环境胁迫下植物的化感作用及其诱导机制

植物化感作用是生态学研究中一个十分活跃的领域,对植物为什么和在什么条件下释放化感物质这一重要问题有不同的认识。在对环境胁迫下植物化感作用的变化及环境胁迫因子对化感物质听诱导机制等方面进行了评述后,指出植物化感化质的产生和释放是植物在环境胁迫的选择压力下形成的,植物化感作用是植物在进化过程中产生的一种对环境的适应性机制。     

菊科植物化感作用研究进展

对菊科植物化感作用的研究进展进行了综述。菊科植物中至少有 39个属存在化感作用 ,特别是一枝黄花属、向日葵属、胜红蓟属、银胶菊属、蒿属植物等有较多的研究报道。鉴定出的化感物质多为萜类、聚乙炔类、酚类、有机酸类等 ,这些化感物质对多种受体植物表现出程度不同的抑制或促进的效应。其化感作用机理表现在破坏受体膜系统的稳定性及水分平衡关系、抑制氧化磷酸化、促进或阻滞叶绿素的合成、影响矿质元素的吸收利用等。并对菊科植物化感物质在植物生长调节剂、天然除草剂和生物杀虫剂 ,或人工合成除草剂和杀虫剂上应用的前景进行了探讨。本文显示菊科植物的化感作用将在控制外来恶性杂草及维护生态平衡上扮演重要的角色。在当前菊科植物化感作用研究的基础上 ,提出了进一步研究的 6个方向 :(1)化感物质的生物合成途径与关键酶的特性研究 ;(2 )具化感潜势物种资源的调查评价及利用研究 ;(3)化感作用在自然生态系统中的演变规律 ;(4 )菊科重要作物自毒的生化机制及克服途径 ;(5 )具应用前景的菊科植物化感关键酶的基因克隆和转基因 ,并对受体植物基因的表达与调控进行研究 ;(6 )化感作用在可持续发展农业应用上的研究与开发 ,特别是作为天然除草剂及杀虫剂     

信号分子活性氧和NO在土荆芥化感胁迫诱导蚕豆根边缘细胞死亡中的调控

为了探讨入侵植物土荆芥(Chenopodium ambrosioides L.)化感作用如何干扰受体植物的防御功能,以蚕豆(Vicia faba L.)为受体,研究了土荆芥挥发油及其主要成分ρ-对伞花素和α-萜品烯对根边缘细胞活性及其胞外诱捕网厚度的影响,并测定了细胞内信号分子活性氧(Reactive oxygen species, ROS)和NO水平的变化。结果表明:在土荆芥挥发油、ρ-对伞花素和α-萜品烯作用下,蚕豆根边缘细胞粘胶层厚度增加,细胞活性下降,而ROS和NO水平升高,且表现为浓度依赖效应,细胞死亡率、ROS水平和NO水平三者之间存在着显著的正相关(P<0.05)。ROS清除剂抗坏血酸(AsA)、硝酸还原酶抑制剂(NaN₃)和泛Caspase抑制剂Z-VAD-FMK均可有效缓解挥发性物质的细胞致死效应,表明ROS和NO诱导根边缘细胞发生了Caspase依赖性细胞凋亡。上述结果表明土荆芥挥发性化感物质诱导蚕豆根边缘细胞内NO和ROS的水平上升,二者协同作用导致细胞凋亡,引起受体防御功能障碍,从而抑制了植物根系的生长。     

