水杨酸对盐胁迫下黄瓜幼苗生长抑制的缓解效应

研究了水杨酸对盐胁迫下黄瓜幼苗生长抑制的缓解效应及其机制。结果证明,盐胁迫条件下水杨酸能提高幼苗相对含水量,降低Na^ 、K^ 向上运输的选择性,通过促进子叶内超氧化物歧化酶、过氧化物酶活性降低膜脂过氧化产物丙二醛含量和质膜透性,缓解了盐胁迫对幼苗生长的抑制。     

外源硅对盐胁迫下黄瓜幼苗叶绿体活性氧清除系统的影响

以黄瓜为材料,研究了外源硅（K2SiO3 1．0mmol／L）对NaCl（50mmol/L）胁迫下黄瓜幼苗叶绿体中Na^＋、K^＋向叶绿体分配及活性氧清除系统的影响。结果表明：盐胁迫下硅处理使叶绿体在K^＋与Na^＋之间选择性吸收K^＋,从而降低了叶绿体内Na^＋的含量;同时Si处理可以显著降低盐胁迫下叶绿体中过氧化氢（H2O2）和丙二醛（MDA）含量,提高超氧化物歧化酶（SOD）、抗坏血酸过氧化物酶（APX）、谷胱甘肽还原酶（GR）和脱氢抗坏血酸还原酶（DHAR）的活性及抗坏血酸（ASA）、还原型谷胱甘肽（GSH）含量。说明Si不仅能降低叶绿体对Na^＋的选择吸收,还能增强叶绿体活性氧清除系统清除活性氧的能力,缓解盐胁迫对叶绿体膜的伤害。     

硅改善盐胁迫下库拉索芦荟生长和离子吸收与分布

Si2．0mmol／L处理明显缓解NaCl 100、200mmol／L胁迫120d对库拉索芦荟（Aloevera）生长的抑制作用。Si可显著降低NaCl胁迫下芦荟植株中的Na^＋和Cl^-含量,提高K^＋含量,从而显著降低K^＋／Na^＋,促进根对K^＋的选择性吸收（ASK,Na）和K^＋向地上部的选择性运输（TSK,Na）,以维持植株体内的离子稳态。根系和叶片横切面的X-射线能谱微区分析结果进一步证实了这一结果。Si改善盐胁迫下芦荟对K^＋的选择性吸收和运输的机制之一是通过显著提高盐胁迫下芦荟根细胞质膜H^＋ATPase、液泡膜H^＋-ATPase和液泡膜H^＋-PPase的活性。     

过量表达星星革PtSOS1提高拟南芥的耐盐性

将星星草中分离的质膜型Na^＋／H^＋逆向转运蛋白基因PtSOSJ（GenBank登录号EF440291）构建到pGWB2植物表达载体上,转化拟南芥,获得抗卡那霉素的抗性植株。PCR和Northem检测表明,PtSOS1已整合到拟南芥基因组中并过量表达。耐盐性实验表明,PtSOS1过量表达提高了拟南芥植株的耐盐性。盐分测定表明,盐胁迫下PtSOS1转基因植株中Na^＋积累低于野生型的,K^＋含量则高于野生型的,转基因植株中K^＋／Na^＋比值高于野生型。     

罗布麻对不同浓度盐胁迫的生理响应

利用网室盆栽实验,研究不同浓度的NaCl（100-400mmol·L^-1）胁迫对罗布麻（Apocynum venetum）生长及生理特性的影响。结果表明,100mmol·L^-1NaCl处理显著降低了罗布麻植株的鲜重,但对其干重影响不大;随着盐浓度继续增加,罗布麻鲜重和干重显著下降。在盐胁迫下,罗布麻叶片内的丙二醛含量、电解质渗漏率、根部和地上部Na^＋的含量明显增加,K^＋的含量随着盐离子浓度的增加而降低。盐胁迫显著降低了地上部Ca^2＋的含量,而对根部Ca^2＋的含量没有影响。植株K^＋/Na^＋和Ca^2＋/Na^＋比值随着盐胁迫强度的增加而降低。盐胁迫显著促进了罗布麻根部对K^＋和Ca^2＋的选择性吸收及对K^＋的选择性运输。当NaCl浓度小于或等于200mmol·L^-1时,随着盐离子浓度的增加,罗布麻叶片内的脯氨酸和可溶性糖积累显著增加,而当NaCl浓度大于200mmol·L^-1时,这2种有机溶质含量显著下降。总体上,罗布麻通过积累无机离子、合成有机溶质及维持较高的K^＋、Ca^2＋选择性吸收和运输来适应一定浓度（≤200mmol·L^-1NaCl）的盐胁迫。     

