马铃薯耐霜冻研究进展

综述国内外马铃薯耐霜冻的研究成果,包括马铃薯霜冻害机理、耐冻性鉴定、耐冻性遗传和QTL定位以及提高耐冻性的有效措施等方面的研究进展,并提出了今后马铃薯耐霜冻研究值得深入探讨的问题。     

南亚热带主要果树冻(寒)害低温指标的确定

根据历史气候和冻(寒)害灾情资料、2007/2008、2008/2009年冬季盆栽移放试验和典型年考察资料,以及冻(寒)害形态学标准,采用数理统计和对比印证方法,对南亚热带主要果树冻(寒)害低温指标进行研究。确定了几种主要南亚热带果树的轻、中、重、严重冻(寒)害低温指标,结果分别为龙眼:-1.5～0℃、-2.5～-1.5℃、-3.5～-2.5℃、<-3.5℃;荔枝:-2.0～0℃、-3.0～-2.0℃、-4.0～-3.0℃、<-4.0℃;香蕉:3.0～5.0℃、1.0～3.0℃、-1.0～1.0℃、<-1.0℃。结果可为果树冻害监测预警及避冻区划提供参考。     

壳聚糖涂膜处理对冷藏砂糖橘冷害和品质影响

为探究壳聚糖对砂糖橘果实冷害的影响,以1℃贮藏的砂糖橘为对象,对果实进行1.0%壳聚糖涂膜处理,以未涂膜的果实作为对照,研究了壳聚糖涂膜处理对果实贮藏品质和膜脂过氧化作用的影响。结果表明,1℃条件下采用1.0%壳聚糖处理砂糖橘可延缓果实冷害的发生,显著提高果实的好果率,同时可以抑制TSS、TA、Vc含量的下降;1.0%壳聚糖处理砂糖橘果实在低温下保持了较高的POD、CAT和SOD活性,壳聚糖处理抑制了果实MDA含量的上升。由此可见,1.0%壳聚糖处理可以降低砂糖橘果实由于1℃不适宜低温造成的膜脂过氧化,保持果实贮藏品质,减轻果实的冷害症状。本研究结果为减缓砂糖橘果实冷害提供了一定的理论依据。     

枇杷幼果冻害低温等级指标的确定

根据福建省近5a枇杷幼果低温箱试验和低温过程山坡地枇杷冻害观测试验结果,以及主产省福建、浙江历史灾情资料,采用归纳分析和对比印证等方法,对枇杷幼果冻害的低温等级指标进行研究。结果表明：枇杷幼果冻害低温等级指标可用日最低气温（Tmin）和低温持续天数（DD）表示,各级冻害指标分别为,轻度：-2.5℃＜Tmin≤-1.0℃,DD≤3d;中度：-3.5℃＜Tmin≤-2.5℃,DD≤3d或-2.5℃＜Tmin≤-1.0℃,DD＞3d;重度：-4.5℃＜Tmin≤-3.5℃,DD≤3d或-3.5℃＜Tmin≤-2.5℃,DD＞3d;极重：Tmin≤-4.5℃,DD≤3d或Tmin≤-3.5℃,DD＞3d。历史灾情资料验证结果表明,冻害等级指标在福建莆田的推算准确率为61%,在浙江临海、黄岩为87.5%,说明枇杷幼果低温冻害等级指标可应用于低温冻害预测。     

高温对茶树叶片光合及抗逆特性的影响和恢复*3

以4个茶树品种福鼎大白茶、鸠坑、龙井43和乌牛早7a生植株为研究对象,采用人工气候箱模拟高温（35℃和40℃）处理6、12、18、24、48h,取出后置于人工气候箱中（25℃）恢复3、6、9d,以未经高温处理置于人工气候箱中（温度25℃）的各品种茶树为对照（CK）,测定茶树叶片的最大净光合速率、荧光参数、抗氧化酶活性以及细胞伤害率。结果表明：高温胁迫显著抑制了茶树的最大净光合速率（Pnmax）和最大光化学效率（Fv/Fm）,处理时间越长、温度越高,Pnmax和Fv/Fm下降越快,除35℃处理的福鼎大白茶外,其它3种茶树经过高温处理后,在恢复期间其Fv/Fm无法恢复至正常水平;茶树叶片的SOD酶活性在高温处理的前12h迅速上升,随着处理时间的延长,其活性降低;叶片MDA含量的平均值在高温处理第48小时达到最大,恢复期间缓慢下降;随着处理温度的升高和处理时间的延长,各茶树叶片的细胞伤害率均呈增加趋势。4种茶树耐热性的强弱由高到低依次为福鼎大白茶＞乌牛早＞鸠坑＞龙井43。     

