植物光毒素

介绍了植物光霉素的概念和结构，阐述了光霉素对病毒、细菌、真菌、线虫、昆虫和植物的作用。     

光动力疗法对肿瘤的作用机制及其影响因素

光动力疗法（photodynamic therapy,PDT）被提出可用于肿瘤治疗已有25年历史。最近几年,PDT在临床上得到了较广泛的应用。一些光敏剂已被某些国家批准作为PDT药物。有关新型光敏剂的合成、体内体外试验、作用机制等方面的研究得到了迅速的发展,并取得了丰硕的成果。现从光动力反应基本原理出发,回顾了有关肿瘤PDT作用机制特别是细胞水平作用机制及其影响因素的最新研究成果。对肿瘤PDT作用机制进行全面深入的探讨,将有助于寻找改善和加强PDT功效的方法,使其在肿瘤治疗中发挥更大的优势。     

光系统Ⅱ颗粒内单线态氧诱导产生超氧阴离子自由基

活性氧是生物体有氧代谢的必然产物。当机体处于疾病或胁迫条件下 ,活性氧的生成将更加活跃[1] 。由于类囊体膜是植物体光合放氧的器官 ,处于高浓度的氧环境中 ,同时类囊体膜上还存在着活跃的电子传递体系 ,因此类囊体膜是超氧阴离子自由基生成的活跃部位[2 ] 。最近的研究表明 ,ＰＳⅠ和ＰＳⅡ都是超氧阴离子自由基的生成部位[3] 。其中 ,对ＰＳⅠ生成超氧的机制研究已比较深入[2 .4 ] ,而对ＰＳⅡ生成超氧阴离子自由基的机制研究是在近几年内刚刚开展[3 ,5- 7] 。ＰＳⅡ中生成的另一活性氧是单线态氧。通常认为由于强光照射下ＰＳⅡ生成的…     

Triton X-100对70℃处理后光系统Ⅰ颗粒耗氧速率的影响

比较了70℃10min处理前后和加与不加Triton X-100时光系统Ⅰ颗粒的耗氧速率、荧光光谱和吸收光谱等.70℃处理后光系统Ⅰ颗粒的耗氧速率明显降低,Triton X-100可以恢复其耗氧速率.在Triton X-100存在时,光系统Ⅰ颗粒耗氧速率的急剧上升是光系统Ⅰ核心复合物和捕光色素蛋白复合体Ⅰ分离后产生的单线态氧引起的.     

利用RNO脱色反应检测类囊体中的单线态氧

光敏剂RB在光照射下与O₂反应产生 ¹O₂, ¹O₂与组氨酸或咪唑反应的中间产物使RNO发生氧化,导致RNO在440 nm处吸光度减小,此即为RNO脱色反应.RNO脱色反应随着光照时间的增加而增大,表明RB受光照射后使 ¹O₂增加;随着组氨酸或咪唑浓度的增加,RNO脱色反应增大;咪唑在RNO脱色反应中的作用更明显. ¹O₂淬灭剂NaN₃或DABCO存在时,RNO脱色反应降低.利用RNO脱色反应检测到莴苣类囊体在强光照射下产生的 ¹O₂,随着光强和照射时间增加,类囊体中 ¹O₂的产生增加.     

Triton X-100对70℃处理后光系统I颗粒耗氧速率的影响

比较了70℃10min处理前后和加与不加TritonX-100时光系统I颗粒的耗氧速率、荧光光谱和吸收光谱等。70℃处理后光系统I颗粒的耗氧速率明显降低,TritonX-100可以恢复其耗氧速率。在TritonX-100存在时,光系统I颗粒耗氧速率的急剧上升是光系统I核心复合物和捕光色素蛋白复合体I分离后产生的单线态氧引起的。     

植物病原真菌致病毒素草酸的研究进展

许多植物病原菌可以分泌草酸,草酸作为致病的关键因子在病原菌的侵染过程中发挥着重要作用,并与病原菌的致病性、毒性有密切关系。草酸可通过氧化和脱羧两条途径进行降解,因此可以将草酸降解酶基因导入植物,从而获得对这类病害的抗性。     

