气候变化背景下黄淮冬麦区冬季长寒型冻害时空变化特征

冻害是影响我国北方冬小麦生产主要的农业气象灾害之一,明确气候变化背景下冻害发生规律和演变特征,对防御冻害具有重要的意义。以黄淮冬麦区为研究区域,利用1960—2010年47个气象台站逐日气温资料,在分析越冬期负积温和越冬期长度变化特征基础上,以越冬期负积温为指标分析了黄淮冬麦区冬季长寒型冻害发生频率及站次比演变特征,并利用冻害实际灾情资料对研究结果进行验证。研究结果表明:(1)黄淮冬麦区越冬期负积温绝对值在过去50a平均为17.3—240.8℃·d,空间上呈南少北多的纬向分布特征,且近50a呈减少趋势,全区负积温绝对值每10年减少1.8—38.3℃·d,这种变化趋势表现为南低北高的空间分布特征;(2)研究时段内全区越冬期长度呈波动性缩短趋势,尤其是研究区域北部地区,南部地区越冬期长度年际间变化不显著,且个别站点有些年份没有稳定越冬期,多集中在1985年以后;(3)黄淮冬麦区较轻冻害发生频率较高,为40%以上,空间上由北向南逐渐增大,站次比年代际呈增加趋势;中度冻害和较重冻害发生频率较低,多数站点在10%以下,空间上由北向南逐渐减小,站次比呈减少趋势;全区无严重冻害和极严重冻害风险。气候变化背景下,黄淮冬麦区冬季长寒型冻害风险较小,各站点冻害程度随年代变化逐渐减轻,较轻冻害的站点逐渐增多。     

1971—2020年西南茶区灌木型茶树晚霜冻害危险性时空演变特征

研究晚霜冻害危险性时空演变特征,对于优化区域农业生产布局和品种调优具有科学的指导意义。本研究利用西南茶区65个气象站点1971—2020年逐日气象数据,结合霜冻终日和茶芽萌发初日的变化特征及其相互关系,构建西南茶区灌木型茶树春梢晚霜冻害概率指数和冻害强度指数,分析西南茶区灌木型茶树晚霜冻害危险性时空演变特征。结果表明:1971—2020年,西南茶区霜冻终日和茶芽萌发初日均呈显著提前趋势,且霜冻终日的提早速率快于茶芽萌发初日的提早速率,萌发后的茶芽暴露于晚霜冻害的天数总体呈不显著下降趋势。西南茶区大部分区域灌木型茶树晚霜冻害危险性呈下降趋势,但贵州茶区呈不显著上升趋势。四川茶区西部边缘山区、贵州茶区西部与云南茶区东北部交界处等地灌木型茶树晚霜冻害危险性一直较高,四川盆地区、云南茶区南部和贵州茶区南部等地晚霜冻害危险性一直较低。云南茶区北部、中东部地区等区域晚霜冻害危险性呈明显下降趋势;而贵州茶区中部和东部区域灌木型茶树晚霜冻害危险性明显增加。     

河北冬小麦冬季不同类型冻害气候指标及风险分析

利用河北省1981—2010年冬季逐日气象资料、冬小麦冻害灾情资料及品种资料,采用秩和检验法,依据Bayes判别准则,建立了初冬剧烈降温型、冬季长寒型和融冻型3大主要类型冬季冻害气候指标;依据风险分析原理,结合概率密度函数,建立了各类型冻害的气候风险概率指数模型,进行风险分析。结果表明:冬小麦初冬剧烈降温型冻害主要受越冬前后降温过程的降温幅度和过程最低气温影响;长寒型冻害主要受越冬期寒冷程度影响,包括越冬天数及越冬期平均气温、最低气温低于临界温度的天数及其累积负积温两个方面;融冻型冻害主要受平均气温回升到0℃以上后出现的低温过程的极端最低气温影响。北部麦区以长寒型冻害风险为主,高风险和较高风险区主要分布在唐山、秦皇岛两市中北部和保定西北部;中南部麦区以融冻型和初冬剧烈降温型冻害风险为主,高风险和较高风险区主要分布在邢台和邯郸两市东部、保定西北部。     