紫茎泽兰提取物对3种杂草的化感胁迫作用

为探讨紫茎泽兰(Eupatorium adenophorum)提取物对植物种子萌发和早期幼苗生长的影响及其生理机理,以稗草(Echinochloa crusgalli)、灰绿藜(Chenopodium glaucum)和反枝苋(Amaranthus retroflexus)3种常见的田间杂草为材料,采用根悬空培养等方法,研究了不同浓度紫茎泽兰提取物对3种杂草种子萌发和幼苗生长、根尖组织结构、根系边缘细胞(root border cell,RBC)生理特性和根冠果胶甲基酯酶(pectin methyl esterase,PME)活性的影响。结果发现:紫茎泽兰提取物对3种植物种子萌发均具有明显的抑制作用;1000 mg/L紫茎泽兰提取物处理后,3种杂草幼苗的根尖均有不同程度的伤害,如根尖肿胀、抽缩或变形;根尖表层细胞脱落、内层细胞排列混乱。紫茎泽兰提取物处理能显著抑制3种杂草幼苗根尖RBC的数量(分别比对照降低了44.5%、48.3%和64.0%);诱导RBC凋亡(凋亡率分别达到81.7%、91.3%和97.1%)并显著增加RBC的黏胶层厚度(分别比对照增加了99.0%、65.5%和61.1%)及诱导PME活性升高。这些结果表明:紫茎泽兰提取物抑制了3种杂草根边缘细胞的产生,并诱导了根尖边缘细胞凋亡,因而破坏了根边缘细胞对根尖的保护系统,最终抑制了根系的生长发育。研究为将紫茎泽兰提取物用于植物源除草剂的开发提供了理论依据。     

外源NO缓解紫茎泽兰提取物对黄瓜根边缘细胞的化感胁迫

以津优35号黄瓜为材料,采用根尖悬空气培养的方法,研究了紫茎泽兰提取物对黄瓜根边缘细胞的化感胁迫,以及外源NO缓解化感胁迫的效应.结果表明: 1000 mg·L^-1紫茎泽兰提取物对黄瓜根尖有明显的伤害作用,根尖组织结构被破坏,根尖表层细胞脱落,细胞排列混乱且疏松;这些伤害能够被外源NO有效缓解.与对照相比,紫茎泽兰提取物处理黄瓜幼苗根尖根边缘细胞(RBC)的数量和细胞活率被显著抑制,分别降低54.5%和97.2%,细胞凋亡率升高12.3倍,RBC的黏胶层厚度增加31.4%,根边缘细胞根冠果胶甲基酯酶(PME)活性显著增加.与紫茎泽兰提取物处理相比,提取物胁迫下添加外源NO处理的RBC数量和细胞活率分别增加72.4%和146.0%,细胞凋亡率和RBC黏胶层厚度分别降低30.7%和15.0%,PME活性在处理72 h时降低了14.3%.紫茎泽兰提取物对黄瓜RBC产生细胞毒性,诱导细胞发生凋亡和死亡,破坏RBC对根尖的保护,提取物进一步对根尖产生胁迫伤害,破坏根尖的组织结构.外源NO可以在一定程度上缓解提取物对黄瓜根尖及RBC的化感胁迫伤害.     

土荆芥挥发性化感物质对蚕豆叶表皮保卫细胞的影响

化感作用是外来植物土荆芥( Chenopodium ambrosioides)成功入侵的机制之一。为了探讨土荆芥挥发油的化感作用机制,该文以蚕豆( Vicia faba)叶的下表皮为材料,将表皮条孵育在分别含土荆芥挥发油、α-萜品烯和对伞花素的MES [2-( N-morpholino) ethanesulfonic acid]缓冲液中,25℃下光照培养30 min,采用吖啶橙/溴乙锭( AO/EB)双荧光染色法和Feulgen染色法,研究土荆芥挥发油、α-萜品烯和对伞花素对保卫细胞活性和细胞核形态的影响。结果表明：在土荆芥挥发油、α-萜品烯和对伞花素的作用下,蚕豆气孔保卫细胞活性降低,细胞核出现固缩、畸形或降解等细胞凋亡特征。随着处理剂量增加,保卫细胞活性显著下降,核异常率显著增加,表明土荆芥挥发油、α-萜品烯和对伞花素均对蚕豆保卫细胞具有细胞毒性,其中,挥发油毒性最大,α-萜品烯的毒性次之,对伞花素的毒性最小;Caspase抑制剂Z-VAD-FMK可缓解挥发油、α-萜品烯和对伞花素对保卫细胞的毒性,提高细胞活性,这种缓解效应随着抑制剂浓度的增加而增大。由此可见,土荆芥挥发油、α-萜品烯和对伞花素诱导蚕豆保卫细胞发生了Caspase依赖性的细胞凋亡。     

