水分亏缺下作物补偿效应类型及机制研究概述

总结了作物在水分亏缺下产生补偿效应的类型、机制及条件,补偿效应类型可分为生长补偿、生理生化补偿、代谢及产量补偿等;从渗透调节、脱水保护等方面对补偿效应的生化及分子机制作了探讨,并阐明了作物产生补偿效应的生物学基础,指出了进一步研究的方向。     

物种组成、丰富度、播种密度和土壤养分对群落补偿效应的影响

为了明确物种组成、丰富度、播种密度和土壤养分对群落补偿效应的影响,以及群落补偿效应随时间的变化趋势,本文以青藏高原高寒草地常见物种垂穗披碱草(Elymus nutans)、中华羊茅(Festuca sinensis)和羊茅(F.ovina)为材料,通过建植不同物种组合的单、混播草地,连续5年对不同群落的生产力进行了测定,结果表明:物种组成显著影响群落的补偿效应;在施肥情况下,物种丰富群落有较高的补偿效应;实验初期,随着播种密度的增加,群落补偿效应有降低趋势,但随着生长年限的增加,密度对补偿效应的影响变得不显著;施肥显著提高了群落的补偿效应;随着生长年限的延长,群落补偿效应有升高趋势。     

马铃薯块茎膨大期不同程度干旱后复水的源库补偿效应

旱后复水的补偿效应在多种作物的不同生育时期都存在,是植物抵抗逆境胁迫和伤害的重要自我调节机制,也是对有限水分高效利用的体现.本研究在马铃薯块茎膨大期进行两轮干旱后复水处理,明确马铃薯补偿效应产生的干旱胁迫阈值,并从源-库角度探索马铃薯旱后复水补偿效应产生的缘由.试验选取‘大西洋’马铃薯脱毒组培苗为材料,设置充分供水(W)、轻度干旱后复水(D₁-W)、中度干旱后复水(D₂-W)和重度干旱后复水(D₃-W)4个水分处理并经过两个循环.结果表明:在经过两轮轻度干旱复水后,马铃薯产量表现出超补偿效应,水分利用效率和产量比充分供水分别提高了17.5%和6.3%;中度水分胁迫表现出近等量补偿效应,产量与充分供水差异不大,而水分利用效率提高了8.4%;而重度水分胁迫没有表现出产量补偿效应.不同程度的干旱胁迫均降低马铃薯叶片叶绿素含量、净光合速率、叶面积等源的大小和活性,而在复水后,轻度和中度胁迫出现了超补偿和补偿效应,增强了源的供应能力.同时,适度干旱后复水显著增强了块茎(库)中蔗糖-淀粉代谢途径关键酶的活性,提高了库活性,进而表现为块茎平均重量的增加.综上,马铃薯块茎膨大期适度的水分亏缺在复水后源-库均存在补偿和超补偿效应,以此来弥补干旱带来的损失,最终在产量上表现为补偿或者超补偿效应,并显著提高了水分利用效率.     

植物抗旱性中的补偿效应及其在农业节水中的应用

在论述植物补偿效应存在类型和研究范畴的基础上,详细评述了植物抗旱性中根系形态结构功能及地上部干物质积累、产量和水分利用效率方面的补偿效应及其影响因素,并对植物抗旱作用中补偿生长的可能生理学机制作了探讨。同时,对补偿效应在提高农业水分利用效率中的应用进行了讨论     

光、温限制后铜绿微囊藻和斜生栅藻的超补偿生长与竞争效应

研究了铜绿微囊藻(Microcystis aeruginosa)和斜生栅藻(Scenedesmus obliquus)低温和低光照限制后的超补偿效应,以及共培养条件下的竞争效应。结果表明,低温和低光照均显著抑制微藻的生长发育,但低温对铜绿微囊藻的抑制效应更强,而斜生栅藻则对低光胁迫更敏感。经过低光和低温培养后,铜绿微囊藻和斜生栅藻在恢复正常培养时藻细胞密度短期内都表现出超补偿增长效应,但不同藻类超补偿模式不同,斜生栅藻补偿生长时间不超过1周,而铜绿微囊藻的补偿效应可以持续10天;此外,统计结果表明铜绿微囊藻细胞密度对低温限制解除表现出更显著的补偿生长,斜生栅藻则在低光解除后表现出更强的超补偿效应。微藻叶绿素a指标在光恢复条件下都表现出显著的补偿效应,但温度恢复过程中叶绿素a含量与藻密度增长不同步,低温胁迫对恢复正常培养后微藻叶绿素a的形成产生了一定的负效应;铜绿微囊藻产毒株(912)在两种恢复模式下脱氢酶活性显著高于对照,产毒株(912)脱氢酶活性的补偿响应明显高于其它两种材料。共培养实验结果表明斜生栅藻同铜绿微囊藻产毒株(912)相比处于竞争劣势,而在同无毒株(469)的共培实验中,尽管连续正常培养情况下两者竞争能力差异不显著,但在恢复培养条件下斜生栅藻竞争能力显著高于后者。因此产毒型铜绿微囊藻低温和低光后的补偿生长效应以及对斜生栅藻的竞争优势可能是蓝藻爆发的内源性机制之一。     