盐胁迫下柚和橘幼苗体内矿质元素变化的比较研究

采用沙培法,对盐胁迫下坪山柚和福橘幼苗体内矿质元素的变化进行了研究。结果表明,随着NaCl浓度的增加,坪山柚和福橘幼苗根部及地上部Na^＋、Cl-含量增加,且相同浓度下,福橘比坪山柚高。40mmol／L NaCI胁迫下,坪山柚和福橘幼苗地上部的K^＋、Fe含量,根部的Ca^2＋、Mg^2＋、Zn含量显著下降,而根部Fe含量及地上部Zn含量显著增加。随NaCl浓度增大,坪山柚根部K^＋含量,地上部Ca^2＋、Mg^2＋含量变化不明显,而福橘根部、地上部上述离子含量在NaCl浓度≥160mmol／L时均显著下降。因此,根部K^＋含量,地上部Ca^2＋、Mg^2＋含量存在品种问差异,或许可作为耐盐性鉴定指标。NaCl胁迫降低坪山柚和福橘幼苗根部及地上部P、Mn含量,而Cu含量在较高浓度NaCl胁迫下显著增加。NaCl胁迫明显降低坪山柚和福橘幼苗地上部K^＋／Na^＋、Ca^2＋／Na^＋和Mg^2＋／Na^＋值,其中K^＋／Na^＋值的变化可考虑作为柑橘耐盐性鉴定的指标。     

库拉索芦荟幼苗对海水胁迫的响应

采用砂培试验,研究库拉索芦荟（Aloe vera）幼苗对海水胁迫的响应特征。结果表明：（1）30％海水处理20d,库拉索芦荟幼苗的干重与对照无显著差异,而30％海水处理库拉索芦荟的根干重明显高于10％海水及淡水处理;（2）海水胁迫下,库拉索芦荟幼苗中离子区域化明显：从地下部和地上部来看,Na^＋、Cl^＋明显在芦荟根部积累,海水比例越高,根部Na^＋、Cl^＋含量越大,而K^＋却相反;海水胁迫下芦荟地上部分功能叶片中Na^＋、Cl^＋含量最低,K^＋含量最高,而淡水处理从老叶到新叶,Na^＋、Cl^＋含量总是呈下降趋势,而K^＋正好相反;随海水胁迫在库拉索幼苗中Ca^2＋含量下降,而Mg^2＋含量七升;（3）随海水胁迫时间增加芦荟叶片质膜透性呈显著上升,MDA含量呈波动变化。     

渗透胁迫下稻苗中铁催化的膜脂过氧化作

在－０．７ＭＰａ渗透胁迫下,水和思苗体内Ｏ２↑－．和Ｈ２Ｏ２大量产生,Ｆｅ＾２＋含量与膜脂过氧化产物ＭＤＡ含量呈极显著的正相关。外源Ｆｅ＾２＋、Ｆｅ＾３＋、Ｈ２Ｏ２、Ｆｅ＾２＋＋Ｈ２Ｏ２、ＤＤＴＣ均能刺激膜脂过氧化作用,而铁离子的螯合剂ＤＴＰＡ则有缓解作用。ＯＨ的清除剂苯甲酸钠和甘露醇能明显地抑制渗透胁迫下Ｆｅ＾２＋催化的膜脂过氧化作用。这都表明渗透胁迫下水稻幼苗体内铁诱导的膜脂过氧化作用主要是由     

渗透胁迫下稻苗中铁催化的膜脂过氧化作用

在－０．７ＭＰａ渗透胁迫下,水稻幼苗体内和Ｈ２Ｏ２大量产生,Ｆｅ２＋积累,膜脂过氧化作用加剧。水稻幼苗体内Ｆｅ２＋含量与膜脂过氧化产物ＭＤＡ含量呈极显著的正相关。外源Ｆｅ２＋、Ｆｅ３＋、Ｈ２Ｏ２、Ｆｅ２＋＋Ｈ２Ｏ２、ＤＤＴＣ均能刺激膜脂过氧化作用,而铁离子的螯合剂ＤＴＰＡ则有缓解作用。ＯＨ的清除剂苯甲酸钠和甘露醇能明显地抑制渗透胁迫下Ｆｅ２＋催化的膜脂过氧化作用。这都表明渗透胁迫下水稻幼苗体内铁诱导的膜脂过氧化作用主要是由于其催化Ｆｅｎｔｏｎ型Ｈａｂｅｒ－Ｗｅｉｓｓ反应形成ＯＨ所致。     