福建平和果树冻害调查

本文分析了１９９９年１２月福建平和出现严重冻害的气象 特点，调查全县亚热带、热果树的冻害情况及影响冻害程度的因素，并提出冻后的管理措施。     

根区缓冲降温处理对葡萄叶片冻害的影响

为探索根区降温条件对葡萄(Vitis vinifera)叶片冻害的影响,以1年生美乐葡萄(V.vinifera cv.‘Merlot’)幼苗为试材,设置根区正常降温和缓冲降温2种降温条件,人工模拟霜冻,分析了叶片冻害指数和叶片的荧光参数。结果表明,根区正常降温会导致根系受冻,同时叶片发生严重的冻害,冻害指数达74.36%;根区缓冲降温使根区温度保持在0°C以上,叶片冻害指数降低53.29%,仅有21.07%的叶片遭受了冻害。根区缓冲降温处理能有效提高叶片霜冻恢复过程中光化学淬灭系数(qP)和天线色素转化效率(F_v~'/F_m~'),加快PSII光合电子传递量子效率(Φ_(PSII))的恢复,提高热耗散能力(NPQ),减轻霜冻后的光抑制(F_v/F_m),有利于叶片霜冻后的恢复。     

花期冻害对杜仲花粉营养成分的影响

通过测定花期冻害前后杜仲花粉营养成分和总黄酮含量,研究花期冻害对杜仲花粉营养成分的影响.结果显示,花期低温对花粉蛋白质、蛋白质氨基酸、维生素含量等没有显著的影响;总黄酮含量略有增加,还原糖含量显著增加(P<0.05);但花粉游离氨基酸含量却有较明显的减少,蔗糖和粗脂肪的含量极显著的减少(P<0.01).所以,在今后的生产中应尽量采取措施预防花粉冻害.     

桂林植物园植物1991年大雪下冻害情况

<正> 一九九一年十二月廿七日,大地连续降了两天两夜大雪,厚达4—5毫米。雪经过一个星期才完全融化。这是近二十年来最冷的一年,桂林地区植物受到严重冻害,作者对桂林植物园的植物进行了普遍的观察调查,现将初步调查结果报道如下: 我们对受冻植物的冻害程度分为0—Ⅵ级分别记录。 0级:枝条叶片无冻害,仅有个别叶片局部损伤; Ⅰ级:少数叶片受冻害约在25％以下;     

冻害与抗冻

温度是植物生长发育的重要环境因子,一般的植物都在适宜的气温下完成生长发育,但在温带与寒带,周年中四季气温变化很大,特别是在严寒的冬季,只有耐寒遗传稳定的植物,才能傲霜斗雪,度过低温季节,硬要把南方的喜温植物在北方露地越冬,则百分之百地会冻死。培育抗冻品种,扩大农作物种植纬度,一直是育种家的理想。自1906年开始冻害研究以来,植物生理学界对冻害与抗冻的机理进行了艰苦的探索,有数千篇论文发表,基本上搞清了植物冻害的原理,在抗冻的理论与技术方法研究方面取得了一定的成就。豆．对冻害原因的研究在大多数情况下,…     

莲雾寒冻害低温等级指标的确定

根据福建、广东、广西、贵州四省(区)2008—2014年的89例莲雾(Syzygium samarangense)寒冻害灾情样本资料,结合莲雾寒冻害形态学标准,采用回归分析方法,初步得到莲雾寒冻害低温等级指标。在此基础上,与地理移置自然低温试验、人工气候箱模拟低温试验及2016年果园灾情调查资料所获取的莲雾形态和生理生态指标变化情况进行检验和验证。结果表明:莲雾寒冻害低温等级指标分别为5级;T_(min)5.5℃,无寒冻害,正常生长;3.0℃T_(min)≤5.5℃,轻度;1.0℃T_(min)≤3.0℃,中度;-1.5℃T_(min)≤1.0℃,重度;T_(min)≤-1.5℃,极重,不可恢复或死亡;研究的等级指标通过典型年、地理移放试验和人工气候箱致灾试验结果验证准确率达90%以上,可以投入实际应用。     

