植物地上部对铝毒的生理响应及其耐性

全世界50％以上潜在的可耕地属于酸性土壤,铝毒害是酸性土壤上植物生长最有害因素之一。近年来,为了阐明植物铝毒害及其耐性,前人已进行了大量的研究,并有一些综述性文章发表。然而,大多数文章主要综述铝对植物根系的影响及其耐性,因为根生长受抑是最早的铝毒害症状之一和溶液培养时最容易辨认的铝毒害症状。为此,本文综述了铝对植物地上部光合作用、光保护系统、水分利用效率、含水量、碳水化合物含量、矿质营养、有机酸和氮代谢的影响,并对富铝植物的解铝毒机制（铝与小分子有机酸螯合和把铝隔离在对铝不敏感的表皮细胞和液泡内）进行了综述。本文还对植物耐铝遗传学和分子生物学及今后需要研究的问题进行了讨论。     

铝胁迫下小麦根部苹果酸和柠檬酸的直接测定

铝的有害性严重制约了约占世界可耕地面积40％的酸性土壤中的作物生产。从植物的培养液巾发现从根部分泌出的有机酸与铝结合从而实现无毒化是其抗铝逆性机理的重要依据。而本文直接测定了铝胁迫下培育的小麦根中的铝和有机酸含量,确认了主要积累的是苹果酸和柠檬酸。发现随着提高培养液中的铝浓度,根部的铝含量也相应增加。同时,虽然根中的柠檬酸含量无明显变化,但苹果酸被诱导增加。通过对有机酸与铝的络合能力的调查,探讨了对植物抗铝逆性强弱的影响。     

茶园土壤耐酸铝酵母菌的分离鉴定及其耐铝特性的初步研究

目的为研究铝毒及耐铝机制提供更好的模式生物材料和进一步研究耐铝机制提供依据。方法通过对云南龙陵县茶园土壤耐酸铝微生物的筛选、分离和纯化,筛选出一株Y31耐酸铝酵母。结果经D1/D2区域克隆测序获取全长26S rDNA区域序列,构建系统发育树,初步鉴定Y31为长形隐球酵母（Cryptococcus longus）。在LPM培养基及GM培养基上耐铝水平检测表明Y31分别能耐100 mmol/L和50 mmol/L铝。用不同铝浓度处理酵母菌后,进行FDA PI双染色并用荧光显微镜观察,当铝浓度达到100 mmol/L时,出现明显的细胞凋亡过程。结论本研究为铝毒和生物体耐铝机制提供了生物材料。     

不同浓度铝胁迫对小麦成熟胚再生植株及生理特性的影响

研究了酸性条件下铝胁迫对小麦的铝抗性品系Atlas66和铝敏感品系EM12的诱导、分化、根和叶细胞的某些生理特性的影响。结果表明,抗性品系小麦Atlas66受铝毒害较小,诱导率、分化率无明显变化,而铝敏感品系小麦EM12随铝浓度增大诱导率、分化率分别降至23．42％、11．87％;在不同浓度铝作用下,铝敏感品系EM12叶片中的脯氨酸含量显著升高,而铝抗性品系Atlas66叶片中的脯氨酸含量变化不大,但其根细胞壁的蛋白及己糖和糖醛酸的含量均升高,表明铝促进根细胞壁成分的合成,提高了抗铝性。     

铝浸种对荞麦种子萌发和幼苗生理的影响

对2个荞麦(Fagopyrum esculentumMoench)品种(小白花叶和溪荞5号)在铝浸种后萌发特性和幼苗的生理变化进行了初步研究。结果表明,10~1000mg.L-1的铝浸种处理对2个荞麦品种的发芽率和发芽指数影响不明显,低浓度铝(≤100mg.L-1)处理可降低荞麦种子细胞膜透性,减少细胞内营养物质的外渗,促进种子的萌发。5000mg.L-1的铝处理降低了荞麦的发芽指数。种子萌发后,铝对荞麦根的伸长有抑制作用,并且随着铝浓度的增加,抑制作用增大。10~1000mg.L-1的铝浸种处理对荞麦叶片内MDA含量影响较小,但高浓度的铝处理(5000mg.L-1)明显增加了MDA的含量;POD、SS、Pro随着铝浓度增加都有先降低后增加的趋势;不同品种叶片内CAT活性变化趋势不同,小白花叶内CAT活性对铝的敏感性大于溪荞5号。试验结果可以看出,荞麦种子和幼苗对环境中的铝都有较强的耐受性,在铝胁迫下,荞麦可以通过升高POD活性以及增加SS和Pro含量来缓解铝毒害,不同荞麦的基因型对铝毒害的反应有一定的差异性。     