小麦化感作用研究进展

小麦是世界第一大粮食作物,在农业生产中占有重要地位.然而,由于人们为保证小麦产量往往施用大量的除草剂和杀菌剂,对环境造成了极大的危害.小麦化感作用是利用小麦活体或残体向环境中释放次生代谢物质对自身或其他生物产生作用,它克服了除草剂和杀菌剂等引起的环境污染问题,具有抑制杂草控制病害的潜力.本文对已有的小麦化感作用的研究进展情况进行了综合评述.其中小麦对杂草、虫害及病害产生防御功能的主要化感物质为异羟肟酸和酚酸类物质.小麦化感物质活性的发挥除了取决于化感物质的种类外,还由小麦自身的遗传因素、环境因素和生物因素的共同作用所决定.小麦化感物质在根际土壤中的滞留、迁移和转化过程、小麦化感作用与土壤生物的关系以及相关的作用机理是小麦化感作用研究的薄弱环节,其研究方法还需进一步探索改进.小麦化感作用在植物保护、环境保护以及作物育种等方面具有广泛的应用前景,促进了小麦抗逆性的增强以及产量和品质的提高.     

土荆芥挥发性化感物质诱导蚕豆保卫细胞死亡及信号调节

为了探讨入侵植物土荆芥的化感作用机制,以其入侵地广泛种植的农作物蚕豆叶片下表皮为受试材料,通过对保卫细胞的活性分析,研究了土荆芥挥发油及其两种主要成分α-萜品烯和对伞花素诱导保卫细胞死亡及其信号调节的机制。结果表明:土荆芥挥发油、α-萜品烯、对伞花素具有显著的细胞毒性,随着处理剂量增加,保卫细胞存活率显著下降,细胞核出现了畸形、碎裂和降解等程序性细胞死亡的典型特征;活性氧(Reactive oxygen species,ROS)、一氧化氮合酶(Nitric oxide synthetase,NOS)和Ca~(2+)的组织化学定位显示,在土芥挥发油、α-萜品烯和对伞花素作用下,保卫细胞内ROS、NOS和Ca~(2+)的水平明显高于对照组;活性氧清除剂(AsA)、Ca~(2+)螯合剂(EGTA)和硝酸还原酶抑制剂(NaN——3)均可有效缓解土荆芥挥发油、α-萜品烯和对伞花素的细胞毒性,显著提高了保卫细胞的存活率(P0.05)。上述结果表明,ROS、NO和Ca~(2+)参与了土荆芥挥发油、α-萜品烯和对伞花素诱导蚕豆保卫细胞死亡的信号调节过程。土荆芥挥发油、α-萜品烯和对伞花素诱导的保卫细胞死亡,可能是通过ROS和NO调控保卫细胞内Ca~(2+)水平的变化而引起的。     

土荆芥挥发油对蚕豆根尖细胞的化感潜力

化感作用是外来植物成功入侵的机制之一。本研究以蚕豆根尖为材料,采用DNA Ladder分析技术和蚕豆根尖微核技术,分析了入侵植物土荆芥挥发油经土壤载体诱导的细胞凋亡以及对细胞的遗传损伤。结果表明：（1）经挥发油处理24 h和48 h,低剂量（＜5 μL）挥发油对蚕豆根的生长与根尖细胞有丝分裂具有显著的促进作用,但随着处理剂量增大（＞5 μL）和处理时间延长,根的生长与细胞有丝分裂过程明显受到抑制。（2）挥发油具有诱导染色体畸变的效应,根尖细胞微核率随处理剂量增加和时间延长而增大,但当挥发油剂量大于15 μL,这种诱导效应降低。（3）通过DNA Ladder分析,经挥发油处理后根尖细胞发生了凋亡,其中24 h处理组DNA未发生特异性降解,当剂量大于15 μL处理48 h和剂量大于10 μL处理72 h后,DNA开始发生特异性降解,形成DNA Ladder,表明随着挥发油剂量增大和作用时间延长,细胞凋亡过程加剧。本研究结果表明土荆芥释放的挥发性化感物质能以土壤为载体对根细胞产生影响。     