温州蜜柑果实生长动态特征及影响因子的分析

金衢盆地柑桔生产历史悠久。近10年来发展很快,已形成浙江第二个柑桔产区。由于受东亚季风气候影响,该区柑桔不但冬季易遭冻害,而且夏秋易受高温干旱危害,冬季的低温冻害和夏季的高温干旱是造成桔柑减产的两个主要     

植物冻害和氧化胁迫——甘蓝叶冻-融循环中超氧的产生

为检验植物冻害的发生和氧化胁迫这一假说,在冰冻前把氮蓝四唑（NBT）真空渗入到甘蓝叶圆片中,在叶圆片冻－融循环中NBT被还原为甲Zan,把其中的单甲Zan用乙醇提取出来,在分光光度计上比色,可作为冻融循环中产生的氧化胁迫的定量指标,NBT本身作为氧化剂,使冻害稍有增加,作为冰冻保护剂的二甲基亚砜真空渗入叶圆片使其抗冻性显著增加,而NBT还原则显著减少,表明二甲基亚砜在保护叶组织免受冻害上的作用和它减缓植物组织氧化胁迫的作用有关。实验结果支持植物冻害的发生和氧化胁迫有关这一假说。实验还表明还原NBT的还原剂很可能是超氧阴离子自由基。     

Isolation of mutations affecting the development of freezing tolerance in Arabidopsis thaliana (L.) Heynh.

We screened for mutations deleterious to the freezing tolerance of Arabidopsis thaliana (L.) Heynh. ecotype Columbia. Tolerance was assayed by the vigor and regrowth of intact plants after cold acclimation and freezing. From a chemically mutagenized population, we obtained 13 lines of mutants with highly penetrant phenotypes. In 5 of these, freezing sensitivity was attributable to chilling injury sustained during cold acclimation, but in the remaining 8 lines, the absence of injury prior to freezing suggested that they were affected specifically in the development of freezing tolerance. In backcrosses, freezing sensitivity from each line segregated as a single nuclear mutation. Complementation tests indicated that the 8 lines contained mutations in 7 different genes. The mutants' freezing sensitivity was also detectable in the leakage of electrolytes from frozen leaves. However, 1 mutant line that displayed a strong phenotype at the whole-plant level showed a relatively weak phenotype by the electrolyte leakage assay.     

草莓开花期发生霜害的温度

用人工霜箱对草莓(Fragaria ananassa)叶片和花托进行模拟春霜实验。结果表明草莓叶片有忍耐胞间结冰的能力, 最低叶温-6.4 ℃以上, 结冰持续90分钟以内的叶片解冻后还能存活。花托不能忍耐胞间结冰, 是通过保持过冷却状态以回避结冰伤害。花托温度越低, 发生霜害的累积百分率越大, 半开花的花托温度降到-5.4 ℃时累计有50%发生结冰而造成霜害。盛开的花及鲜重大的花发生霜害的温度较高。     

Alterations in membrane transport properties by freezing injury in herbaceous plants:

