系统疾病的发生有关。     

SO2体内衍生物诱发蚕豆根尖细胞微核

以蚕豆为材料 ,研究 SO2 体内衍生物 -亚硫酸钠与亚硫酸氢钠混合液 (3:1)对根尖细胞的遗传毒效应。结果表明 :0 .0 5～2 .0 0 mmol/ L的 SO2 衍生物处理可诱发两品种蚕豆根尖中的微核细胞明显增加 ;不同浓度 (0 .0 5～ 15 .0 0 mmol/ L ) SO2 衍生物处理 12、2 4、36 h后 ,根尖微核细胞率是对照组的 2 .5～ 5 .0倍 ,显著高于对照组。在一定浓度范围内 ,蚕豆根尖细胞微核率与SO2 衍生物浓度之间具有正的线性相关。研究结果表明 ,SO2 衍生物能够破坏蚕豆根尖细胞的遗传稳定性。     

SO_2对胸主动脉血管平滑肌细胞钾离子通道的影响

为了探讨二氧化硫(SO2)引起大鼠血管平滑肌的降压机制,采用急性酶分离法分离大鼠单个血管平滑肌细胞,运用全细胞膜片钳技术记录平滑肌细胞外向钾电流(IKv),观察SO2及其衍生物对平滑肌细胞膜钾电流的作用,从离子通道角度研究SO2对血压的影响。结果发现:SO2衍生物可使外向IKv显著增大,10μmol/L SO2衍生物可使电流-电压曲线(I-V曲线)显著上移,即增大IKv,且呈一定的电压依赖性,并且,SO2衍生物可使IKv增大呈现出剂量-效应关系。当使用5 mmol/L 4-氨基吡啶(4-AP)抑制IKv后,加入10μmol/L SO2衍生物,IKv有一定程度增加。TEA能抑制SO2衍生物对IKv的增大效应。10μmol/L SO2衍生物可使IKv的激活曲线显著向超极化方向移动,但并不影响其斜率因子。说明SO2衍生物作用于血管平滑肌细胞,可引起外向钾电流幅度增大,使钾电流提前激活,这是SO2及其衍生物降压的作用机制之一;TEA、4-AP对SO2衍生物引起的血管平滑肌细胞钾电流的增大具有拮抗作用。     

突触小泡膜蛋白与神经递质释放的局部调节

突触小泡膜蛋白及其在神经递质释放过程中的作用已取得若干研究进展.突触素I、SY蛋白、SO蛋白、SB蛋白、SG蛋白等都是突触小泡膜的重要蛋白质,这些蛋白质在突触小泡的贴靠、膜融合及胞吐作用中起着局部自主性调节作用.     

二氧化硫吸入对小鼠脑组织的氧化损伤

对昆明小鼠进行不同浓度SO2 吸入试验 ,然后测定脑组织中还原型谷胱甘肽 (GSH)含量、谷胱甘肽过氧化物酶 (GSH Px)活性、超氧化物歧化酶 (SOD)活性及脂质过氧化产物丙二醛 (MDA)含量 ,研究SO2 对小鼠中枢神经系统的氧化损伤作用 .雄鼠脑组织匀浆上清液GSH含量在SO2 浓度为 14mg m3 时明显上升 (P <0 0 5 ) ,浓度为 2 8、5 6和 84mg m3 时极显著降低 (P <0 0 1) ,而雌鼠在14和 2 8mg m3 时无明显变化 (P >0 0 5 ) ,在 5 6和 84mg m3 时极显著降低 (P <0 0 1) .雌雄小鼠的GSH Px活性在 14和 2 8mg m3 时无明显变化 (P >0 0 5 ) ,在 5 6、84mg m3 时均极显著降低 (P <0 0 1,P <0 0 0 1) .在SO2 上述 4种吸入浓度下 ,雌雄小鼠的SOD活性均显著降低 (P <0 0 5 )或极显著降低 (P <0 0 1,P <0 0 0 1) ;雄鼠和雌鼠的脂质过氧化产物丙二醛 (MDA)含量均极显著增高 (P <0 0 1,P <0 0 0 1) .结果表明 ,小鼠脑组织对SO2 的氧化损伤作用非常敏感 ,是SO2 的靶器官之一 ,SO2 的污染可能与某些脑疾患有关     

杜鹃对SO2胁迫的抗氧化防护效应

以SO2耐受性植物杜鹃(Rhododendron sp.)为材料,在2个高浓度SO2熏气后,检测了叶组织中丙二醛(MDA)、可溶性蛋白和叶绿素含量以及抗氧化酶活性.结果表明:40和80mg?m-3SO2熏气4h(1d)后,杜鹃叶片超氧化物歧化酶(SOD)活性和MDA含量均分别比对照显著增加了11.26%、11.86%和73.32%、76.43%;随熏气时间的延长,SOD、过氧化物酶(POD)、过氧化氢酶(CAT)活性持续增高,且SOD和CAT活性显著高于对照,MDA含量逐渐降至对照水平;SO2熏气导致叶片可溶性蛋白含量显著降低,但叶绿素含量却无显著改变.熏气后恢复期间,抗氧化酶活性相对降低,可溶性蛋白含量恢复至对照水平.研究发现,杜鹃对SO2的耐受性与细胞中抗氧化酶活性的诱导性增强有关,抗氧化能力增强是植物适应SO2胁迫的重要原因.     

