Na2CO3胁迫下星星草幼苗活性氧及保护酶活性的变化

对低浓度Na₂CO₃胁迫下星星草幼苗相对电导率、O^-₂产生速率、H₂O₂含量以及保护酶CAT、SOD和POD活性的研究结果表明,低盐胁迫1 d后,星星草幼苗细胞膜的通透性、O^-₂产生速率、H₂O₂含量及保护酶活性都随着盐胁迫的加剧而升高,其具体的变化规律与盐胁迫强度和幼苗细胞膜的受损伤程度密切相关,但相关关系的性质上具有差异。     

Hydrogen peroxide inhibits cAMP-induced Cl- secretion across colonic epithelial cells

We examined the effects ofH₂O₂on Cl secretion acrosshuman colonic T84 cells grown on permeable supports and mounted in modified Ussing chambers. Forskolin-induced short-circuit current, ameasure of Cl secretion,was inhibited in a concentration-dependent fashion when monolayers werepretreated withH₂O₂for 30 min (30-100% inhibition between 500 µM and 5 mM).Moreover,H₂O₂inhibited 76% of the Clcurrent across monolayers when the basolateral membranes were permeabilized with nystatin (200 µg/ml). When the apical membrane waspermeabilized with amphotericin B,H₂O₂inhibited the Na⁺ current (ameasure ofNa⁺-K⁺-ATPaseactivity) by 68% but increased theK⁺ current more than threefold. Inaddition to its effects on ion transport pathways,H₂O₂also decreased intracellular ATP levels by 43%. We conclude that theprincipal effect ofH₂O₂on colonic Cl secretion isinhibitory. This may be due to a decrease in ATP levels followingH₂O₂treatment, which subsequently results in an inhibition of the apicalmembrane Cl conductance andbasolateral membraneNa⁺-K⁺-ATPaseactivity. Alternatively,H₂O₂may alter Cl secretion bydirect action on the transporters or alterations in signal transductionpathways.

     

Hydroxyl Radicals and a Thylakoid-Bound Endopeptidase are Involved in Light- and Oxygen-Induced Proteolysis in Oat Chloroplasts

The hypothesis that light- and oxygen-induced proteolysis inchloroplasts is mediated by active oxygen species was examined.In order to determine whether or not H₂O₂ and/or ^{dot}OH radicalsare involved in these degradative processes we compared thedegradation of proteins in isolated oat chloroplasts exposedto white light at 80 W m^-2 with that in chloroplasts incubatedin darkness in the absence or presence of H₂O₂ or a ^{dot}OH-generatingsystem composed by ascorbic acid, FeCl₃ and H₂O₂ (Asc-Fe-H₂O₂).Light enhanced the rate of degradation of at least 18 polypeptides,while proteolysis was almost negligible in darkness in the abscenceof additives. H₂O₂ had a very small effect. However, Asc-Fe-H₂O₂-treatedchloroplasts in darkness showed a pattern of protein degradationalmost identical to that observed in the light. A thylakoid-boundendopeptidase (EP), the activity of which increased under photooxidativeenvironmental conditions and treatment with an ^{dot}OH-generatingsystem, was partially purified and characterized as a serinetypeprotease. Treatments with inhibitors of serine-type proteaseprevented both light- and Asc- Fe-H₂O₂-induced proteolysis.EP was more active against both soluble and membranous proteinsthat had been pretreated with Asc-Fe-H₂O₂ than against untreatedproteins. It is proposed that a high dose of light irradiationpromotes proteolysis by increasing the formation of ^{dot}OH,which may modify proteins such that they become more susceptibleto EP-catalyzed hydrolysis. ¹Fisiología Vegetal, Dept. de Biología Vegetal,Universidad de Alcalá de Henares, Present address: 28871Alcalá de Henares (Madrid), España.     

