Cd2+、Hg2+对菱幼苗生长及其超氧化物歧化酶、过氧化物酶活性的影响

利用不同浓度Ｃｄ２＋、Ｈｇ２＋处理菱幼苗,研究重金属离子对菱生长、超氧化物歧化酶（ＳＯＤ）、过氧化物酶（ＰＯＤ）活性的影响,比较Ｃｄ２＋、Ｈｇ２＋对同一植物的毒性差异。Ｃｄ２＋、Ｈｇ２＋各处理浓度均抑制菱幼苗生长,使叶绿素含量下降,但Ｃｄ２＋的抑制作用比Ｈｇ２＋的作用明显。Ｃｄ２＋、Ｈｇ２＋对ＳＯＤ、ＰＯＤ活性有不同的影响效果：Ｃｄ２＋处理最初诱导ＳＯＤ、ＰＯＤ活性升高,但随浓度加大时间延长酶活性急剧下降;Ｈｇ２＋处理的酶活性变化相对平缓,其中５μｍｏｌ／Ｌ和１０μｍｏｌ／ＬＨｇ２＋处理的ＰＯＤ活性持续上升。实验结果表明,在相同处理时间和浓度条件下,Ｃｄ２＋比Ｈｇ２＋对菱的毒性要大。依据实验结果,作者探讨了重金属对植物的毒害机制     

Cd2+、Hg2+对菱幼苗生长及其超氧化物歧化酶、过氧化物酶活性的影响

利用不同浓度Ｃｄ＾２＋、Ｈｇ＾２＋处理菱幼苗,研究重金属离子对菱生长、超氧化物歧化酶（ＳＯＤ）、过氧化物酶（ＰＯＤ）活性的影响,比较了Ｃｄ＾２＋、Ｈｇ＾２＋对同一植物的毒性差异,Ｃｄ＾２＋、Ｈｇ＾＾２＋各处理浓度与均抑制菱幼苗生长,使叶绿素含量下降,Ｃｄ＾２＋的抑制作用比Ｈｇ＾２＋的作用明显。Ｃｄ＾２＋、Ｈｇ＾２＋对ＳＯＤ、ＰＯＤ活性有不同的影响效果;Ｃｄ＾２＋处理最艉地ＳＯＤ、ＰＯＤ活性升高,但     

Hg2+污染对莼菜冬芽幼叶细胞超微结构伤害的研究

报道了Ｈｇ＾２＋污染对莼菜冬芽幼叶毒害引起的叶片受害症状和叶肉细胞的超微结构变化。冬芽在Ｈｇ＾２＋浓度５ｍｇ／Ｌ处理１５ｄ时,叶片开始褪绿,腺毛收缩扭曲,粘液减少,细胞中高尔基体消失,核糖体减少,线粒体出现解体。在相同处理时间中,随着Ｈｇ＾２＋浓度增加,细胞出现质膜收缩,胞间连丝断裂,核仁裂解成多个小核仁,叶绿体膨胀,类囊体解体。在Ｈｇ＾２＋浓度１５ｍｇ／Ｌ时,细胞核解体,细胞死亡。经观察,Ｈｇ＾     

Cd^2＋污染对莼菜叶片形态学伤害反应的研究

重点研究了Ｃｄ＾２＋胁迫下莼菜叶片的受害症状及叶肉细胞超微结构的变化。当Ｃｄ＾２＋浓度大于２μｇ·ｇ＾－１时,莼菜叶面将在短期内出现不同程度的受害症状。莼菜叶片遭受Ｃｄ＾２＋毒害初期,叶肉细胞质体中的少数基粒会发生膨胀或解体,线粒体的脊出现瓦解,部分核仁裂解成数块大小不等的颗粒。随着叶肉细胞遭受毒害程度的加深,质体中较多的类囊体便出现解体,多种膜性结构如：质体、线粒体的外包膜以及核膜、液泡膜等均遭     