长期施用含硫和含氯化肥对稻田杂草生长动态的影响

利用湖南祁阳红壤稻田长期定位试验,研究了在等量氮磷钾养分条件下,长期施用含Cl-、SO2-4和Cl-+SO2-4化肥水稻生育期间杂草种类和生物量的变化.结果表明:施肥34年后,施用含Cl-化肥处理水稻生育期间杂草的种类最多、总生物量(浮生杂草和湿生杂草的生物量之和)最大,早稻期间杂草平均总干物质量分别比含SO2-4和Cl-+SO2-4化肥处理增加了51.4%和17.6%,晚稻期间分别增加了144%和242%.含SO2-4和Cl-+SO2-4化肥处理稻田中浮生杂草生物量较大,而含Cl-化肥处理田间几乎没有浮生杂草生长.杂草总干物质量和湿生杂草干物质量均与土壤Cl-含量呈显著正相关(相关系数分别为0.764**和0.948**),与土壤SO2-4-S含量呈显著负相关(相关系数分别为0.849**和0.641*).土壤碱解氮和有效磷受土壤SO2-4-S、Cl-及pH的共同作用对杂草总干物质量产生影响.通过各种施肥措施维持土壤适宜pH及碱解氮、有效磷含量,提高土壤SO2-4-S含量、降低Cl-含量,能有效抑制南方红壤稻田中湿生杂草的生长,降低杂草总生物量.     

p53、bax和bcl-2基因在SO 2染毒大鼠肝中的表达

为了进一步探讨SO₂的毒理学作用机制,运用荧光实时定量RT-PCR和免疫组化技术研究SO2吸入对大鼠肝细胞中p53、bax和bcl-2三种细胞凋亡相关基因mRNA和蛋白表达的影响.结果显示,肝中p53和bax mRNA水平呈剂量依赖性增加,在SO ₂浓度为28.00和56.00 mg/m3时显著增加（p53 mRNA在28 mg/m ³为1.30倍,在56 mg/m^3为3.43倍;bax mRNA在28 mg/m3为1.63倍,在56 mg/m ³为2.17倍）;而bcl-2 mRNA水平显著降低（在28 mg/m3为0.63倍,在56 mg/m ³为0.45倍）.免疫组化实验结果表明,吸入SO ₂后,大鼠肝中p53和bax蛋白表达水平呈剂量依赖性增加,而bcl-2蛋白表达水平呈剂量依赖性降低.结果表明,SO2可以改变凋亡相关基因的表达,诱导大鼠肝组织细胞凋亡,这可能与一些凋亡相关疾病的发生有关.     

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 .     

含硫气体信号分子对心血管调节的效应及机制研究进展

含硫气体信号分子硫化氢(hydrogen sulfide,H2S)和二氧化硫(sulfur dioxide,SO2)过去被认为是废气,但是研究先后发现这两种含硫气体能在哺乳动物体内通过含硫氨基酸代谢内源性生成。心血管系统存在H2S和SO2的生成体系,并且H2S和SO2具有重要的心血管生理学效应,包括舒张血管和心肌负性肌力作用。H2S和SO2的心血管病理生理学效应也逐渐被认识,如缓解高血压和肺动脉高压、抑制动脉粥样硬化进展、保护心肌缺血再灌注损伤和异丙肾诱导的心肌损伤。ATP敏感性钾通道、L型钙通道、c GMP、NF-κB信号通路及MAPK信号通路等都参与H2S和SO2的生物学效应。以上发现表明H2S和SO2是重要的心血管内源性气体信号分子,为阐明心血管疾病的发病机制和治疗靶点提供新的思路。     

Studies on the assembly and stability of the metal-thiolate clusters of metallothionein in dimethyl sulfoxide.

Solvent perturbation studies in 100% dimethyl sulfoxide (Me2SO) have been carried out on rabbit liver metallothionein (MT) in an effort to learn more about the factors stabilizing the three-dimensional structure and the mechanism of cluster formation. As indicated by the electronic absorption spectra of Co7-metallothionein, the reconstituted protein preserves its structural integrity in this solvent. Minor spectral differences between water and Me2SO were fully reversible. The titration of apoMT with cobalt(II) in Me2SO, followed by UV-visible-near-infrared electronic absorption, circular dichroism, magnetic circular dichroism, and EPR spectroscopy, indicate that the protein can refold in this solvent. A comparison with the previous titration data in water reveals that the first four titration steps in both solvents are identical, indicating a thermodynamically controlled folding process. However, the reversed order of the cluster completion between Me2SO and water may suggest the involvement of a kinetically controlled folding process in the last three titration steps. A new cluster form developed with approximately nine Co(II) equivalents.     