外源NO对南方红豆杉幼苗光合色素及抗氧化酶的影响

以4年生南方红豆杉幼苗为实验材料,通过对南方红豆杉幼苗喷施不同浓度外源一氧化氮（NO）供体硝普钠溶液（0、0.01、0.1、0.5和1 mmol·L^-1SNP）,测定光合色素含量、抗氧化酶活性、丙二醛（MDA）含量和过氧化氢（H₂O₂）含量等生理指标,以探讨不同浓度外源NO对南方红豆杉叶片光合色素和抗氧化酶的影响。结果表明：喷施低浓度（0.01、0.1 mmol·L^-1）SNP可显著提高南方红豆杉叶片的叶绿素a、叶绿素b、类胡萝卜素和总叶绿素含量,增加叶绿素a/b的比值,而喷施高浓度（0.5、1 mmol·L^-1）SNP降低了叶片的光合色素含量。随着外源NO供体浓度的增加,叶片过氧化氢酶(CAT)活性显著增加,过氧化物酶(POD)活性先增加后降低。此外,处理前期,低浓度SNP处理明显提高了抗坏血酸过氧化物酶(APX)活性,而高浓度SNP处理显著降低了APX活性,处理后期APX活性随SNP浓度的增加而显著下降。喷施低浓度SNP可有效提高超氧化物歧化酶(SOD)活性和增加可溶性蛋白含量,降低MDA和H₂O₂的含量,而喷施高浓度SNP显著增加了MDA和H₂O₂的含量。因此,低浓度的SNP（<0.5 mmol·L^-1）处理南方红豆杉幼苗,可增加其叶绿素含量,提高抗氧化酶活性,降低MDA和H₂O₂的含量,而高浓度的SNP（≥0.5 mmol·L^-1）处理会降低叶绿素含量,提高H₂O₂含量,增加细胞膜质过氧化程度,从而对南方红豆杉幼苗造成一定伤害。     

Presence of the distinct systems responsible for superoxide anion and hydrogen peroxide generation in red tide phytoplankton Chattonella marina and Chattonella ovata

Raphidophycean flagellates, Chattonella marina and C. ovata,are harmful red tide phytoplankters; blooms of these phytoplanktersoften cause severe damage to fish farming. Previous studieshave demonstrated that C. marina and C. ovata continuously producereactive oxygen species (ROS) such as superoxide anion (O₂^–)hydrogen peroxide (H₂O₂) under normal growth conditions, andan ROS-mediated toxic mechanism against fish and other marineorganisms has been proposed. Although the exact mechanism ofROS generation in these phytoplankters still remains to be clarified,our previous study suggested that NADPH oxidase-like enzymelocated on the cell surface of C. marina may be involved inO₂^– generation. To investigate the localization of O₂^–and H₂O₂ generation in C. marina and C. ovata, we employed 2-methyl-6(p-methoxyphenyl)-3,7-dihydroimidazo[1,2-a]pyrazin-3-oneand 5-(and-6)-carboxy-2',7'-dichlorodihydrodihydrofluoresceindictate, acetyl ester, which are specific fluorescent probefor detecting O₂^– and H₂O₂, respectively. Observationby fluorescence microscopy of live phytoplankters incubatedwith each probe revealed that O₂^– is mainly generatedon the cell surface, whereas H₂O₂ is generated in the intracellularcompartment in these phytoplankters. When the cells were rupturedby ultrasonic treatment, O₂^– levels of C. marina and C.ovata decreased significantly, whereas a few times higher levelsof H₂O₂ were detected in the ruptured cell suspensions whencompared with the levels of the live cell suspension. In immunoblottinganalysis, the protein recognized by anti-human gp91 phox wasdetected in both species. These results suggest that, in bothphytoplankters, the underlying mechanisms of O₂^– and H₂O₂generation may be distinct and such systems are independentlyoperating in the cells.     