甘薯幼苗对NaCl胁迫的生理响应及外源钙的缓解效应

以甘薯品种‘徐薯22’为试验材料,研究了不同浓度NaCI胁迫对甘薯幼苗生根、叶片抗氧化能力、渗调物质含量、光合气体交换参数、荧光参数及叶片离子含量的影响及不同浓度Ca^2＋处理对300mmol·L^-1NaCl胁迫的缓解效应。结果表明,低浓度NaCl（50和100mmol·L^-1）胁迫对甘薯幼苗生根及叶片相对电导率和MDA含量影响较小,随着盐度的增加,叶片SOD活性呈先增加后降低趋势,脯氨酸和可溶性糖含量持续增加,叶片Pn、Tr、Gs、F√Fm、RC／CS0、TR0／CS0、ET0／CS0、ФE0及K^＋、Ca^2＋含量、K^＋／Na^＋不断降低,ФD0和Na^＋含量升高;高浓度NaCl（300mmol·L^-1）胁迫下,甘薯幼苗的正常生理代谢受到显著抑制。适当浓度外源ca2’能显著缓解Nacl胁迫对甘薯幼苗的毒害作用,能促进盐胁迫下甘薯幼苗生根,改善细胞的渗透平衡,提高渗透调节能力,降低膜脂过氧化程度,使甘薯叶片维持较高的Fv√Fm、RC／CS0、TR0／CS0、ET0／CS0、ФE0和较低的ФD0,增强光合作用和气孔蒸腾作用效率,说明外施Ca^2＋是提高甘薯耐盐性的一种有效方法。     

Anti- and pro-oxidative effects of flavonoids on metal-induced lipid hydroperoxide-dependent lipid peroxidation in cultured hepatocytes loaded with alpha-linolenic acid

Lipid hydroperoxide (LOOH)-dependent lipid peroxidation was induced in alpha-linolenic acid (LNA)-loaded hepatocytes by adding Fe, Cu, V, or Cd ions at concentrations from 20 to 500 microM. The effects of structurally related flavonoids at concentrations from 10 to 500 microM on the lipid peroxidation were examined. The results with regard to each flavonoid subclass are as follows: (i) Flavonols such as myricetin, quercetin, fisetin, and kaempferol, but not morin, showed dose-dependent antioxidative activity against metal-induced lipid peroxidation at all metal concentrations. Myricetin, quercetin, and fisetin were the most effective antioxidants, although their efficacies depended on the metal ion. Kaempferol and morin had antioxidative activity equal to the other flavonols in the presence of Cu ions, but were much less effective for the other three metal ions. (ii) Flavones, luteolin, apigenin, and chrysin were antioxidative at low Fe concentrations, but were pro-oxidative at high Fe concentrations. Luteolin exhibited antioxidative activity similar to that of catechol-containing flavonols in the presence of the other three metal ions. Apigenin and chrysin also acted as pro-oxidants with V or with all metal ions, respectively. (iii) Taxifolin, a flavanone, also showed both anti- and prooxidative activity, depending on Fe concentrations, but with other metal showed only antioxidative activity ions. (iv) Epigallocatechin, a flavanol, was antioxidative with all metal ions, and its activity was similar to that of catechol-containing flavonols. The various effects of flavonoids on metal-induced lipid peroxidation in LNA-loaded hepatocytes is discussed with regard to the change in redox potential of flavonoid-metal complexes.     

Anti- and pro-oxidative effects of flavonoids on metal-induced lipid hydroperoxide-dependent lipid peroxidation in cultured hepatocytes loaded with α-linolenic acid

Lipid hydroperoxide (LOOH)–dependent lipid peroxidation was induced in α-linolenic acid (LNA)-loaded hepatocytes by adding Fe, Cu, V, or Cd ions at concentrations from 20 to 500 μM. The effects of structurally related flavonoids at concentrations from 10 to 500 μM on the lipid peroxidation were examined. The results with regard to each flavonoid subclass are as follows: (i) Flavonols such as myricetin, quercetin, fisetin, and kaempferol, but not morin, showed dose-dependent antioxidative activity against metal-induced lipid peroxidation at all metal concentrations. Myricetin, quercetin, and fisetin were the most effective antioxidants, although their efficacies depended on the metal ion. Kaempferol and morin had antioxidative activity equal to the other flavonols in the presence of Cu ions, but were much less effective for the other three metal ions. (ii) Flavones, luteolin, apigenin, and chrysin were antioxidative at low Fe concentrations, but were pro-oxidative at high Fe concentrations. Luteolin exhibited antioxidative activity similar to that of catechol-containing flavonols in the presence of the other three metal ions. Apigenin and chrysin also acted as pro-oxidants with V or with all metal ions, respectively. (iii) Taxifolin, a flavanone, also showed both anti- and prooxidative activity, depending on Fe concentrations, but with other metal showed only antioxidative activity ions. (iv) Epigallocatechin, a flavanol, was antioxidative with all metal ions, and its activity was similar to that of catechol-containing flavonols. The various effects of flavonoids on metal-induced lipid peroxidation in LNA-loaded hepatocytes is discussed with regard to the change in redox potential of flavonoid–metal complexes.     