氮素营养与水分胁迫对大豆产量补偿效应的影响

在大豆营养生长期,对大豆进行不同程度的干旱锻炼,同时改变土壤中的施氮水平,研究大豆产量及其构成因子对干旱胁迫复水的反应机制,为大豆节水增产及抗旱机制的实践探索提供理论依据。水分胁迫强度、历时和氮素营养都对大豆产量及其构成因子的补偿效应产生明显影响,水分胁迫抑制了大豆单株粒数的增长,但可以显著提高百粒重;氮素营养会抑制大豆百粒重的增加,但在一定水分条件下可以显著提高单株籽粒的数量,然而随着水分胁迫程度的加重,单株粒数的增加幅度也会相应减少。虽然氮素营养和水分胁迫使大豆产量构成因子产生补偿效应的阈值范围不同,但二者具有一定的耦合区域,在耦合区域内(水分胁迫时间14d左右、土壤含水量为田间持水量的50%—55%、施氮量在97.5—225kg/hm2之间)单株粒数和百粒重都产生较强的补偿效应,二者的协同作用显著提高了大豆的经济产量,使大豆产量表现出较强的补偿效应。结果表明:氮素营养和适度水分胁迫可以通过不同途径提高大豆植株的生长能力,当二者结合后大豆的补偿生长机制更为复杂,最终表现为水分胁迫提高了大豆的百粒重,而氮素增加了大豆单株粒数,二者协同作用使大豆经济产量显著增加。     

沙地云杉幼树对食叶害虫危害的补偿与超补偿效应

从沙地云杉食叶害虫优化管理出发 ,在植物与害虫相互作用的生态系统中 ,通过人工模拟摘叶实验研究 ,结果表明 ,沙地云杉幼树在一定失叶率的条件下存在补偿和超补偿效应 ,进而以沙地云杉宏观生长指标组建了一组不同生长指标的补偿与超补偿效应模型 ,同时寻求了相应的补偿点与超补偿点 .     

苗期刈割伤害对春小麦生长及产量的影响

通过1996年大田试验研究了黄土高原半干旱区春小麦苗期（三叶－心期）受到不同强度刈割伤害（模拟动物的采食）后的补偿作用,结果,在大田试验条件下,受轻度刈割（刈割一半叶面积,H0,H1）,春小麦的补偿效应大于受重度刈割（刈割全部叶面积T0,T1）春小麦的补偿效应,且都低于未受刈割处理（对照,CK0,CK1）,即CK0＞H0＞T0;CK1＞H1＞T1,刈割处理后,灌溉一次水（CK1,H1,T1）虽可增强其补偿能力,促进小麦的生长,但仍为低补偿。     

生态补偿理论、方法研究进展

对近年来国内外生态补偿的概念内涵、理论依据、补偿标准、补偿模式和补偿效应评价等多方面研究内容做了梳理和评析,进而对国内生态补偿研究提出几点展望,包括生态补偿的GIS时空分配模型、风险式补偿和差别化补偿、补偿模式的系统整合研究、模式选择模型和补偿预期效率研究、补偿社会经济效果和环境影响评价研究,并结合我国建设生态友好型社会和区域共同发展的需要角度,提出了开展符合我国生态国情的区域生态补偿理论与方法研究的必要性和基本内容.     

滴灌甜菜叶丛生长期对干旱胁迫的生理响应

在人工控水条件下,于叶丛生长期设置0~40 cm土层含水量为70%田间持水量、50%田间持水量和30%田间持水量3个处理,研究干旱胁迫下甜菜叶片相关生理性状的变化.结果表明:甜菜叶丛生长期中度缺水处理(50%田间持水量)的补偿指数最大,甜菜叶片丙二醛(MDA)含量、相对电导率、过氧化氢酶(CAT)活性及可溶性糖含量均在复水后24 h产生补偿效应,脯氨酸产生的补偿效应在复水后48 h,过氧化物酶(POD)未发生补偿效应.酶促活性氧清除系统以CAT反应最为灵敏.因此,在甜菜叶丛快速生长期,当土壤含水量下降至田间持水量的50%时应及时进行补充灌溉,促使叶片产生补偿效应,从而降低干旱胁迫对甜菜产量和含糖量的影响.     