Photoreduction of 18O2 and H218O2 with Concomitant Evolution of 16O2 in Intact Spinach Chloroplasts: Evidence for Scavenging of Hydrogen Peroxide by Peroxidase

Illuminated intact spinach chloroplasts decomposed one moleculeof H₂¹⁸O₂ which resulted in the evolution of a half moleculeof ¹⁶O₂, but little ¹⁸O₂. The chloroplasts showed the same rateof photoreduction of ¹⁸C₂ as that of the evolution of ¹⁶O₂ withoutaccumulation of H₂¹⁸O₂. These reactions were suppressed by DCMU,and also by several inhibitors of ascorbate peroxidase and dehydroascorbateand monodehydroascorbate reductases in chloroplasts. These observationsindicate that the hydrogen peroxide produced in chloroplastsis reduced to water by a peroxidase using a photoreductant asthe electron donor. The hydrogen peroxide scavenging systemof chloroplasts was inactivated if hydrogen peroxide was addedin the dark, but not if added during the light. (Received May 4, 1984; Accepted July 10, 1984)     

维生素C保护Aβ1-40Cu(Ⅱ)复合物引起的神经元氧化损伤

老年斑中存在大量β 淀粉样蛋白（β-amyloid, Aβ）是老年痴呆症（Alzheimer′s disease, AD）的重要病理特征.大量数据表明,Aβ上具有与过渡态金属离子共价结合的位点,二者能结合成为寡聚复合物. Aβ_1-40Cu（Ⅱ）复合物通过Cu²⁺的还原催化O₂产生H₂O₂但反应机制不清.本文尝试以天然抗氧化剂维生素C（VC）来对抗Aβ_1-40及Aβ_1-40Cu（Ⅱ）复合物产生的H₂O₂对原代培养的神经细胞的毒性.结果表明,VC能够起到显著的保护作用,其有效浓度为1mmol/L.本文用胞外乳酸脱氢酶泄漏量和H₂O₂生成量的数据证实了细胞存活率（MTT实验）的实验结果.这些结果表明,Aβ_1-40Cu（Ⅱ）复合物能够释放更多的H₂O₂,引发细胞膜破裂并最终引起细胞死亡.加入VC后,神经元受到的损伤较轻,提示VC在保护细胞免受氧化损伤方面发挥了重要作用.     

Sulfhydryls associated with H2O2-induced channel activation are on luminal side of ryanodine receptors

The mechanism underlying H₂O₂-inducedactivation of frog skeletal muscle ryanodine receptors was studiedusing skinned fibers and by measuring single Ca²⁺-releasechannel current. Exposure of skinned fibers to 3-10 mM H₂O₂ elicited spontaneous contractures.H₂O₂ at 1 mM potentiated caffeine contracture.When the Ca²⁺-release channels were incorporated into lipidbilayers, open probability (P_o) and open timeconstants were increased on intraluminal addition ofH₂O₂ in the presence of cis catalase,but unitary conductance and reversal potential were not affected.Exposure to cis H₂O₂ at 1.5 mM failedto activate the channel in the presence of trans catalase.Application of 1.5 mM H₂O₂ to the transside of a channel that had been oxidized by cisp-chloromercuriphenylsulfonic acid (pCMPS; 50 µM) still led to anincrease in P_o, comparable to that elicited bytrans 1.5 mM H₂O₂ without pCMPS.Addition of cis pCMPS to channels that had been treated with orwithout trans H₂O₂ rapidly resulted inhigh P_o followed by closure of the channel. Theseresults suggest that oxidation of luminal sulfhydryls in theCa²⁺-release channel may contribute toH₂O₂-induced channel activation and musclecontracture.

