几种药剂防治柑橘黑斑病的田间药效试验

为筛选出防治柑橘黑星病的有效药剂,以南丰蜜橘为研究对象,对柑橘黑斑病进行田间防治试验。结果表明:10%苯醚甲环唑1000倍防治效果最好,防治效果为92.32%;80%代森锰锌+70%甲基托布津复配500倍防治效果次之,防治效果为91.45%;依次是80%代森锰锌400倍、70%甲基托布津400倍和10%苯醚甲环唑1500倍,防治效果分别为87.32%、84.65%和83.56%。     

棉花曲叶病毒对棉花造成的经济损失评估

棉花曲叶病毒(Cotton leafcurl virus)是我国进境检疫性病毒,严重危害棉花的生长,给棉花生产带来巨大经济损失。文中分析此病毒可能给棉花生产所造成的损失,包括直接经济损失、间接经济损失和防治费用。估算了棉花曲叶病毒对棉花造成的经济损失值为77.27亿元~498.61亿元。     

广东西瓜上检测到甜瓜黄斑病毒

在广东发现了可能被番茄斑萎病毒属(Tospovirus)病毒侵染的西瓜,采用ELISA和RT-PCR法对该西瓜病样进行了检测,西瓜病叶粗汁液不与番茄斑萎病毒(Tomato spotted wilt virus,TSWV)和西瓜银斑驳病毒(Watermelon silver mottle virus,WSMoV)的血清发生反应;利用引物J13/UHP通过RT-PCR可以扩增出约1400 bp的基因片段,该片段包括一个840 bp的核衣壳蛋白ORF,其推导的氨基酸序列与已报道的Melon yellow spot virus(MYSV)NP基因氨基酸序列的同源率都为99%,进化树分析表明侵染广东西瓜的病毒(命名为MYSV-GZ)属于Tospovirus的MYSV血清组。     

叶面积指数测定方法综述

叶面积指数(LAI)被定义为单位地面面积上叶面面积总和,是极其重要的植被特征,是表征植被冠层结构最基本的参量之一,它控制着植被的许多生物、物理过程,如光合、呼吸、蒸腾、碳循环和降水截获等。因此如何有效的测定叶面积指数将是我们面临的重大课题。本文阐述了直接收获法、调落叶法等叶面积测定方法,同时也将例举这些叶面积测定方法已测定过的物种范围,并就这些方法中所存在的局限性进行说明。     

不同发育时期椰子叶片精油的提取与成分分析

为明确引诱椰心叶甲[Brontispa longissima(Gestro)]取食的化学信息物质,利用同时蒸馏萃取法分别提取椰子(Cocos nucifera L.)的心叶、半展叶、老熟叶的精油,并采用气相色谱-质谱联用法对3者化学成分进行种类和含量的比较分析.结果表明,不同发育时期椰子叶片精油的主要成分为:2,3-二...     

遮阴对麦冬叶面积和叶绿素含量的影响

研究不同遮阴度对麦冬叶面积和叶绿素含量的影响。以邢台市区绿地的麦冬为研究对象,在全遮阴(25%～45%全光照)、半遮阴(60%～80%全光照)、不遮阴(全光照)3种不同遮阴度下,测定并分析麦冬叶面积的大小、叶绿素a和叶绿素b的含量以及叶绿素a/b的值。结果表明,随着遮阴程度的增加,麦冬的叶面积增大,叶绿素a和叶绿素b均增加,且叶绿素b的增加率大于叶绿素a,叶绿素a/b的值变小。这表明麦冬具有强的耐阴性,适合于室内摆设和遮阴处的园林配置。     

Effects of the aglycone of ascaulitoxin on amino acid metabolism in Lemna paucicostata

Ascaulitoxin and its aglycone (2,4,7-triamino-5-hydroxyoctanoic acid, CAS 212268-55-8) are potent phytotoxins produced by Ascochyta caulina, a plant pathogen being developed for biocontrol of weeds. The mode of action of this non-protein amino acid was studied on Lemna paucicostata. Ascaulitoxin is a potent growth inhibitor, with an I₅₀ for growth of less than 1 μM, almost completely inhibiting growth at about 3 μM. Its action is slow, starting with growth inhibition, followed by darker green fronds, and then chlorosis and death. Most amino acids, including non-toxic non-protein amino acids, reversed the effect of the toxin when supplemented in the same medium. Supplemental sucrose slightly increased the activity. d-Amino acids were equally good inhibitors of ascaulitoxin activity, indicating the amino acid effects may not be due to inhibition of amino acid synthesis. Oxaloacetate, the immediate precursor of aspartate, also reversed the activity. LC-MS did not detect interaction of the compound with lysine, an amino acid that strongly reversed the effect of the phytotoxin. Metabolite profiling revealed that the toxin caused distinct changes in amino acids. Reduction in alanine, paralleled by enhanced levels of the branched chain amino acids valine, leucine and isoleucine and nearly unchanged levels of pyruvate, might indicate that the conversion of pyruvate to alanine is affected by ascaulitoxin aglycone. In addition, reduced levels of glutamate/glutamine and aspartate/asparagine might suggest that synthesis and interconversion reactions of these amino group donors are affected. However, neither alanine aminotransferase nor alanine: glyoxylate aminotransferase were inhibited by the toxin in vitro. Our observations might be explained by three hypotheses: (1) the toxin inhibits one or more aminotransferases not examined, (2) ascaulitoxin aglycone affects amino acid transporters, (3) ascaulitoxin aglycone is a protoxin that is converted in vivo to an aminotransferase inhibitor.     