5-heteroatom substituted pyrazoles as canine COX-2 inhibitors. Part 1: Structure-activity relationship studies of 5-alkylamino pyrazoles and discovery of a potent, selective, and orally active analog

Structure-activity relationship (SAR) studies of the novel 2-[3-di and trifluoromethyl-5-alkylamino pyrazo-1-yl]-5-methanesulfonyl (SO(2)Me)/sulfamoyl (SO(2)NH(2))-pyridine derivatives for canine COX enzymes are described. The studies led to the identification of 2e as lead with potent in vitro activity, selectivity, and in vivo activity in dogs and cats.     

Role of prothrombin fragment 1 in the pathway of regulatory exosite I formation during conversion of human prothrombin to thrombin

Prothrombin (Pro) activation by factor Xa generates the thrombin catalytic site and exosites I and II. The role of fragment 1 (F1) in the pathway of exosite I expression during Pro activation was characterized in equilibrium binding studies using hirudin(54-65) labeled with 6-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)hexanoate ([NBD]Hir(54-65)(SO3-)) or 5-(carboxy)fluorescein ([5F]Hir(54-65)(SO3-)). [NBD]Hir(54-65)(SO3-) distinguished exosite I environments on Pro, prethrombin 1 (Pre 1), and prethrombin 2 (Pre 2) but bound with the same affinities as [5F]Hir(54-65)(SO3-). Conversion of Pro to Pre 1 caused a 7-fold increase in affinity for the peptides. Conversely, fragment 1.2 (F1.2) decreased the affinity of Pre 2 for [5F]Hir(54-65)(SO3-) by 3-fold. This was correlated with a 16-fold increased affinity of F1.2 for Pre 2 in comparison to thrombin, demonstrating an enhancing effect of F1 on F1.2 binding. The active intermediate, meizothrombin, demonstrated a 50- to 220-fold increase in exosite affinity. Free thrombin and thrombin.F1.2 complex bound [5F]Hir(54-65)(SO3-) with indistinguishable affinity, indicating that the effect of F1 on peptide binding was eliminated upon expression of catalytic activity and exosite I. The results demonstrate a new zymogen-specific role for F1 in modulating the affinity of ligands for exosite I. This may reflect a direct interaction between the F1 and Pre 2 domains in Pro that is lost upon folding of the zymogen activation domain. The effect of F1 on (pro)exosite I and the role of (pro)exosite I in factor Va-dependent substrate recognition suggest that the Pro activation pathway may be regulated by (pro)exosite I interactions with factor Va.     

Cryopreservation in micro-volumes: impact upon Caco-2 colon adenocarcinoma cell proliferation and differentiation

Recent advances in cell-based therapies require new approaches for cell cryopreservation, capable of dealing with large number of samples and providing specific conditions for each cell type. Reduction of sample volume from the commonly used 1 mL to 25 microL in 30-well micro-cryosubstrates improves cryopreservation by allowing automation, data handling and access to individual wells without thawing the whole cryosubstrate. This system was evaluated for the storage of Caco-2 colon adenocarcinoma cells, which differentiate spontaneously after long-term culture. The impact of the cryosample small volume upon post-thawing membrane integrity of the cells and their capacity to proliferate and differentiate was studied. Two different cryoprotectants commonly employed, dimethyl sulfoxide (Me(2)SO) and glycerol, were evaluated as well as the possibility of decreasing their concentration from the 10% concentration, usually used, down to 3% (v/v). The process automation by pipette robotic addition of the cryoprotectant to the micro-cryosubstrates was also evaluated. The micro-cryosubstrates have proven to be at least as efficient as typical 1 mL cryovials for cryopreservation of Caco-2 cells using either Me(2)SO or glycerol. Compared to the manual process, the automatic addition of glycerol to the micro-cryosubstrates allowed higher cell viabilities after thawing while with Me(2)SO no significant changes were observed. Me(2)SO has shown to be more effective than glycerol in maintaining high post-thaw cell membrane integrity, either in micro-cryosubstrates or cryovials, for any of the concentrations tested. The ability of Me(2)SO in maintaining high cell membrane integrity post-thawing was confirmed by long-term (up to 22 days) proliferation and differentiation studies performed with cells cultured immediately after thawing.     

Insights into the cryoprotective mechanism of dimethyl sulfoxide for phospholipid bilayers.