The effect of calcium on phospholipid peroxidation

The effect of calcium ions on the peroxidation of ox-brain phospholipid liposomes in different free-radical catalysing systems has been assessed. Using thiobarbituric acid-reactivity (TBA) as a measure of lipid peroxidation, calcium ions both inhibited and enhanced peroxidation in the different systems.Changing the composition of the ox-brain phospholipid liposome with synthetic non TBA-reactive phosphatidylcholine, significantly altered its susceptibility to peroxidation both in the presence and absence of calcium ions.The results are discussed with reference to the possibility that calcium ions induce conformational changes in membrane phospholipids. Susceptibility to peroxidation is then influenced by a complex interrelationship between the qualitative lipid composition of the membrane, the pro-oxidant catalyst and the presence of calcium or other active ions.     

Activation of lipid peroxidation in the adrenal cortex by metal ions

The processes of lipid peroxidation have been studied in bovine adrenal cortex in vitro. The lipid peroxidation rate in this tissue is shown to be dependent on the content of metal ions. EDTA, deferroxamine and penicyllamine inhibit spontaneous lipid peroxidation by 25, 50 and 42%, respectively. The ability to activate the process permits arranging metal ions in the following sequence: Fe2+ greater than Fe3+ greater than Cu2+ greater than Mg2+ greater than Mn2+. The maximum activation of lipid peroxidation is observed at Fe2+ and Fe3+ concentrations within the range of 5 x 10(-6) x 10(-4) M.     

Lipid peroxidation inhibits norepinephrine-stimulated lipolysis in rat adipocytes. Reduction of beta-adreno-ceptor number

The effect of lipid peroxidation on lipolysis depends on the intactness of the adipocyte plasma membrane. In the intact cells, the norepinephrine-stimulated lipolysis was inhibited, while the basal one was elevated. In the lysed cells, lipid peroxidation had no effect upon hormone-stimulated lipolysis, but the basal one was strongly inhibited. The effects of free radical damage (iron plus ascorbate ions) were compared to those of malondialdehyde, a non-radical product of lipid peroxidation. Although qualitatively similar, deterioration of plasma membrane induced by malondialdehyde was much lower than by free radicals. The changes in lipolytic response to norepinephrine were accompanied by a drastic reduction in the number of beta-adrenergic receptors.     

In vitro assessment of the toxicity of metal compounds

This review has focused on several parameters related to the delivery of carcinogenic metal compounds to the cell nucleus as a basis for understanding the intermediates formed between metals and cellular components and the effect of these intermediates on DNA structure and function. Emphasis has been placed on metal interactions at the cellular membrane, including lipid peroxidation, metal interactions with glutathione and their relation to membrane injury, and metal effects on the membrane bound enzyme, Na⁺/K⁺ ATPase. Metal binding to metallothionein is also considered, particularly as related to transport and utilization of metal ions and to genetic defects in these processes exemplified in Menkes disease. The ability of cadmium to induce the synthesis of metallothionein more strongly than zinc is also discussed in relation to other toxic and carcinogenic metals. The effects of metal ions on purified DNA and RNA polymerase systems are presented with some of the recent studies using biological ligand-metal complexes. This review points out the importance of considering how metals affect in vitro systems when presented as ionic forms or complexed to relevant biological ligands.     

模拟酸雨及其酸化土壤对小麦幼苗膜脂过氧化水平的影响

以小麦为试材,采用盆栽的方法研究了模拟酸雨及其酸化土壤对小麦幼苗膜脂过氧化水平的影响。结果表明以黄棕壤为材料通过模拟酸雨的淋溶,引起了土壤酸化和盐基流失。当模拟酸雨的pH值由5.6下降到2.5时,土壤pH值由6.06下降到3.41,土壤中交换性盐基总量便从56.5mmol/kg下降到41.1mmol/kg。将小麦幼苗栽培在该酸化土壤上,并分别用5种不同pH值的模拟酸雨喷淋地上器官,导致小麦幼苗体内的膜脂过氧化水平增高和保护酶的活性变化。其中模拟酸雨喷淋小麦幼苗对叶片中的膜脂过氧化水平及保护酶活性的影响大于酸化土壤对其产生的影响。而酸化土壤对小麦幼苗根系中的膜脂过氧化水平和保护酶活性的影响大于模拟酸雨喷淋对其产生的影响。同时,pH≤3.0的高强度酸雨以及由其产生的酸化土壤(T4、T5土壤)对小麦幼苗的膜脂过氧化水平和保护酶的活性产生了严重的影响。     

Induction of lipid peroxidation during heavy metal stress in Saccharomyces cerevisiae and influence of plasma membrane fatty acid unsaturation.