苜蓿化感作用研究进展

苜蓿是一种优良的多年生豆科牧草 ,具有多重生态功能 ,在世界范围内广泛种植。苜蓿在第 2～ 4年后产量逐渐下降 ,而且种过苜蓿的土壤 ,间隔较短时间再种苜蓿 ,很难建植成功。许多研究表明 ,苜蓿体内含有的一些水溶性化学物质不仅能够对其产生自毒作用 ,而且也能对其他植物具有化感作用。本文综述了苜蓿化感作用研究进展 ,包括苜蓿中主要的化感物质、影响苜蓿化感作用的因素、苜蓿化感作用的应用三个方面。同时就苜蓿化感作用今后的研究重点提出一些看法和展望。     

Selective oxidative stress induces dual damage to telomeres and mitochondria in human T cells

Oxidative stress caused by excess reactive oxygen species (ROS) accelerates telomere erosion and mitochondrial injury, leading to impaired cellular functions and cell death. Whether oxidative stress‐mediated telomere erosion induces mitochondrial injury, or vice versa, in human T cells—the major effectors of host adaptive immunity against infection and malignancy—is poorly understood due to the pleiotropic effects of ROS. Here we employed a novel chemoptogenetic tool that selectively produces a single oxygen (¹O₂) only at telomeres or mitochondria in Jurkat T cells. We found that targeted ¹O₂ production at telomeres triggered not only telomeric DNA damage but also mitochondrial dysfunction, resulting in T cell apoptotic death. Conversely, targeted ¹O₂ formation at mitochondria induced not only mitochondrial injury but also telomeric DNA damage, leading to cellular crisis and apoptosis. Targeted oxidative stress at either telomeres or mitochondria increased ROS production, whereas blocking ROS formation during oxidative stress reversed the telomeric injury, mitochondrial dysfunction, and cellular apoptosis. Notably, the X‐ray repair cross‐complementing protein 1 (XRCC1) in the base excision repair (BER) pathway and multiple mitochondrial proteins in other cellular pathways were dysregulated by the targeted oxidative stress. By confining singlet ¹O₂ formation to a single organelle, this study suggests that oxidative stress induces dual injury in T cells via crosstalk between telomeres and mitochondria. Further identification of these oxidation pathways may offer a novel approach to preserve mitochondrial functions, protect telomere integrity, and maintain T cell survival, which can be exploited to combat various immune aging‐associated diseases.     

Quiescence induced by iron challenge protects neuroblastoma cells from oxidative stress

The brain uses massive amounts of oxygen, generating large quantities of reactive oxygen species (ROS). Because of its lipid composition, rich in unsaturated fatty acids, the brain is especially vulnerable to ROS. Furthermore, oxidative damage in the brain is often associated with iron, which has pro-oxidative properties. Iron-mediated oxidative damage in the brain is compounded by the fact that brain iron distribution is non-uniform, being particularly high in areas sensitive to neurodegeneration. This work was aimed to further our understanding of the cellular mechanisms by which SHSY5Y neuroblastoma cells adapt to, and survive increasing iron loads. Using an iron accumulation protocol that kills about 50% of the cell population, we found by cell sorting analysis that the SHSY5Y sub-population that survived the iron loading arrested in the G(0) phase of the cell cycle. These cells expressed neuronal markers, while their electrical properties remained largely unaltered. These results suggest that upon iron challenge, neuroblastoma cells respond by entering the G(0) phase, somehow rendering them resistant to oxidative stress. A similar physiological condition might be involved in neuronal survival in tissues known to accumulate iron with age, such as the hippocampus and the substantia nigra pars compacta.     

Mitochondria-targeted antioxidant mito-TEMPO alleviate oxidative stress induced by antimycin A in human mesenchymal stem cells