重金属对蚕豆的细胞遗传学毒理作用和对蚕豆根尖微核技术的探讨

Ｐｂ２＋ 、Ｃｄ２＋ 和Ｈｇ２＋ 显著地缩短蚕豆（Ｖｉｃｉａ ｆａｂａ Ｌ．）根尖细胞分裂的持续时间,延长细胞间期的时间间隔,在总体上延长了细胞分裂周期;除Ｈｇ２＋ 随浓度升高一直表现为对有丝分裂抑制外,在Ｐｂ２＋ 、Ｃｄ２＋ 和Ｚｎ２＋ 浓度分别小于１．０、０．０１、１０．０ ｐｐｍ 时,细胞有丝分裂指数随处理浓度升高而上升,当超出上述浓度时则随浓度升高而下降;微核率（ＭＣＮＦ）在Ｐｂ２＋ 、Ｃｄ２＋ 、Ｈｇ２＋ 和Ｚｎ２＋ 的浓度分别小于１．０、５．０、０．５０、１００．０ ｐｐｍ 时,染色体畸变率（ＣＡＦ）在Ｐｂ２＋ 、Ｃｄ２＋ 、Ｈｇ２＋ 和Ｚｎ２＋ 的浓度分别小于５．０、５．０、０．５０、１００．０ ｐｐｍ 时,这两参数随处理浓度的升高而增大;超过上述浓度后,则随处理浓度升高而下降。Ｍｎ２＋ 对各项参数无显著影响。对蚕豆根尖细胞遗传学毒性顺序为Ｈｇ２＋ ＞ Ｃｄ２＋ ＞ Ｐｂ２＋ ＞ Ｚｎ２＋ ＞ Ｍｎ２＋ 。经综合分析,３ 个参数在不同剂量范围下相关性程度有很大的差异。认为蚕豆根尖微核技术检测危险化学品和监测环境污染时取得可靠结果的条件是：受检物质在检测条件下不严重抑制细胞分裂和ＣＡＦ和ＭＣＮＦ呈正相关     

低温逆境中不同抗寒性植物细胞内Ca^2＋稳定平衡的区别

电镜细胞化学观察揭示,不抗寒的玉米（Ｚｅａ ｍａｙｓ Ｌ．ｅｖ． Ｂｌａｃｋ Ｍｅｘｉｃａｎ Ｓｗｅｅｌ）和抗寒的小偃麦（Ｔｒｉｔｉｃｕｒｎ ｓｅｅｔ．Ｔｒｉｔｉｔｒｉｇｉａ ｍａｃｋｅｙ）细胞在２６℃悬浮培养时,标志Ｃａ＾２＋定位的锑酸钙沉淀物主要分布在液泡内,细胞质和细胞核中很少见到Ｃａ＾２＋沉淀;标志Ｃａ＾２＋－ＡＴＰａｓｅ活性的反应的磷权沉淀物丰富地分布在质膜上,显示这两种植物物质膜Ｃａ＾     

牛磺酸对血管紧张素Ⅱ改变培养心肌细胞内游离Ca^2＋深度作？…

目的和方法：用Ｆｕｒａ－２／ＡＭ荧光显示测定细胞内游离Ｃａ＾２＋浓度（〖Ｃａ＾２＋〗ｉ）的方法,我们研究了牛磺酸（Ｔａｕ）对血管紧张素Ⅱ（ＡｎｇⅡ）引起的培养心肌细胞（〖Ｃａ＾２＋〗ｉ）变化的影响。结果：在有Ｃａ＾２＋和无Ｃａ＾２＋的缓冲液中,ＡｎｇⅡ（１,１０,１００,１０００ｎｍｏｌ／Ｌ）引起的〖Ｃａ＾２＋）ｉ和蔼同。在含Ｃａ＾２＋的缓冲液中,Ｔａｕ（１０,２０ｍｏｌ／Ｌ）可隽浓度地抑制Ａｎｇ     

Ca2+对非细胞体系细胞核重建影响机制的研究

研究Ｃａ＾２＋与非细胞体系细胞核重建的关系以及Ｃａ＾２＋的作用机制,结果显示：Ｃａ＾２＋对非细胞体系中核装配有抑制作用,随着Ｃａ＾２＋浓度的增加,抑制核装配作用增加,在Ｃａ＾２＋作用的早期（作用１０分钟后）中入ＥＧＴＡ,可以部分地逆转Ｃａ＾２＋的抑制作用,Ｃａ＾２＋作用１小时后再加入ＥＧＴＡ,不再有逆转作用。对Ｃａ＾２＋作用机制的研究结果显示,不是由于ＡＴＰ和ＧＴＰ被沉淀而导致细胞核组装被抑制,Ｃ     

亚精胺对苹果花粉萌发与花粉管伸长的抑制效应及其与Ca^2 …

２０～１００μｍｏｌ．ｌ＾－１外源亚精胺（Ｓｐｄ）抑制苹果（品种：国光、富士、金冠）花粉萌发与花粉管伸长,其效应随浓度增加而增强;Ｃａ＾２＋（１ｍｍｏｌ．Ｌ＾－１）在一定程度上削弱这种抑制效应,而Ｃａ＾２＋的良好作用则又为Ｃａ＾２＋通道竞争性抑制剂Ｌａ＾２＋所消除,Ｃａ＾２＋载体Ａ２３１８７仅削弱Ｃａ＾２＋对花粉管 工的良好作用。     