铝诱导植物程序性细胞死亡信号转导的研究进展

铝是制约酸性土壤上作物生产的主要因素。铝诱导氧化胁迫产生大量活性氧/一氧化氮,引起胞质钙超载,通过线粒体信号转导途径激发相关凋亡基因,从而引起细胞主动死亡,以减轻铝对植物的进一步毒害。本文综述了铝诱导程序性细胞死亡的信号分子、相关基因以及信号转导途径,对未来的研究方向提出了展望,为深入研究植物铝毒害机理和耐铝机制提供参考。     

一株耐铝隐球酵母菌株5-2的分离鉴定及耐铝特性分析

目的分离高耐铝的微生物菌株,为耐铝基因克隆和耐铝机制研究奠定基础。方法用含5 mmol/L铝的平板逐级筛选和纯化,PCR扩增ITS序列和26S r DNA D1/D2序列,用菌株在不同铝浓度的固体培养基和液体培养基中的生长状况鉴定耐铝能力,用ICP-AES测量菌液上清中剩余活性铝的含量。结果通过ITS序列和26S r DNA D1/D2序列比对及形态观察,初步鉴定该菌株为Cryptococcus podzolicus,该菌株的最大耐铝能力达到100 mmol/L,而且该菌株能够吸附溶液中的活性铝,这可能是其耐铝的原因之一。结论该菌种是首次发现具有耐铝能力,从而为土壤微生物耐铝机制的研究及克隆耐铝基因提供了很好的实验材料。     

铝胁迫对小麦胚诱导及超微结构的影响

目的：铝毒害在酸性土壤中普遍存在,已经成为影响小麦产量和品质的重要因素,因此小麦铝毒害与耐铝分子机制的研究逐渐成为了小麦抗逆研究的热点内容之一。从细胞水平上阐明铝毒害的机理。方法：设置了3种铝浓度梯度(100、200 300μmol/1),通过组织培养及透射电镜的方法观察了铝对铝敏感材料Scout66,耐铝材料Adas66及湖北主栽品种EM12胚发生阶段及超微结构的影响。结果：铝降低了胚的诱导率,抑制了胚的进一步分化,其中幼胚的诱导率从对照的94．0%降到了25．3% (300μmaol/1),成熟胚的诱导率从对照的75．0%降到了17．3%(300μtmol/1);铝严重破坏了小麦根尖的超微结构,与对照相比,最明显的变化是细胞核结构变得不完整,同时空泡增多,线粒体数量增加,脊的结构变模糊甚至消失。结论：以上结果说明铝破坏了细胞的超微结构,特别是细胞核和线粒体结构的破坏阻止了细胞的进一步分裂和分化。     

模拟酸雨对主要酸性土壤中铝的溶出及形态的影响

本文研究了模拟酸雨对主要酸性土壤中铝的溶出及形态变化的影响。结果表明,模拟酸雨对土壤酸化的影响较小,但对土壤铝的溶出却影响明显,尤其在pH<4.0时;模拟酸雨对不同类型土壤的影响是不同的,其中以高度风化的酸性土壤较为敏感。模拟酸雨对土壤游离铝形态的影响是重要的,酸处理后,交换性铝略有增加,无定形活性铝增加较多,而有机络合态铝有减少的趋势。这表明在酸雨的长期作用下,铝终将转化为交换性铝和水溶性铝而进入环境并危害生态系统。     

生长素及其运输蛋白对植物铝胁迫的响应

铝对植物的毒害作用主要表现为抑制根尖生长,而根尖生长与生长素及其运输密切相关,铝可能影响了生长素及其代谢过程,但目前尚不清楚生长素及其运输蛋白如何参与植物应对铝胁迫响应。本文通过分析、总结前人研究,并结合自己的前期研究结果,初步阐述生长素或其运输蛋白对植物铝胁迫的响应,即铝影响生长素代谢的相关基因,干扰根尖生长素运输蛋白在细胞内分布及其囊泡运输,调控生长素的极性运榆,进而抑制根尖生长。另一方面,生长素或其运输蛋白又参与了植物应对铝胁迫过程,这主要体现在参与了植物铝毒信号传递、根系铝内置化过程和减缓铝诱导的氧化胁迫。最后,本文提出了生长素及其运输蛋白对植物铝胁迫响应的可能模型。     

Microbial interactions with aluminium

Although aluminium is the most abundant metal in the Earth's crust, it lacks biological functions and shows a low bioavailability. Acid rain, however, solubilizes aluminium to toxic levels. Most research on the biological effects of aluminium has been centred on the analysis of aluminium-tolerant plants as well as its possible relationship with neurological disorders in humans. Also, several studies have been reported concerning aluminium effects on microorganisms, with more interest directed to cyanobacteria, soil bacteria and mycorrhizal fungi. Competition with iron and magnesium, and binding to DNA, membranes or cell walls are considered the main toxic effects of aluminium in microbes.     