棉花盐害的控制技术及其机理

棉花是耐盐作物,但土壤耕层中积累过多的盐离子会通过离子毒害、渗透胁迫和引起营养失衡等机制导致盐害。控制棉花盐害的途径主要有两条,一是提高棉花自身的耐盐性,另一方面是躲避或减轻盐胁迫。本文评述了提高棉花耐盐性和躲避或减轻盐胁迫的途径、原理和方法,提出在工程措施改良盐碱地的基础上,综合运用适宜品种、水肥运筹、种子处理及地膜覆盖和诱导根区盐分差异分布等农艺措施是现阶段控制盐碱地棉花盐害的有效途径。     

二苯胺处理对鸭梨果实冷害的影响

研究了贮前二苯胺（DPA）处理对在低温条件下（0℃）贮藏鸭梨果实的果心褐变及生理变化的影响。结果表明：急骤降温（0℃）可产生严重的早期果心褐变,贮前二苯胺处理在一定条件下可减轻鸭梨果实的早期褐变,贮藏60 d时DPA处理果实的褐变指数为0.233,而对照为0.417;同时DPA处理可降低果实的乙烯释放量、抑制多酚氧化酶活性、保持果实酚类物质含量,对丙二醛（MDA）含量和果实相对电导率也有一定影响。     

The protection of the hepatic ischemic preconditioning is concerned with the NO/ET-1 system

AIM: To study the relationship between the disturbance of nitric oxide/endothelin-1(NO/ET-1) and hepatic ischemia/reperfusion(I/R) injury as well as the regulation of NO/ET-1 system by hepatic ischemic preconditioning(IPC). METHODS: The changes of NO/ET-1 system and their relationship with hepatic I/R injury were compared between I/R group and IPC+I/R group in a rat hepatic I/R model. Two hours after reperfusion, the liver tissues were detected by RT-PCR to see whether there was inducible nitric oxide synthase (iNOS) mRNA expression. RESULTS:In the acute phase of hepatic reperfusion, the ratio of NO/ET-1 was reduced, which was due to a significant reduction of NO₂^-/NO₃^- (the metabolic product of NO) and significant elevation of ET-1 in the blood plasma. The content of ALT, AST, LDH and TNF-α in blood plasma, and of MDA in liver tissue were increased but ATP in liver tissue was reduced, the hepatic damage was deteriorated. The protection of the hepatic IPC was concerned with the elevation of the ratio of NO/ET-1 caused by the elevation of NO₂^-/NO₃^-, and reduction of ET-1 as well. There was no iNOS mRNA detected in the liver tissues.CONCLUSION: Hepatic I/R injury is related to the disturbance of NO/ET-1. The protection of the hepatic IPC in the acute phase might be conducted by its regulation of NO/ET-1 system. The cNOS rather than the iNOS generated the NO in this situation.     

Effects of oxidative stress and inflammatory response on kidney injury in mice with hyperthyroidism

AIM To explore the effects of oxidative stress and inflammatory response on kidney injury induced by hyperthyroidism in mice. METHODS Forty male Kunming mice were randomly divided into control group （n=20） and L-thyroxine （T4） group （n=20）. The mice in T4 group were intraperitoneally injected with T4 diluent at a dose of 1 mg/kg to induce hyperthyroidism, and those in control group were injected with normal saline of the same volume. After 7 weeks, the mice were weighed and dissected, the kidneys were removed and weighed, and the length of tibia was also measured. The activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） in the kidney tissues were detected. The pathological changes of the kidney tissues were observed by HE staining. The levels of 4-hydroxynonenal （4-HNE）-modified proteins, interleukin-1 receptor-associated kinase 1 （IRAK1） and tumor necrosis factor receptor-related factor 6 （TRAF6） were determined by Western blot and immunohistochemistry. RESULTS Compared with control group, the body weight of the mice was decreased, while the kidney size and weight were increased significantly in T4 group. In addition, the ratios of kidney weight/body weight and kidney weight/tibia length were also increased （P<0.05）. In T4 group, the renal tubules were enlarged, and the epithelial cells of renal tubules were swollen and exfoliated, with vacuolar degeneration. Furthermore, reduced SOD activity, and increased MDA content and 4-HNE-modified proteins were found in T4 group, all of which were related to oxidative stress （P<0.05）. The levels of inflammation-related proteins IRAK1 and TRAF6 were significantly increased in T4 group （P<0.05）. CONCLUSION Excessive T4 may lead to kidney hypertrophy and injury in mice, and the mechanism may be related to oxidative stress and inflammatory response.