Cd^2＋或Hg^2＋水污染对菱体细胞的细胞核及叶绿体超微结构的影响

用Ｃｄ２＋、Ｈｇ２＋两种重金属离子溶液培育菱（ＴｒａｐａｂｉｃｏｒｎｉｓＯｓｂｅｃｋ．）植物体后,观察体细胞的细胞核及叶绿体超微结构的变化。处理后第８天,菱浮水叶叶片和不定根细胞中细胞核的染色质与核质遭到破坏,不定根中细胞核的核仁消失。但在各处理浓度（１０μｍｏｌ／Ｌ～５０μｍｏｌ／ＬＣｄ２＋或Ｈｇ２＋）下,核膜均保持完整。叶片细胞的叶绿体基粒数目减少,基粒片层解体,叶绿体双层膜断裂,叶绿体中的质体球流入细胞基质中。两种结构的破坏程度随处理的离子浓度提高而增大。说明菱体细胞超微结构的变化观测可作为监测重金属污染的一种方法。     

Isolation and identification of urinary metabolites of AF-2 (3-(5-nitro-2-furyl)-2-(2-furyl)acrylamide) in rabbits

After oral administration of AF-2 (3-(5-nitro-2-furyl)-2-(2-furyl)acrylamide) to rabbits, the two unique metabolites, M-I and M-II, were isolated from the urine. M-I, yellow needles of mp 117°, was identified as a new type metabolite of nitrofuran derivative, 2-(β-carboxypropionyl)-3-(5-methylthio-2-furyl) acrylamide by its mass, ir and nmr spectrometries. M-II, yellow solid, appears to be cis-trans isomer of M-I considering from its uv and mass spectral data, and the behavior on tlc.     

3-(2-Methoxytetrahydrofuran-2-yl)pyrazoles: a novel class of potent, selective cyclooxygenase-2 (COX-2) inhibitors

A series of 3-(2-methoxytetrahydrofuran-2-yl)pyrazoles (4–10) was synthesized. The compounds were evaluated for their ability to inhibit cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) activity in human whole blood (HWB). The compound, 5-(4-methanesulfonylphenyl)-3-(2-methoxytetrahydrofuran-2-yl)-1-p-tolyl-1H-pyrazole 5 showed potent and selective COX-2 inhibition (IC₅₀ for COX-1: >100 μM and COX-2: 1.2 μM).     

Synthesis and Properties of Modified Oligodeoxyribonucleotides Containing 2"-O-(2,3-Dihydroxypropyl)uridine and 2"-O-(2-Oxoethyl)uridine

A new uridine derivative, 2"-O-(2,3-dihydroxypropyl)uridine, and its 3"-phosphoramidite were obtained for direct introduction into oligonucleotides during automated chemical synthesis. Oligonucleotides 10 to 15 nt long harboring 2"-O-(2,3-dihydroxypropyl)uridine residues were synthesized; periodate oxidation of these oligomers gave oligonucleotides containing 2"-O-(2-oxoethyl)uridine residues. The presence of a reactive aldehyde group in 2" position of the carbohydrate moiety was confirmed by the interaction withp-nitrophenylhydrazine and methionine methyl ester. The thermostability of DNA duplexes containing modified units does not practically differ from that of the natural analogues.     

Seven in Absentia Homolog 2 (Siah2) Protein Is a Regulator of NF-E2-related Factor 2 (Nrf2)

Under pathological conditions such as ischemia-reperfusion, Nrf2 acts as a key regulator of cellular oxidative response. Provided that Nrf2 is sensitive to hypoxia during ischemia, Nrf2 may affect reactive oxygen species metabolism during reoxygenation. In this study, hypoxia suppressed Nrf2 protein, and its hypoxic suppression was not recovered with knockdown of the Nrf2 repressor Keap1. Moreover, an Nrf2 mutant lacking the Keap1 binding domain was suppressed under hypoxia, suggesting that Keap1 does not contribute to hypoxic Nrf2 suppression. HIF-1α and Siah2 are both key regulators of hypoxic responses. Hypoxia induced the Siah2 protein. Although inhibition or knockdown of Siah2 prevented the suppression of Nrf2, knockdown of HIF-1α did not. Moreover, Siah2 interacted with Nrf2 through a binding motif, suggesting that Siah2 contributes to the suppression of Nrf2. Some cytosolic kinases also play important roles in Nrf2 regulation. In this study, PKC phosphorylates serine residues of Nrf2 during hypoxia. Knockdown of Siah2 rescued hypoxic decreases in an Nrf2 mutant that mimicked phosphorylation at serine 40 or lacked this phosphorylation site, suggesting that Siah2 contributes to the degradation of Nrf2 irrespective of its phosphorylation status. Moreover, knockdown of Siah2 attenuated ubiquitination of the Nrf2 mutant, suggesting that association of Siah2 with Nrf2 causes proteasome-mediated degradation of Nrf2.     