Furazolidone induces the activity of microsomal enzymes that metabolize furazolidone in chickens

The nitrofuran antibacterial agent furazolidone (FZ) is still used in veterinary medicine in some countries in the Middle and Far East. The present study aimed to show the effect of FZ on the activity of microsomal enzymes that metabolize FZ, and to identify the enzyme that contributes to FZ metabolism in chickens. Wistar rats and White Leghorn chickens were administered FZ once a day for four consecutive days. FZ metabolism was accelerated by FZ administration in chickens, but not in rats. The elevation of FZ metabolism coincided with the induction of NADPH cytochrome P450 reductase (CPR) activity in chickens, but such induction was not observed in rats. FZ metabolizing activities were inhibited in the presence of a CPR inhibitor (diphenylene iodonium chloride) but not by the addition of archetypal cytochrome P450 inhibitors (CO or n-octylamine). The preset study concluded that FZ accelerated its own metabolism in the chicken by induction of the activity of CPR.     

Probing mode of action in plant cell cycle by the herbicide endothall, a protein phosphatase inhibitor

The mode of action of endothall, an herbicide which was reported to inhibit plant protein phosphatases 1 (PP1) and 2A (PP2A), was investigated. For initial characterization, a series of bioassays was used for comprehensive physiological profiling of endothall effects which suggested a phytotoxic mode of action similar to mitotic disrupter herbicides. Unlike known microtubule disrupters, endothall did not inhibit soybean tubulin polymerization in vitro. As shown in meristematic corn root tips, endothall distorted the orientation of cell division plane and microtubule spindle structures which led to cell cycle arrest in prometaphase. In tobacco BY-2 cells, malformed spindles together with prometaphase arrest of nuclei and abnormal perinuclear microtubule patterns were detected as early as 4 h of endothall treatment. These effects were also observed after treatment with other protein phosphatase inhibitors, cantharidin and okadaic acid, which phenocopied the mitotic changes described in tonneau1 (ton1) and tonneau2 (ton2) Arabidopsis mutants. These mutants are defective in TONNEAU2 (TON2) protein, a regulatory subunit of PP2A, which governs cell division plane and microtubule orientation. Therefore, PP2A/TON2 phosphatase complex is suggested to be an in planta molecular target of endothall. However, in BY-2 cells, additional effects of endothall, including inhibition of S-phase initiation and DNA synthesis, detected by 5-ethynyl-2′-deoxyuridine (EdU) incorporation, and condensed nuclei arrested in late mitosis were observed which were not reported in Arabidopsiston1 and ton2 mutants. This result indicates that two additional checkpoints in cell cycle were blocked by endothall which are probably not associated with TON2-pathway inhibition. Possibly, inhibition of PP1 and/or other PP2A protein phosphatases are involved in the regulation of these cell cycle phenomena.     

Hepatoprotective activity of angiotensin-converting enzyme (ACE) inhibitors, captopril and enalapril, against paraquat toxicity

Paraquat is a highly toxic herbicide that is used in most countries without restriction. The cytotoxic action of paraquat is mediated by reactive radicals that are products of its metabolic reduction in cells. It has already been hypothesized that some angiotensin-converting enzyme inhibitors (e.g., captopril and enalapril) could show antioxidant and radical scavenging activity through their structural thiol groups, increasing antioxidant enzymes production or nitric oxide synthesis. In this study the hepatoprotective effect of captopril and enalapril against paraquat induced oxidative stress cytotoxicity was evaluated in isolated rat hepatocyte. Subtoxic concentrations of captopril (0.2 mM) and enalapril (0.2 mM) significantly (p < 0.05) protected the hepatocytes against paraquat (2 mM) induced oxidative stress cytotoxicity markers including: cell lysis, reactive oxygen species (ROS) generation, lipid peroxidation, glutathione depletion, mitochondrial membrane potential decrease, lysosomal membrane oxidative damage and cellular proteolysis. Moreover, we showed that non-thiol enalapril acts as well as thiol containing captopril at inhibiting oxidative stress cytotoxicity markers. Finally, our results support the hypothesis that it is the increase in nitric oxide synthesis and not the presence of the thiol group that accounts for the antioxidant activity of ACE inhibitors.