The degree of plasma membrane fatty acid unsaturation and the copper sensitivity of Saccharomyces cerevisiae are closely correlated. Our objective was to determine whether these effects could be accounted for by differential metal induction of lipid peroxidation. S. cerevisiae S150-2B was enriched with the polyunsaturated fatty acids (PUFAs) linoleate (18:2) and linolenate (18:3) by growth in 18:2- or 18:3-supplemented medium. Potassium efflux and colony count data indicated that sensitivity to both copper (redox active) and cadmium (redox inactive) was increased in 18:2-supplemented cells and particularly in 18:3-supplemented cells. Copper- and cadmium-induced lipid peroxidation was rapid and associated with a decline in plasma membrane lipid order, detected by fluorescence depolarization measurements with the membrane probe trimethylammonium diphenylhexatriene. Levels of thiobarbituric acid-reactive substances (lipid peroxidation products) were up to twofold higher in 18:2-supplemented cells than in unsupplemented cells following metal addition, although this difference was reduced with prolonged incubation up to 3 h. Conjugated-diene levels in metal-exposed cells also increased with both the concentration of copper or cadmium and the degree of cellular fatty acid unsaturation; maximal levels were evident in 18:3-supplemented cells. The results demonstrate heavy metal-induced lipid peroxidation in a microorganism for the first time and indicate that the metal sensitivity of PUFA-enriched S. cerevisiae may be attributable to elevated levels of lipid peroxidation in these cells.     

Effect of succinate on mitochondrial lipid peroxidation. 1. Comparative studies on ferrous ion and ADP · Fe/NADPH-induced peroxidation

Lipid peroxidation in isolated rat liver mitochondria, mitoplast, and mitochondrial inner membrane fragments was induced either by ferrous ions, or in an NADPH-dependent process by complexing with adenine nucleotides (ADP or ATP) iron. The Fe²⁺-induced lipid peroxidation is nonenzymic when inner membrane fragments are used, while the differences in the inhibitory effect of Mn²⁺ ions and the stimulatory effect of the ionophore A-23187 in mitochondria and inner membrane fragments suggest an enzymic mechanism for ferrous ion-induced lipid peroxidation in intact mitochondria. Contrary to this the ADP/Fe/NADPH-dependent lipid peroxidation is an enzymic process both in mitochondria and inner membrane preparations. We have shown that cytochrome P₄₅₀ is involved in the ADP/Fe/NADPH-induced lipid peroxidation. Succinate, a known inhibitor of NADPH-dependent lipid peroxidation, inhibited the Fe²⁺-induced process also, and there was no difference in this effect when inner membrane preparations, mitochondria, or mitoplasts were used.     

The effect of ionic strength on the lipid peroxidation of porcine intestinal brush-border membrane vesicles

The effects of salt concentration gradient (inside to outside) on the lipid peroxidation of porcine intestinal brush-border membrane vesicles have been studied and several interesting features of the peroxidation have been elucidated. The addition of dithiothreitol and Fe2+ is far more effective in induction of the lipid peroxidation than any of the other metal ion species tested (Fe3+, Cu2+, Ni2+, Zn2+ and Cr3+). The peroxidation rate of the membrane vesicles induced by dithiothreitol plus Fe2+ was sensitive for the incubation temperature and was increased with increase of the temperature. Imposition of an inward salt concentration gradient on the membrane vesicles preloaded with 300 mM mannitol by addition of 100 mM chloride of K+, Na+, Li+, Rb+, NH4+ or choline to medium produces a very large reduction of the lipid peroxidation induced by dithiothreitol plus Fe2+. The membrane peroxidation is depressed more with the mannitol (300 mM)-preloaded vesicles than with the K2SO4 (100 mM)-preloaded vesicles when they are incubated in medium containing 20-100 mM of K2SO4. Addition of membrane-permeant anions such as SCN- and I-, but not addition of NO3-, to incubation medium has been found to decrease markedly the lipid peroxidation of the mannitol-preloaded vesicles. From these results it is suggested that the lipid peroxidation of the brush-border membranes by addition of dithiothreitol plus Fe2+ is sensitively changed with change in ionic strength.