MOB2基因在真核细胞中的表达研究

通过RT-PCR从培养的HUVECs中扩增MOB2基因片段,将该片段克隆在真核表达载体pEGFP-C1中,转染NIH3T3细胞,经G418筛选,构建稳定表达细胞系,并用荧光显微镜和Western blot对其进行鉴定。经RT-PCR扩增出734 bp基因片段,经测序分析并与GenBank的DNA序列比对分析后,在NIH3T3细胞中表达。G418筛选后,细胞荧光信号较强,Western blot检测,细胞中的融合蛋白能够与抗MOB2的多抗结合。成功地扩增了HUVECs中的MOB2基因全长cDNA并进行真核表达与鉴定。     

Facile synthesis of (R)N-2-hydroxyacyl-L-cysteine derivatives: (R)N-2-hydroxyacyl transfer from enzymatically-synthesized (R)S-2-hydroxyacylglutathione derivatives to L-cysteine

Summary N-(R)-2-Hydroxyacyl-L-cysteine derivatives were conveniently synthesized by the reaction of the corresponding S-(R)-2-hydroxyacyl-glutathione with cysteine. The (R)2-hydroxyacyl group was transferred from the S-glutathionyl moiety to S-cysteinyl, forming the corresponding (R)S-2-hydroxyacylcysteine; this rearranged to the (R)N-hydroxyacylcysteine. These compounds have anti-proliferative activity associated with the inhibition ofde novo pyrimidine synthesis.Abbreviations TRIS tris(hydroxymethyl) aminomethane - DTNB 5,5-dithiobis(2-nitrobenzoic acid)     

(E)-2-(2-(2-hydroxyphenyl)hydrazono)-1-phenylbutane-1,3-dione: Tautomery and coordination to copper(II)

(E)-2-(2-(2-hydroxyphenyl)hydrazono)-1-phenylbutane-1,3-dione (H₂L) was synthesized by azocoupling of diazonium salt of 2-hydroxyaniline with 1-phenylbutane-1,3-dione and characterized by IR, ¹H and ¹³C NMR spectroscopies and X-ray diffraction analysis. In solution, H₂L exists as a mixture of the enol-azo and hydrazone tautomeric forms and a decrease of temperature and of solvent polarity shifts the tautomeric balance to the hydrazone form. In the solid state, H₂L crystallizes from ethanol-water in the monohydrate hydrazone form, as shown by X-ray analysis. The dissociation constants of H₂L (pK₁ = 5.98 ± 0.04, pK₂ = 9.72 ± 0.03) and the stability constants of its copper(II) complex (log β₁ = 11.01 ± 0.07, log β₂ = 20.19 ± 0.08) were determined by the potentiometric method in aqueous-ethanol solution. The copper(II) complex [Cu₂(μ-L)₂]_n was isolated in the solid state and found by X-rays to be a coordination polymer of a binuclear core with a distorted square pyramidal metal coordination geometry.     

Adaptor Protein2 (AP2) Orchestrates CXCR2‐Mediated Cell Migration

The chemokine receptor CXCR2 is vital for inflammation, wound healing, angiogenesis, cancer progression and metastasis. Adaptor protein 2 (AP2), a clathrin binding heterotetrameric protein comprised of α, β2, μ2 and σ2 subunits, facilitates clathrin‐mediated endocytosis. Mutation of the LLKIL motif in the CXCR2 carboxyl‐terminal domain (CTD) results in loss of AP2 binding to the receptor and loss of ligand‐mediated receptor internalization and chemotaxis. AP2 knockdown also results in diminished ligand‐mediated CXCR2 internalization, polarization and chemotaxis. Using knockdown/rescue approaches with AP2‐μ2 mutants, the binding domains were characterized in reference to CXCR2 internalization and chemotaxis. When in an open conformation, μ2 Patch 1 and Patch 2 domains bind tightly to membrane PIP2 phospholipids. When AP2‐μ2, is replaced with μ2 mutated in Patch 1 and/or Patch 2 domains, ligand‐mediated receptor binding and internalization are not lost. However, chemotaxis requires AP2‐μ2 Patch 1, but not Patch 2. AP2‐σ2 has been demonstrated to bind dileucine motifs to facilitate internalization. Expression of AP2‐σ2 V88D and V98S dominant negative mutants resulted in loss of CXCR2 mediated chemotaxis. Thus, AP2 binding to both membrane phosphatidylinositol phospholipids and dileucine motifs is crucial for directional migration or chemotaxis. Moreover, AP2‐mediated receptor internalization can be dissociated from AP2‐mediated chemotaxis.