     

Role of calreticulin in the sensitivity of myocardiac H9c2 cells to oxidative stress caused by hydrogen peroxide

Calreticulin (CRT), a Ca²⁺-binding molecular chaperone in the endoplasmic reticulum, plays a vital role in cardiac physiology and pathology. Oxidative stress is a main cause of myocardiac apoptosis in the ischemic heart, but the function of CRT under oxidative stress is not fully understood. In the present study, the effect of overexpression of CRT on susceptibility to apoptosis under oxidative stress was examined using myocardiac H9c2 cells transfected with the CRT gene. Under oxidative stress due to H₂O₂, the CRT-overexpressing cells were highly susceptible to apoptosis compared with controls. In the overexpressing cells, the levels of cytoplasmic free Ca²⁺ ([Ca²⁺]_i) were significantly increased by H₂O₂, whereas in controls, only a slight increase was observed. The H₂O₂-induced apoptosis was enhanced by the increase in [Ca²⁺]_i caused by thapsigargin in control cells but was suppressed by BAPTA-AM, a cell-permeable Ca²⁺ chelator in the CRT-overexpressing cells, indicating the importance of the level of [Ca²⁺]_i in the sensitivity to H₂O₂-induced apoptosis. Suppression of CRT by the introduction of the antisense cDNA of CRT enhanced cytoprotection against oxidative stress compared with controls. Furthermore, we found that the levels of activity of calpain and caspase-12 were elevated through the regulation of [Ca²⁺]_i in the CRT-overexpressing cells treated with H₂O₂ compared with controls. Thus we conclude that the level of CRT regulates the sensitivity to apoptosis under oxidative stress due to H₂O₂ through a change in Ca²⁺ homeostasis and the regulation of the Ca²⁺-calpain-caspase-12 pathway in myocardiac cells. apoptosis; calcium; endoplasmic reticulum     

活性氧在UV-B诱导的玉米幼苗叶片乙烯产生中的作用

 研究了活性氧在UV-B(280～320 nm)诱导的玉米(Zea mays)幼苗叶片乙烯合成中的作用。结果表明,UV-B促进了玉米幼苗活性氧和乙烯的产生;乙 烯合成抑制剂氨氧乙烯基甘氨酸 (AVG)和氨氧乙酸(AOA)能明显减弱UV-B对玉米幼苗乙烯产生的诱导作用,但对活性氧(ROS)的 产生没有明显影 响;ROS的清除剂不但能抑制UV-B诱导的 ROS的产生,而且还可以抑制UV_B诱导的乙烯的产生,但这种抑制作用可以被外源O₂^.-的供体所逆转。这 说明,乙烯的积累不能作为UV-B胁迫下ROS的诱导的因素,相反,ROS的积累则导致了乙烯的积累;因此,ROS可能参与了UV-B胁迫诱导的乙烯的产生 。质膜NADPH氧化酶的抑制剂二苯碘鎓(DPI)和H₂O₂的特异性清除剂过氧化氢酶（CAT）对UV-B胁迫诱导的乙烯积累 几乎没有影响, 这说明H₂O₂ 可能与UV-B诱导的玉米幼苗叶片乙烯的产生无关, 在UV-B诱导的玉米幼苗叶片乙烯的生物合成过程中O₂^.-起着很重要的作用,相关的O₂^.-不是由 NADPH氧化酶催化产生的。     

Relationship between light-induced potential change and internal ATP concentration in tonoplast-free Chara cells

The effect of the intracellular concentration of ATP ([ATP]₁)on the light-induced potential change (LPC) in tonoplast-freeChara cells was studied. The LPC was hardly affected by loweringthe [ATP]₁ by about 1/10 or by raising it to about 10 timesthe normal cytoplasmic concentration (0.5–1.3 mM). Theinsensitivity of LPC to [ATP]₁ excludes the possibility thatan increase in [ATP]₁ due to photosynthesis may induce the LPC.However, extreme lowering of the [ATP]₁ to about 1–2 µMcompletely inhibited LPC, although photosynthetic O₂ evolutionwas not significantly inhibited. This fact supports the hypothesisthat light stimulates the putative H⁺pump fueled by ATP. Theuncoupling agents DNP and CCCP greatly depolarized the membrane,and inhibited LPC strongly, but they did not decrease [ATP]₁.Photosynthetic O₂ evolution was inhibited to some extent by2 µM CCCP and strongly inhibited by 0.1 mM DNP. Sincethe membrane resistance increased significantly, these chemicalsare believed to act on the membrane as an inhibitor of the electrogenicH⁺ pump not as an H⁺conductor. Introduction of 1 mM ATP intocells treated with uncouplers, to a large extent restored theirability to produce LPC although the membrane potential in darknesswas maintained at a low level. ¹Present address: Niigata College of Pharmacy, 5829 Kamishinei-cho,Niigata 950-21, Japan. ²Present address: Department of Agricultural Chemistry, Collegeof Agriculture, Kyoto University, Kyoto 606, Japan. ³Present address: Department of Botany, Faculty of Science,University of Tokyo, Hongo, Tokyo 113, Japan. (Received March 9, 1979; )     