Model studies of the precipitation of silica in the presence of aluminium; implications for biology and industry

The unique chemical affinity between the oxides of silicon and aluminium has been cited as a potential route for the amelioration of the detrimental effects of aluminium in the environment and in biological systems. A greater understanding of silicon-aluminium interactions may assist in this endeavour and also provide a means of overcoming silica fouling problems encountered by industry which are exacerbated by the presence of aluminium. It is also conceivable that this increased knowledge may demonstrate a positive use for aluminium in the processing of the silicon dioxide phase. In this study we report the effect of aluminium ions, derived from aluminium chloride, on silicic acid species obtained from potassium catecholato complexes of silicon at circumneutral pH at the molar ratios 1000Si:Al, 100Si:Al and 50Si:Al. Silica and low levels of aluminium-rich silica materials were formed with Si:Al ratios of about 3.5:1 comparable with the element ratios detected in senile plaques and aluminium-rich scale. A kinetic study showed that aluminium in the reaction medium slowed down the rate of formation of one of the silica species formed early in the condensation process, e.g. trimers, but increased the rate at which silicic acid was removed from sub 1 nm diameter particles. The materials precipitated in the presence of aluminium were composed of smaller particles and aggregates with smaller pores (Si100:Al and Si50:Al systems) or larger pores (Si1000:Al) compared to the control. The nature of the interactions responsible for these differences is discussed. The effects described here demonstrate the ability of silica and aluminium to interact under conditions such as those found in biological systems. That silica reacts with aluminium in the presence of catechol supports the protective role assigned to silicon.     

Does neurotransmission impairment accompany aluminium neurotoxicity?

Neurobehavioral disorders, except their most overt form, tend to lie beyond the reach of clinicians. Presently, the use of molecular data in the decision-making processes is limited. However, as details of the mechanisms of neurotoxic action of aluminium become clearer, a more complete picture of possible molecular targets of aluminium can be anticipated, which promises better prediction of the neurotoxicological potential of aluminium exposure. In practical terms, a critical analysis of current data on the effects of aluminium on neurotransmission can be of great benefit due to the rapidly expanding knowledge of the neurotoxicological potential of aluminium. This review concludes that impairment of neurotransmission is a strong predictor of outcome in neurobehavioral disorders. Key questions and challenges for future research into aluminium neurotoxicity are also identified.     

Regional alterations in calcium homeostasis in the primate brain following chronic aluminium exposure

The present study investigates the possible effects of chronic aluminium exposure on the various aspects of calcium homeostasis in the primate central nervous system. Aluminium administration caused a marked decline in the activity of Ca2+ ATPase in the monkey brain. The total calcium content was also significantly raised following aluminium exposure. Concomittant to the increase in the calcium content, the levels of lipid peroxidation were also augmented in the aluminium treated animals, thereby further accentuating the aluminium induced neuronal damage. In addition, aluminium had an inhibitory effect on the depolarization induced 45Ca2+ uptake via the voltage operated channels. The results presented herein, indicate that the toxic effects of aluminium could be mediated through modifications in the intracellular calcium homeostasis with resultant altered neuronal function.     

Aluminium speciation in the Vienne river on its upstream catchment (Limousin region, France)

The aim of this study was to investigate the speciation of aluminium in the river Vienne on its upstream catchment (Limousin region, France) over a period of seven years (May 1998-September 2004) in order to assess harmful effects on aquatic life. Two sampling points were selected: the first at 4 km from the spring (Peyrelevade), and the second one at 89 km from the spring (Royères). The aluminium speciation was computed with Mineql+ 4.5 speciation software. Organic matter and phosphorous play a major role in aluminium speciation. If we consider the free aluminium ion (Al3+) as being the only toxic form of aluminium, the concentrations of toxic forms recorded at Peyrelevade and Royères were always below the toxic values for fish. However, if the sum of the concentrations of Al3+, Al(OH)2+, Al(OH)2+ and Al(OH)4- is taken into consideration, the concentration of aluminium recorded may have adverse effects on aquatic life in the upstream catchment of the river Vienne. Al(OH)4- is the major contributor to the concentration in toxic aluminium recorded. In general, Al(OH)4- forms appears in water during the summer with water alkalinisation due to an increase in photosynthetic activities.     