Leakage of ions from a thawed tissue is a common phenomenon of freezing injury. This leakage is usually assumed to be due to loss of membrane semipermeability or membrane rupture by freezing injury. Freeze injured, yet living, onion (Allium cepa L.) epidermal cells were used to study alterations in cell membranes that result in leakage of ions. In spite of a large efflux of ions, freeze injured cells could be plasmolysed and they remained plasmolysed for several days just like the unfrozen control cells. Injured cells also exhibited protoplasmic streaming. Passive transport of KCl, urea and methyl urea across the cell membranes of injured and control cells was also studied. No difference could be detected for the transport rates of urea and methyl urea between control and injured cells. However, a dramatic increase in the transport rate of KCl was found for the injured cells. Depending upon the extent of initial freezing injury, an increase or a decrease in injury symptoms was found in the post-thaw period. During the progress of freezing injury, 10 days after thawing, a swelling of the protoplasm was seen in the irreversibly injured cells. In spite of this swelling, these cells could be plasmolysed. It appears that the high amount of K⁺ that leaks out into the extracellular water, due to freezing injury, causes protoplasmic swelling by replacing Ca²⁺ in the plasma membrane. We conclude that protoplasmic swelling is a sign of secondary injury. The results presented in this study show that membrane semipermeability is not completely lost and membrane rupture does not occur during the initial stage of freezing injury. In fact, the cells have the ability to repair damage depending upon the degree of injury. Our results show there are specific alterations in membrane semipermeability (e.g., transport of K⁺) which could be repaired completely depending on the degree of injury. These findings suggest that ion leakage due to freezing injury is due to alteration in the membrane proteins and not in the membrane lipids.     

Contribution of extracellular ice formation and the solution effects to the freezing injury of PC-3 cells suspended in NaCl solutions

The mechanism of cell injury during slow freezing was examined using PC-3 human prostate adenocarcinoma cells suspended in NaCl solutions. The objective was to evaluate contribution of extracellular ice and the 'solution effects' to freezing injury separately. The solution effects that designate the influence of elevated concentration were evaluated from a pseudo-freezing experiment, where cells were subjected to the milieu that simulated a freeze-thaw process by changing the NaCl concentration and the temperature at the same time. The effect of extracellular ice formation on cell injury was then estimated from the difference in cell survival between the pseudo-freezing experiment and a corresponding freezing experiment. When cells were frozen to a relatively higher freezing temperature at -10 degrees C, about 30% of cells were damaged mostly due to extracellular ice formation, because the concentration increase without ice formation to 2.5-M NaCl, i.e., the equilibrium concentration at -10 degrees C, had no effect on cell survival. In contrast, in the case of the lower freezing temperature at -20 degrees C, about 90% of cells were injured by both effects, particularly 60-80% by the solution effects among them. The present results suggested that the solution effects become more crucial to cell damage during slow freezing at lower temperatures, while the effect of ice is limited to some extent.     

Morphologic characterization of acute injury to vascular endothelium of skin after frostbite

Cyclo-oxygenase inhibitors and free-radical scavengers protect the skin against necrosis induced by frostbite. However, the tissue component(s) that determine the evolution of skin necrosis and the mechanism of this pharmacologic protection are not precisely defined. We have studied freezing injury to rabbit ears by serial biopsies examined by light and electron microscopy. The morphologic evidence of skin injury due to freezing was localized exclusively in the endothelial cells, particularly in the arterioles. Within 1 hour, the entire microvasculature demonstrated endothelial damage. Intravascular platelet aggregation occurred just after thawing and closely paralleled the endothelial cell injury. Very few neutrophils were seen initially (at 10 minutes). By 1 hour, leukocyte aggregates were present, and they further increased at 6 hours. Swelling of the interstitium started 10 minutes after thawing, while extravasation of erythrocytes began to appear by 6 hours. Parenchymal elements of skin were relatively free of damage. In the ear cartilage, the chondrocytes showed evidence of damage immediately after freezing. The administration of superoxide dismutase (SOD) during thawing (reperfusion) did not qualitatively alter any of the initial morphologic changes induced by freezing. We conclude that the endothelial cell is the initial target of injury induced by freezing, an initial injury that is mediated by a non-free-radical-mediated mechanism. It is likely that this acute injury ultimately compromises blood flow and leads to skin necrosis.     

Heat shock protects germinating conidiospores of Neurospora crassa against freezing injury.