Requirement of Manganese for Electron Donation of Hydrogen Peroxide in Photosystem II Reaction Center Complex

Mn²⁺ was required for the electron donating reaction from H₂O₂,but not for that from diphenylcarbazide (DPC), in the PS IIreaction center complex which was prepared from spinach chloroplastsby Triton X-100 extraction. The reaction center complex showeda high activity of 2,6-dichloroindophenol (DCIP) photoreductionin the presence of DPC, but a low activity with H₂O₂. The H₂O₂-supportedDCIP photoreduction was suppressed by EDTA and enhanced by asmall amount of Mn²⁺. Ca²⁺ and Mg²⁺ could not replace Mn²⁺.The activation by Mn²⁺ and its binding showed two binding sitesof Mn²⁺ in the reaction center complex, with high (1.5?10⁷ M^–1)and low (1 ? 10⁶ M^–1) binding constants. (Received November 8, 1986; Accepted April 10, 1987)     

Oxidation-reduction reactions between electron transfer components and hydrogen peroxide in photosystem II of chloroplasts

The light-induced oxygen evolution, photoreduction of 2,6-dichlorophenolindophenol (DPIP) and carotenoid photobleaching induced by carbonylcyanide m-chlorophenylhydrazone (CCCP) were investigated withspinach chloroplast fragments in the presence of H₂O₂. Oxygenevolution in the presence of H₂O₂ was not inhibited by CCCPand was only partially inhibited by 5 µM 3-(3,4-dichlorophenyl)-1,1-dimethylurea(DCMU) which completely inhibited the Hill reaction with DPIP.The degree of inhibition by DCMU was decreased by a simultaneousaddition of CCCP. Carotenoid photobleaching in the presenceof CCCP was stimulated by H₂O₂. The CCCP-induced carotenoidphotobleaching was completely inhibited by DCMU. However, itwas only partially inhibited by DCMU in the presence of H₂O₂.These data indicate that H₂O₂ donates electrons at a site betweenthe CCCP-sensitive site and the reaction center of photosystemII and is reduced at a site between the DCMU-blocked site andthe reaction center of photosystem II. ¹Present address: Department of Biology, Kyushu Dental College,Kitakyushu 803, Japan. (Received June 20, 1974; )     

Effect of hydrogen peroxide on the fluorescence and the G550 absorption change of spinach chloroplast fragments

Effects of H₂O₂ on the transient phase of fluorescence and thelight-induced absorption change of C550 in the presence of ferricyanidewere studied in spinach chloroplast fragments at room temperature.In the presence of 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU),the parameter of the variable fluorescence, work integral, wasincreased by the addition of H₂O₂ and the rate of its recoveryin the dark was decreased. The steady-state fluorescence yieldwas decreased by H₂O₂. Essentially the same results were obtainedin the absence of ferricyanide. In the presence of DCMU, H₂O₂ decreased the steady-state absorptionchange of C550 and inhibited its reoxidation in the dark. Thesame effects were observed when H₂O₂ was added to chloroplastfragments in the presence of DCMU and carbonyl cyanide m-chlorophenylhydrazone.From these data we concluded that the fluorescence quencherQ and C550 are not identical. ¹Present address: Department of Biology, Kyushu Dental College,Kitakyushu 803, Japan. (Received June 20, 1974; )     