Physiological and structural responses of the cyanobacterium Anabaena cylindrica to aluminium

When adding aluminium (3.7–370 μ M ) as AlCl₃–6H₂0 to cultures of the nitrogen-fixing cyanobacterium Anabaena cylindrica , strain 1403/2a (CCAP), the following responses were observed: The effects of aluminium were dependent on pH. being most drastic at pH 6.0. At this pH the growth of A. cylindrica was significantly reduced by 3.7 μ M aluminium and completely inhibited by 370 μ M . The content of chlorophyll a and phycocyanin decreased after treatment with aluminium. Also, aluminium lowered the rates of both CO₂-fixation and N₂-fixation with total inhibition of both processes by 370 μ M . At the lower concentrations used the nitrogenase activity started to recover after about 100 h. The aluminium content in the cells increased with increasing concentration and with time. At 190 μ M the aluminium concentration in the cells represented 2.4 and 3.3% of the dry weight after 6 and 24 h, respectively. Clogging of filaments and lysis of vegetative cells were apparent at higher aluminium concentrations while the frequency of heterocysts increased in all concentrations used. The most pronounced ultrastructural changes included accumulation of cyanophycin granules and degradation of the thylakoids. The ultrastructure of the heterocysts was however not affected. It is concluded that major reasons for the toxicity are interactions with membranes and phosphate deficiency.     

Inhibitory effect of aluminium on the axonal transport of HRP microinjected into dorsal root ganglion neurons in vitro

In the present study the function of axonal transport in individual neurons under aluminium intoxication was investigated experimentally in comparison with controls. We used the technique of microinjection of horseradish peroxidase (HRP) in dissociated dorsal root ganglia (DRG) neurons and neurons of explant cultures of DRG. Different exposure periods (1 and 6 hours as well as 6 and 10 days) to aluminium were analysed quantitatively. This analysis revealed an impaired anterograde transport of HRP already after a short aluminium intoxication period of only 1 hour in DRG cells in vitro, an effect that increased with a prolonged aluminium exposure for up to 10 days. Hence, functional alterations of the anterograde transport caused by aluminium could be detected even after short exposure periods. Furthermore, the effects of aluminium on anterograde transport mechanisms were reversible 8 days after removal of aluminium. To determine how aluminium affects the cytoskeleton, we performed immunohistochemistry and electron microscopy on cultured DRG neurons. Distinct morphological alterations of the cytoskeleton, especially the accumulation of phosphorylated neurofilaments, appeared after 6 days of aluminium exposure. Our results suggest that neurofilaments are indispensable to the functional integrity of the cytoskeleton and its ability to mediate microtubule-based axonal transport processes.     

Toxicity of aluminium oxide nanoparticles demonstrated using a BY-2 plant cell suspension culture model

Aluminium oxide nanoparticles have been applied in many branches of industry. They are also used in personal care products, such as cosmetics. Because of these uses, their impact on the environment must be considered and investigated. Almost nothing is known about the effects of aluminium oxide nanoparticles on plants at the cellular level; the objective of this work was thus to study the effects of nanoparticles on the plant cell model tobacco BY-2 cell suspension culture, which serves as a model comparable with the HeLa cells used for animal cell studies. We observed the impact of these nanoparticles at different levels. The inhibitory effect on growth was observed in both time- and concentration-dependent studies. In addition, the ability of the nanoparticles to generate reactive oxygen (hydrogen peroxide, superoxide anion radical) and nitrogen species (nitric oxide) has been established. The principal part of the work was focused on the ability of aluminium oxide nanoparticles to induce the processes of programmed cell death. Changes observed in the permeability of the plasma membrane are connected with the effects of the reactive oxygen species and lipid peroxidation. In addition, the loss of mitochondrial potential, the enhancement of the caspase-like activity and the fragmentation of DNA determined in both time- and concentration dependent studies are closely connected with the execution of the programmed cell death. Our results indicate the ability of aluminium oxide nanoparticles to induce programmed cell death in plant cells and may explain the toxic effect of these nanoparticles on plants.     

Effects of aluminium on nodulation of two Stylosanthes species grown in nutrient solution

Summary Effects of three solution aluminium concentrations (0, 25 and 100 M) on nodulation ofStylosanthes hamata andStylosanthes scabra inoculated with Rhizobium CB 756 were studied using nutrient solution culture. Aluminium strongly affected nodulation by delaying nodule appearance and reducing the number and dry weight of nodules in both species. The effects of aluminium toxicity on nodulation were more pronounced inStylosanthes scabra than inStylosanthes hamata. These effects of aluminium on nodulation occurred before any significant effect of aluminium on top growth, root growth or root elongation. A plant transfer experiment suggested that aluminium interfered with root infection and/or nodule initiation in both species. The detrimental effect of aluminium on nodulation appeared to be associated with a reduction in lateral root density, thus decreasing the potential number of sites for root infection and nodule formation.