植物抗逆性与光呼吸作用之间的关系

用Na_2SO_3溶液浸泡,可以影响菠菜叶片中超氧物歧化酶的活性。较低浓度(0.1、1、10ppm)的该溶液使酶活性增加,而100ppm的该溶液则降低此酶的活性。同时发现叶片中光呼吸关键酶,即乙醇酸氧化酶活性也随着发生正相关的变化。讨论植物受SO_3~(2-)胁迫后,乙醇酸氧化酶的活性变化与植物抗逆性的产生可能存在密切的关系。     

寄主选择性植物病原真菌的毒素化学

Wheeler和Luke把那些在病害中起重要病因作用的毒素称为致病毒素（path。toxin）‘”,那么由真菌产生的致病毒素则称为真菌毒素（MyC0t0Xin）。长期以来,人们一直对那些重要的植物病原真菌毒素进行分离、提纯和化学结构鉴定,发现它们大多数为低分子量的次生代谢产物m．自从＊all欢。从梨上的菊池键格抱（Alternariakikl,chiana）中发现第一个寄生选择性真菌毒素阳StSCICChVCt0Xill）以来l’］,现已报道有9个属的对种植物病原真菌可以产生寄主选择性毒素14－’］其中已有15种明确了其化学结构,（见表1）。实践证明来源于某一病原…     

Lidocaine: a hydroxyl radical scavenger and singlet oxygen quencher

Lidocaine, a local anaesthetic, has been shown to reduce ventricular arrhythmias associated with myocardial infarction and ischemic myocardial injury and its protective effects has been attributed to its membrane stabilizing properties. Since oxygen radicals are known to be produced during ischemia induced tissue damage, we have investigated the possible antioxidant properties of lidocaine and found that lidocaine does not scavenge 0₂^–· radicals at 1 to 20 mM concentrations. However, lidocaine was found to be a potent scavenger of hydroxyl radicals and singlet oxygen. Hydroxyl radicals were produced in a Fenton type reaction and detected as DMPO-OH adducts by electron paramagnetic resonance spectroscopic techniques. Lidocaine inhibited DMPO-OH adduct formation in a dose dependent manner. The amount of lidocaine needed to cause 50% inhibition of that rate was found to be approximately 80 M and at 300 M concentration it virtually eliminated the DMPO-OH adduct formation. The production of OH-dependent TBA reactive products of deoxyribose was also inhibited by lidocaine in a dose dependent manner. Lidocaine was also found to inhibit the ¹O₂-dependent 2,2,6,6-tetramethylpiperidine N-oxyl (TEMPO) formation in a dose dependent manner. ¹O₂ was produced in a photosensitizing system using Rose Bengal or Methylene Blue as photosensitizers and was detected as TEMP-¹O₂ adduct by EPR spectroscopy. The amount of lidocaine required to cause 50% inhibition of TEMP-¹O₂ adduct formation was found to be 500 M. These results suggest that the protective effect of lidocaine on myocardial injury may, in part, be due to its reactive oxygen scavenging properties. These results may also explain the membrane stabilizing actions of lidocaine by scavenging OH · and ¹O₂ that are implicated in membrane lipid peroxidation.     

Generation of superoxide and singlet oxygen from α-tocopherolquinone and analogues

Three potential routes to generation of reactive oxygen species (ROS) from α-tocopherolquinone (α-TQ) have been identified. The quinone of the water-soluble vitamin E analogue Trolox C (Trol-Q) is reduced by hydrated electron and isopropanol α-hydroxyalkyl radical, and the resulting semiquinone reacts with molecular oxygen to form superoxide with a second order rate constant of 1.3 × 10⁸ dm³/mol/s, illustrating the potential for redox cycling. Illumination (UV-A, 355 nm) of the quinone of 2,2,5,7,8-pentamethyl-6-hydroxychromanol (PMHC-Q) leads to a reactive short-lived (ca. 10^{? 6} s) triplet state, able to oxidise tryptophan with a second order rate constant greater than 10⁹ dm³/mol/s. The triplet states of these quinones sensitize singlet oxygen formation with quantum yields of about 0.8. Such potentially damaging reactions of α-TQ may in part account for the recent findings that high levels of dietary vitamin E supplementation lack any beneficial effect and may lead to slightly enhanced levels of overall mortality.     