Scavenging of Hydrogen Peroxide in Prokaryotic and Eukaryotic Algae: Acquisition of Ascorbate Peroxidase during the Evolution of Cyanobacteria

Ascorbate (AsA) peroxidase was found in six species of cyanobacteriaamong ten species tested. Upon the addition of H₂¹⁸O₂ to thecells of AsA peroxidase-containing cyanobacteria, ¹⁶O₂ derivedfrom water and ¹⁸O₂ derived from H₂^I8O₂ were evolved in thelight. The evolution of ¹⁶O₂ was inhibited by DCMU and did notoccur in the dark, but ^I8O₂ was evolved even in the dark orin the presence of DCMU. Similar light-dependent evolution of¹⁶O₂ was observed in the cells of AsA peroxidase-containingEuglena and Chlamydomonas. However, the cells of AsA perox-idase-lackingcyanobacteria evolved only ¹⁸O₂ in either the light or dark.Furthermore, the quenching of chlorophyll fluorescence inducedby hydrogen peroxide was observed only in the cells of the AsAperoxidase-containing Synechocystis 6803, and not in the cellsof Anacystis nidulans which lacks AsA peroxidase. Thus, cyanobacteriacan be divided into two groups, those that has and those thatlacks AsA peroxidase. The first group scavenges hydrogen peroxidewith the peroxidase using a photoreductant as the electron donor,and the second group only scavenges hydrogen peroxide with catalase. (Received July 23, 1990; Accepted October 18, 1990)     

Superoxide, hydroxyl radical, and hydrogen peroxide effects on single-diaphragm fiber contractile apparatus

Reactive oxygenspecies contribute to diaphragm dysfunction in certainpathophysiological conditions (i.e., sepsis and fatigue). However, the precise alterations induced by reactive oxygen species orthe specific species that are responsible for the derangements inskeletal muscle function are incompletely understood. In this study, weevaluated the effect of the superoxide anion radical (O₂·), hydroxyl radical (·OH), and hydrogenperoxide (H₂O₂) on maximum calcium-activatedforce (F_max) and calcium sensitivity of the contractileapparatus in chemically skinned (Triton X-100) single rat diaphragmfibers. O₂· was generated using thexanthine/xanthine oxidase system; ·OH was generated using 1 mMFeCl₂, 1 mM ascorbate, and 1 mMH₂O₂; and H₂O₂ wasadded directly to the bathing medium. Exposure to O₂· or ·OH significantly decreasedF_max by 14.5% (P < 0.05) and 43.9%(P < 0.005), respectively. ·OH had no effect onCa²⁺ sensitivity. Neither 10 nor 1,000 µMH₂O₂ significantly altered F_max orCa²⁺ sensitivity. We conclude that the diaphragm issusceptible to alterations induced by a direct effect of ·OH andO₂·, but not H₂O₂, on thecontractile proteins, which could, in part, be responsible forprolonged depression in contractility associated with respiratorymuscle dysfunction in certain pathophysiological conditions.

     

Possible physiological mechanisms for production of hydrogen peroxide by the ichthyotoxic flagellate Heterosigma akashiwo

Blooms of the toxic red tide phytoplankton Heterosigma akashiwo(Raphidophyceae) are responsible for substantial losses withinthe aquaculture industry. The toxicological mechanisms of H.akashiwoblooms are complex and to date, heavily debated. One putativetype of ichthyotoxin includes the production of reactive oxygenspecies (ROS) that could alter gill structure and function,resulting in asphyxiation. In this study, we investigated thepotential of H.akashiwo to produce extracellular hydrogen peroxide,and have investigated which cellular processes are responsiblefor this production. Within all experiments, H.akashiwo producedsubstantial amounts of hydrogen peroxide (up to 7.6 pmol min^–110⁴ cells^–1), resulting in extracellular concentrationsof ~0.5 µmol l^–1 H₂O₂. Measured rates of hydrogenperoxide production were directly proportional to cell density,but at higher cell densities, accuracy of H₂O₂ detection wasreduced. Whereas light intensity did not alter H₂O₂ production,rates of production were stimulated when temperature was elevated.Hydrogen peroxide production was not only dependent on growthphase, but also was regulated by the availability of iron inthe medium. Reduction of total iron to 1 nmol l^–1 enhancedthe production of H₂O₂ relative to iron replete conditions (10µmol l^–1 iron). From this, we collectively concludethat production of extracellular H₂O₂ by H.akashiwo occurs througha metabolic pathway that is not directly linked to photosynthesis.     