The cell therapy of damaged tissue, which is linked to hypoxia condition might fail, in large part due to the emergence of oxidative stress (OS) and/or mitochondrial dysfunctions. Thus, the invigoration of stem cells against oxidative stress could be a reliable strategy to improve the cell therapy outcome. Of various antioxidants, mito-Tempo (mito-T) is one of the potent antioxidants that could target and neutralize the mitochondrial oxidative stress. In this study, for the induction of hypoxia and oxidative stress in mitochondria of the mesenchymal stem cells (MSCs) isolated from human adipose tissue, antimycin A (AMA) was used and then several parameters were analyzed, including cell viability and cell cycle arrest of MSCs exposed to AMA, mito-T, antioxidant potential, redox homeostasis, and signaling pathways in MSCs under oxidative stress. Based on our findings, the treated MSCs were found to impose a high resistance to the OS-induced apoptosis, which correlated with the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway required to manage OS. Upon exposure of the MSCs to high oxidative stress conditions using AMA, the cells failed to scavenge. The use of mito-T was found to alleviate the damage induced by oxidative stress through both direct functions of the free radical scavenging and the interplay in terms of cell signaling pathways including the upregulation of the Nrf2 pathway. These findings may pave the way in the stem cell therapy for the hypoxia-mediated tissue damage.     

Cytoprotective effect of phloroglucinol on oxidative stress induced cell damage via catalase activation

We investigated the cytoprotective effect of phloroglucinol, which was isolated from Ecklonia cava (brown alga), against oxidative stress induced cell damage in Chinese hamster lung fibroblast (V79-4) cells. Phloroglucinol was found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, hydrogen peroxide (H(2)O(2)), hydroxy radical, intracellular reactive oxygen species (ROS), and thus prevented lipid peroxidation. As a result, phloroglucinol reduced H(2)O(2) induced apoptotic cells formation in V79-4 cells. In addition, phloroglucinol inhibited cell damage induced by serum starvation and radiation through scavenging ROS. Phloroglucinol increased the catalase activity and its protein expression. In addition, catalase inhibitor abolished the protective effect of phloroglucinol from H(2)O(2) induced cell damage. Furthermore, phloroglucinol increased phosphorylation of extracellular signal regulated kinase (ERK). Taken together, the results suggest that phloroglucinol protects V79-4 cells against oxidative damage by enhancing the cellular catalase activity and modulating ERK signal pathway.     

The role of oxidative stress in acrolein-induced DNA damage in HepG2 cells

This study evaluated the role of oxidative stress in acrolein-induced DNA damage, using HepG2 cells. Using the standard single cell gel electrophoresis (SCGE) assay, a significant dose-dependent increment in DNA migration was detected at lower concentrations of acrolein; but at the higher tested concentrations, a reduction in the migration was observed. Post-incubation with proteinase K significantly increased DNA migration in cells exposed to higher concentrations of acrolein. These results indicated that acrolein caused DNA strand breaks and DNA-protein crosslinks (DPC). To elucidate the oxidatively generated DNA damage mechanism, the 2,7-dichlorofluorescein diacetate (DCFH-DA) and o-phthalaldehyde (OPT) were used to monitor the levels of reactive oxygen species (ROS) and glutathione (GSH), respectively. The present study showed that acrolein induced the increased levels of ROS and depletion of GSH in HepG2 cells. Moreover, acrolein significantly caused 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) formation in HepG2 cells. These results demonstrate that the DNA damage induced by acrolein in HepG2 cells is related to the oxidative stress.     

The role of oxidative stress in acrolein-induced DNA damage in HepG2 cells

This study evaluated the role of oxidative stress in acrolein-induced DNA damage, using HepG2 cells. Using the standard single cell gel electrophoresis (SCGE) assay, a significant dose-dependent increment in DNA migration was detected at lower concentrations of acrolein; but at the higher tested concentrations, a reduction in the migration was observed. Post-incubation with proteinase K significantly increased DNA migration in cells exposed to higher concentrations of acrolein. These results indicated that acrolein caused DNA strand breaks and DNA-protein crosslinks (DPC). To elucidate the oxidatively generated DNA damage mechanism, the 2,7-dichlorofluorescein diacetate (DCFH-DA) and o-phthalaldehyde (OPT) were used to monitor the levels of reactive oxygen species (ROS) and glutathione (GSH), respectively. The present study showed that acrolein induced the increased levels of ROS and depletion of GSH in HepG2 cells. Moreover, acrolein significantly caused 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodGuo) formation in HepG2 cells. These results demonstrate that the DNA damage induced by acrolein in HepG2 cells is related to the oxidative stress.