Germinating conidiospores of Neurospora crassa that were exposed to 45 degrees C, a temperature that induces a heat shock response, were protected from injury caused by freezing in liquid nitrogen and subsequent thawing at 0 degrees C. Whereas up to 90% of the control spores were killed by this freezing and slow thawing, a prior heat shock increased cell survival four- to fivefold. Survival was determined by three assays: the extent of spore germination in liquid medium, the number of colonies that grew on solid medium, and dry-weight accumulation during exponential growth in liquid culture. The heat shock-induced protection against freezing injury was transient. Spores transferred to normal growth temperature after exposure to heat shock and before freezing lost the heat shock-induced protection within 30 min. Spores subjected to freezing and thawing stress synthesized small amounts of the heat shock proteins that are synthesized in large quantities by cells exposed to 45 degrees C. Pulse-labeling studies demonstrated that neither chilling the spores to 10 degrees C or 0 degrees C in the absence of freezing nor warming the spores from 0 degrees C to 30 degrees C induced heat shock protein synthesis. The presence of the protein synthesis inhibitor cycloheximide during spore exposure to 45 degrees C did not abolish the protection against freezing injury induced by heat shock. Treatment of the cells with cycloheximide before freezing, without exposure to heat shock, itself increased spore survival.     

Protein-bound SH groups in frozen-thawed egg cells of the sea urchin

Unfertilized egg cells of the sea urchin St. intermedius could survive slow freezing to ?15 °C for a short period of time, but at the same freezing temperature extracellular freezing became fatal within a few hours. Such freezing injury resulted in “black” or “white” cytolysis in frozen-thawed cells. “Black” cytolysis took place in the process of both freezing and thawing, while “white” cytolysis occurred only on thawing. Rapid rewarming consistently produced “white” cytolysis in extracellularly frozen cells. The observed behavior of the injured cells during freeze-thawing appeared favorable for the explanation of freezing injury by the SH-SS hypothesis. Protein-bound SH groups were quantitatively determined in both whole cell and cortex with plasma membrane before and after freeze-thawing. However, no significant change in the SH value was observed between freeze-thaw cytolysed materials and unfrozen ones.     

Ultrastructural Evidence That Intracellular Ice Formation and Possibly Cavitation Are the Sources of Freezing Injury in Supercooling Wood Tissue of Cornus florida L

Although cellular injury in some woody plants has been correlated with freezing of supercooled water, there is no direct evidence that intracellular ice formation is responsible for the injury. In this study we tested the hypothesis that injury to xylem ray parenchyma cells in supercooling tissues is caused by intracellular ice formation. The ultrastructure of freezing-stress response in xylem ray parenchyma cells of flowering dogwood (Cornus florida L.) was determined in tissue prepared by freeze substitution. Wood tissue was collected in the winter, spring, and summer of 1992. Specimens were cooled from 0 to -60[deg]C at a rate of 5[deg]C h-1. Freezing stress did not affect the structural organization of wood tissue, but xylem ray parenchyma cells suffered severe injury in the form of intracellular ice crystals. The temperatures at which the ice crystals were first observed depended on the season in which the tissue was collected. Intracellular ice formation was observed at -20, -10, and -5[deg]C in winter, spring, and summer, respectively. Another type of freezing injury was manifested by fragmented protoplasm with indistinguishable plasma membranes and damaged cell ultrastructure but no evidence of intracellular ice. Intracellular cavitation may be a source of freezing injury in xylem ray parenchyma cells of flowering dogwood.     

Ultrastructural preservation of plasma membranes by non-lethal slow freezing to liquid nitrogen temperature

Secondary hyphae of Lyophyllum ulmarium were shown to tolerate slow freezing, which allowed extracellular freezing, to -196 degrees C. A freeze-fracture study showed that under this non-lethal freezing condition, the plasma membrane of the secondary hyphae did not show any ultrastructural changes as compared with the control, except gross cellular shrinkage. Tertiary hyphae of Lyophyllum ulmarium, on the other hand, were completely injured by slow freezing to -196 degrees C, and the plasma membrane showed distinct intramembrane particle aggregation as a result of direct membrane contact caused by severe cellular deformation. It is suggested that the absence of freezing injury in the secondary hyphae was due to ultrastructural preservation of the plasma membrane, which resulted from avoidance of severe cellular deformation, while occurrence of freezing injury in the tertiary hyphae is considered to be due to ultrastructural changes in the plasma membrane caused by severe cellular deformation.