LIGHT-INDUCED OXYGEN EVOLUTION CAUSED BY HYDROGEN PEROXIDE IN CATALASE-INHIBITED CHLORELLA CELLS

1. Chlorella cells and spinach chioroplasts, whose catalase activityhad been more than 90% inhibited by 10^–5 M azide, werefound to decompose H₂O₂ photochemically to liberate oxygen,indicating that H₂O₂ was used as an oxidant of the HILL reaction.
2. That, however, the observed phenomena cannot be fully accountedfor in terms of the HILL reaction with H₂O₂ was revealed bythe observation that an extract of Chiorella cells, which hadbeen completely freed from chlorophyll, also showed a light-acceleratedO2 evolution from H₂O₂ in the presence of 10^–5 M azide.This extract contained a large quantity of catalase, which seemedto have been, in some way, involved in the reaction in question.
3. The catalatic H₂O₂ decomposition caused by crystalline catalaseof mammalian liver (in the presence of 10^–5 M azide) wasnot accelerated by the effect of light.

¹ Present address: Department of Biology, Faculty of Science,Niigata University, Niigata. (Received June 4, 1961; )     

硝普钠缓解镧引起的黑麦草幼苗生长抑制和根系氧化损伤

采用水培方法,研究了外源一氧化氮（NO）供体硝普钠（SNP）对300 μmol·L^-1 LaCl₃胁迫下黑麦草幼苗生长和根系活性氧代谢的影响。结果表明：在LaCl₃胁迫下,喷施50 μmol·L^-1 SNP能够抑制镧（La）从黑麦草根系向地上部的转运,缓解La对幼苗生长的抑制作用;提高幼苗根系超氧化物歧化酶和抗坏血酸过氧化物酶活性,降低过氧化物酶活性及谷胱甘肽、脯氨酸、H₂O₂、丙二醛含量、超氧阴离子产生速率和质膜相对透性,对过氧化氢酶活性和抗坏血酸含量无显著影响。表明NO可通过活性氧代谢的调节,缓解高浓度La胁迫对黑麦草幼苗生长的抑制作用。     

Physiological Mechanisms of a Sub-Systemic Oxidative Burst Triggered by Elicitor-Induced Local Oxidative Burst in Potato Tuber Slices

Physiological mechanisms of triggering and occurrence of a short-distancesystemic (sub-systemic) oxidative burst (OXB) caused by inductionof local OXB induced by the elicitor were investigated usingpotato tuber tissues. The sub-systemic OXB was detected as luminol-mediatedchemiluminescence (CL) on the non-treated side of tissue slicesfollowing a transient appearance of local OXB on the other sidedirectly treated with an elicitor. The sub-systemic OXB wasnot induced when the elicitor was applied in the presence ofa radical scavenger, H₂O₂-catabolising enzyme, or inhibitorsof activation of local OXB and NADPH oxidase (diphenyleneiodonium:DPI), Ca²⁺ che-lator and Ca²⁺ channel blockers). Treatment withH₂O₂ solution rapidly caused the sub-systemic OXB, which wasinhibited by the presence of the above inhibitors either duringthe treatment with H₂O₂ or detection of CL. These results suggestedthat the elicitor-stimulated sub-systemic OXB may be dependenton Of generating NADPH oxidase activated by an unknown systemicsignal stimulated by H₂O₂ generated via local activation ofthe NADPH oxidase. ¹Present address: Iwate Biotechnology Research Center, Kita-gami, Iwate, 024 Japan.