Shapes of curves of pH-dependence of reactions

A simple case is considered in which the rate of a two-step reaction depends on pH because the intermediate formed in the first step has to gain (or lose) a proton before it can react in the second step, and in which the rate-determining step therefore changes with pH. The curves of reaction rate against pH are shown to be symmetrical, and the sharpest peak possible has a width at half its height of 1.53pH units, i.e. of 2log(3+2 radical2). Any particular curve for this situation proves to be identical with a curve that could be generated for the pH-dependence of a single-step reaction in which the rate is proportional to the concentration of a particular ionic form of a reactant. Curves for the latter situation, however, can have forms impossible for the former case in which the rate-determining step changes, but only if the protonations that activate and deactivate the reactant are co-operative. The peak can then become even sharper, and its width at half its height can fall to 1.14pH units, i.e. to 2log(2+ radical3).     

Overview of mechanisms of action of lycopene

Dietary intakes of tomatoes and tomato products containing lycopene have been shown to be associated with decreased risk of chronic diseases such as cancer and cardiovascular diseases in numerous studies. Serum and tissue lycopene levels have also been inversely related to the risk of lung and prostate cancers. Lycopene functions as a very potent antioxidant, and this is clearly a major important mechanism of lycopene action. In this regard, lycopene can trap singlet oxygen and reduce mutagenesis in the Ames test. However, evidence is accumulating for other mechanisms as well. Lycopene at physiological concentrations can inhibit human cancer cell growth by interfering with growth factor receptor signaling and cell cycle progression specifically in prostate cancer cells without evidence of toxic effects or apoptosis of cells. Studies using human and animal cells have identified a gene, connexin 43, whose expression is upregulated by lycopene and which allows direct intercellular gap junctional communication (GJC). GJC is deficient in many human tumors and its restoration or upregulation is associated with decreased proliferation. The combination of low concentrations of lycopene with 1,25-dihydroxyvitamin D3 exhibits a synergistic effect on cell proliferation and differentiation and an additive effect on cell cycle progression in the HL-60 promyelocytic leukemia cell line, suggesting some interaction at a nuclear or subcellular level. The combination of lycopene and lutein synergistically interact as antioxidants, and this may relate to specific positioning of different carotenoids in membranes. This review will focus on the growing body of evidence that carotenoids have unexpected biologic effects in experimental systems, some of which may contribute to their cancer preventive properties in models of carcinogenesis. Consideration of solubility in vitro, comparison with doses achieved in humans by dietary means, interactions with other phytochemicals, and other potential mechanisms such as stimulation of xenobiotic metabolism, inhibition of cholesterogenesis, modulation of cyclooxygenase pathways, and inhibition of inflammation will be considered. This review will point out areas for future research where more evidence is needed on the effects of lycopene on the etiology of chronic disease.     

Investigation of the mechanism of temperature sensitivity of the electroreceptors of ampullae of lorenzini

In experiments on Black Sea skates (Raja clavata), the potential of the receptor epithelium of the ampullae of Lorenzini and spike activity of single nerve fibers connected to them were investigated during electrical and temperature stimulation. Usually the potential within the canal was between 0 and –2 mV, and the input resistance of the ampulla 250–400 k. Heating of the region of the receptor epithelium was accompanied by a negative wave of potential, an increase in input resistance, and inhibition of spike activity. With worsening of the animal's condition the transepithelial potential became positive (up to +10 mV) but the input resistance of the ampulla during stimulation with a positive current was nonlinear in some cases: a regenerative spike of positive polarity appeared in the channel. During heating, the spike response was sometimes reversed in sign. It is suggested that fluctuations of the transepithelial potential and spike responses to temperature stimulation reflect changes in the potential difference on the basal membrane of the receptor cells, which is described by a relationship of the Nernst's or Goldman's equation type.I. P. Pavlov Institute of Physiology, Academy of Sciences of the USSR, Leningrad. I. M. Sechenov, Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Pacific Institute of Oceanology, Far Eastern Scientific Center, Academy of Sciences of the USSR, Vladivostok. Translated from Neirofiziologiya, Vol. 12, No. 1, pp. 67–74, January–February, 1980.