Reaction of para-hydroxybenzoic acid esters with singlet oxygen in the presence of glutathione produces glutathione conjugates of hydroquinone, potent inducers of oxidative stress

The determination and toxicological characterization of products of the reaction between p-hydroxybenzoic acid esters (parabens) and singlet oxygen (¹O₂) are very important because of the frequent use of parabens in cosmetics and possible generation of ¹O₂ in the skin. We observed ¹O₂-dependent production of mono-, di-, and tri-substituted glutathione (GSH) conjugates of hydroquinone (HQ) during visible light-irradiation of a mixture of methyl or ethyl paraben and GSH in the presence of rose bengal (RB). 1,4-Benzoquinone (BQ) and HQ were produced during the irradiation in the absence of GSH. While a mixture of BQ and GSH produced only mono-substituted conjugate, irradiation of the mixture with RB produced mono-, di-, and tri-substituted conjugates. These observations indicate that ¹O₂ is involved both in the production of BQ and HQ from parabens and in the formation of multi-substituted GSH conjugates from mono-substituted conjugate. Tri-substituted conjugate generated larger amounts of hydrogen peroxide in an aqueous solution than mono-substituted conjugates or HQ did. Detection of semiquinone radical suggests that the autoxidation of conjugates is related to the generation of hydrogen peroxide. The results obtained in this study indicate that parabens may induce oxidative stress in the skin after conversion to GSH conjugates of HQ by reacting with ¹O₂ and GSH.     

Unifying model for the photoinactivation of Photosystem II in vivo under steady-state photosynthesis

We present a unifying mechanism for photoinhibition based on current obsevations from in vivo studies rather than from in vitro studies with isolated thylakoids or PS II membranes. In vitro studies have limited relevance for in vivo photoinhibition because very high light is used with photon exposures rarely encountered in nature, and most of the multiple, interacting, protective strategies of PS II regulation in living cells are not functional. It is now established that the photoinactivation of Photosystem II in vivo is a probability and light-dosage event which depends on the photons absorbed and not the irradiance per se. As the reciprocity law is obeyed and target theory analysis strongly suggests that only one photon is required, we propose that a single dominant molecular mechanism occurs in vivo with one photon inactivating PS II under limiting, saturating or sustained high light. Two mechanisms have been proposed for photoinhibition under high light, acceptor-side and donor-side photoinhibition [see Aro et al. (1994) Biochim Biophys Acta 1143: 113–134], and another mechanism for very low light, the low-light syndrome [Keren et al. (1995) J Biol Chem 270: 806–814]. Based on the exciton-radical pair equilibrium model of exciton dynamics, we propose a unifying mechanism for the photoinactivation of PS II in vivo under steady-state photosynthesis that depends on the generation and maintenance of increased concentrations of the primary radical pair, P680⁺Pheo_–, and the different ways charge recombination is regulated under varying environmental conditions [Anderson et al. (1997) Physiol Plant 100: 214–223]. We suggest that the primary cause of damage to D1 protein is P680⁺, rather than singlet O₂ formed from triplet P680, or other reactive oxygen species.     

Commentary the Measurement of Oxidative Damage to DNA by HPLC and GC/MS Techniques

Oxidative damage to DNA has been measured by quantitating 8-hydroxy-2′-deoxyguanosine (8-OHdGuo) after enzymic digestion of DNA, followed by HPLC separation and electrochemical detection. Alternatively, 8-hydroxyguanine (and a wide range of other base-derived products of free radical attack) may be measured after acidic hydrolysis of DNA or chromatin, followed by derivatization and gas-chromatography/mass spectrometry. Both techniques have comparable sensitivity, but GC/MS enables determination of a wide variety of chemical changes to all four DNA bases and it can be applied to DNA-protein complexes. However, the two techniques do not always give similar results. Potential reasons for this are discussed. Greater attention to methodological questions is required before using measurement of 8-OHdGuo as a “routine” marker of oxidative DNA damage in vivo.     

Activation of Molecular Oxygen by Infrared Laser Radiation in Pigment-Free Aerobic Systems

With the goal of mimicking the mechanisms of the biological effects of low energy laser irradiation, we have shown that infrared low intensity laser radiation causes oxygenation of the chemical traps of singlet oxygen dissolved in organic media and water saturated by air at normal atmospheric pressure. The photooxygenation rate was directly proportional to the oxygen concentration and strongly inhibited by the singlet oxygen quenchers. The maximum of the photooxygenation action spectrum coincided with the maximum of the oxygen absorption band at 1270 nm. The data provide unambiguous evidence that photooxygenation is determined by the reactive singlet ¹_g state formed as a result of direct laser excitation of molecular oxygen. Hence, activation of oxygen caused by its direct photoexcitation may occur in natural systems.