Dimethyl sulfoxide (Me2SO) is a widely used cryoprotectant for biological structures such as membranes. Despite hundreds of studies on the effects of this molecule, surprisingly little is known about its cryoprotective mechanism. This study investigates the ability of various Me2SO analogs to serve as cryoprotectants for liposomes. The data show that an increase in hydrophobicity progressively reduces the cryoprotective effect of sulfoxides. Additional experiments using phospholipid vesicles of varying composition demonstrate the Me2SO is markedly less effective on liposomes carrying a net negative charge. In fact, cryoprotection by Me2SO was virtually eliminated in vesicles composed of 30% phosphatidylserine (a negatively charged lipid). Based on these results, we suggest that the polar sulfoxide moiety of Me2SO interacts electrostatically with phospholipid membranes and that this interaction is critical for Me2SO's cryoprotective effect for membranes.     

Glass-forming property of the system diethyl sulphoxide/water and its cryoprotective action on Escherichia coli survival

In this work the thermal properties of diethyl sulphoxide (Et2SO), as well as its cryoprotective ability are studied and related to other well-known cryoprotectant substances, like dimethyl sulphoxide (Me2SO). We have investigated the thermal properties of Et2SO/water systems using Differential Scanning Calorimetry at a very low heating/cooling rate (2 degrees C/min). Liquid/solid or glassy/crystalline transitions have been observed only for the solutions with content of Et2SO ranging from 5 up to 40% w/w and/or greater than 85%. In the 45-75% w/w Et2SO range we have found a noticeable glass-forming tendency and a great stability of the amorphous state to the reheating. In samples with Et2SO content ranging from 80 to 85%, we observed a great stability of the glass forming by cooling, but a lesser stability to the subsequent reheating. The glass-forming tendency of these solutions is discussed in terms of existing competitive interactions between molecules of Et2SO, on the one hand, and Et2SO and water molecules, on the other hand. The results are well explainable on the basis of the model structure of water/Et2SO solutions, deduced by Raman and infrared studies [J. Mol. Struct. 665 (2003) 285-292]. The cryoprotective ability of Et2SO on Escherichia coli survival has been also investigated, and a comparison among Et2SO and other widely used cryoprotectants, like Me2SO and glycerol has been done. Survival of E. coli, determined after freezing-thawing process, was maximal at 45% w/w Et2SO (more than 85% viability). It should be noted that at the same concentration the survival is only about 35% in the presence of Me2SO and not more than 15% in the presence of glycerol. These features are well consisted with the glass-forming properties of Et2SO.     

二氧化硫对墨西哥豆瓢虫的影响

空气污染对害虫的影响,国内尚无研究报道。本文报道了作者在美国农业研究中心植物胁迫实验室进行的部分工作。实验结果表明,在0.30ppmSO_2的作用下,墨西哥豆瓢虫(Epilachna varivestis)的取食量和蛹重增加;与未受污染的寄主植物相比,豆瓢虫偏食受污染的植物;而且有嗜食含较高糖分寄主植物的倾向;在污染空气中长成的成虫可消耗更多的植物物质。     

Phosphate Buffers Effect on Protective Enzyme System and Relationship of Enzyme System with SO2 Pollution in Wheat Seedlings

The effect of phosphate buffer on protective enzyme system was different as the way of treatment and wheat (Triticum aestivum L. ) species. Normally superoxide dismutase (SOD) and peroxidase (POD) activity increased markedly. The former decreased with the increase of SO2 fumigation dosage but it was higher than control and producted new isoenzyme pedigree. The latter increased according to SO2 fumigation and showed relative gain effect with phosphate buffer the isoenzyme pedigree increased markedly. The change of protective enzyme system of scavenging free radicals was possible one cause that phosphate buffer eased SO2 insult of wheat seedlings.     

DNA strand scission and ADP-ribosyltransferase activity during murine erythroleukemia cell differentiation

The accumulation of DNA strand breaks and activation of ADP-ribosyltransferase (ADPRT) have recently been associated with cellular differentiation. Murine erythroleukemia (MEL) cells undergo erythropoietic differentiation when exposed to dimethyl sulfoxide (Me2SO) and several studies have suggested that DNA strand scission induced by this agent is a prerequisite for expression of the differentiated phenotype. Me2SO induction of MEL cells has also been associated with increases in ADPRT activity in one study, but not in another. We have monitored the effects of Me2SO on DNA strand breaks in preformed and replicating MEL cell DNA. The results clearly demonstrate that DNA fragmentation is not detectable during Me2SO induction of MEL differentiation, even in the presence of 3-aminobenzamide, an inhibitor of ADPRT. Further, these results are consistent with an absence of detectable changes in both endogenous and total potential ADPRT activity during Me2SO-induced MEL differentiation. These findings would argue against Me2SO induction of DNA strand scission and ADPRT in MEL cells undergoing differentiation.