华北平原几种主要类型土壤的硝化及反硝化活性

取用华北平原5种主要土壤进行实验室培养试验,研究不同类型土壤间硝化反硝化活性的差异。结果表明,培养28h后砂姜黑土、潮土、褐土、盐渍土和风沙土的硝化率分别为7.9%、20.8%、46.4%、22.5%和20.3%;148h后砂姜黑土的硝化率为18.7%,其它4种土壤达98.4%—100%,基本硝化完全;培养268h释放的N2O总量分别为0.04、0.27、0.24、0.41和0.45μgN·g-1土。培养650h的反硝化损失量分别为0.6、0.3、0.08、0.02和0.05μgN·g-1土。可见,不同的土壤中砂姜黑土的硝化作用活性较弱,而反硝化活性较强;潮土、褐土、盐渍土和风沙土的硝化作用活性较强,而反硝化活性相对较弱。土壤的硝化及反硝化作用与土壤质地和pH有关,与硝化和反硝化菌数量无明显相关性。     

NO在植物体内产生的途径及其作用

近年来的研究表明一氧化氮(nitric oxide,NO)是生物体内的重要的信号分子,参与多种生理功能的调控。文章主要介绍了在植物体内NO的产生途径、信号传导机制、与其他信号分子之间的相互作用及其与植物激素之间的作用。     

一氧化氮(NO)在植物抗病防卫反应中的功能

一氧化氮(NO)是一种高度活性分子,能通过细胞膜快速扩散,在植物中NO可通过酶促途径和非酶促途径产生。已在多种受病原物诱导的植物中检测到NO的产生。研究发现在植物-病原物互作中NO在过敏性(HR)细胞死亡和系统获得抗性(SAR)的建立中起非常重要的信号调节作用。     

一氧化氮延缓草莓成熟衰老的生理效应

 以硝普钠（SNP）为一氧化氮（NO）供体，研究了不同浓度NO对丰香草莓采后果实乙烯产生、呼吸强度、维生素C（Vc）、可溶性蛋白、失水腐烂和相对电导率，以及超氧物歧化酶（SOD）、过氧化氢酶（CAT）和过氧化物酶（POD）活性的影响。结果表明，5 μmol·L-1 SNP释放NO可以抑制草莓果实乙烯的产生和呼吸强度，延缓乙烯产生和呼吸高峰的出现，并推迟了果实固酸比、Vc和可溶性蛋白含量下降时期，抑制果实腐烂失水和相对电导率升高；使果实CAT活性显著增强，SOD活性在后期高于对照，但POD活性低于对照。10 μmol·L-1 SNP对果实产生轻微毒害作用，1 μmol·L-1 SNP延迟草莓衰老的效果不明显。证明了NO抑制果实衰老与其浓度的相关性，揭示了NO保护细胞膜结构完整的作用机理。     

L—精氨酸对肉鸡肺动脉压和腹水综合征发生的影响

AA肉鸡 180羽随机等分为对照组 (C)和试验组 (A、B)。参试鸡 14日龄前常规饲养。 14日龄后C组鸡继续常规饲养 ;A、B组鸡舍温度按每日 1～ 2℃由 2 5℃逐步降至 12℃ ,同时日粮中添加 1 5mg kg-1三碘甲状腺原氨酸 (T3 )以诱发腹水综合征 ;B组自 14日龄起至试验结束在日粮中再添加 1% (质量分数 )L 精氨酸。分别于 3,4,5 ,6,7周龄测定各组肉鸡肺动脉平均压 (mPAP)、红细胞压积、右心全心比及血浆一氧化氮 (NO)水平 ,并记录腹水发病率。结果发现 :低温添加T3 处理后 ,A组肉鸡腹水发病率增加 ,mPAP在 5周龄时升高 ,右心全心比在 6周龄时升高 ;B组肉鸡腹水发病率明显低于A组 ,血浆NO水平高于A组 (P <0 0 1) ,mPAP在 6周龄时升高 ,右心全心比在 7周龄时升高 ,此变化比A组晚一周出现。上述结果提示 ,日粮添加精氨酸后血浆NO水平升高 ,可能在一定程度上抑制了肺动脉高压的形成 ,因而在一定程度上降低了腹水综合征发病     

Effects of puerarin on apelin-12, angiotensin II,NO and blood pressure in renovascular hypertensive rat

AIM: To investigate the effects of puerarin on blood pressure in renovascular hypertensive rats, and to measure puerarin-induced changes of apelin-12, angiotensin II (Ang II) and nitric oxide(NO), the factors related to development of hypertension. METHODS: Sixty-five male Sprague-Dawley rats were used, of which 8 rats were randomly selected as sham operation group, and the remaining were used to make two-kidney, one-clip model. The rats that met the criterion for Goldblatt hypertensive rat model were randomly allocated into 5 groups: high-, middle- and low-dose puerarin groups, captopril group, and model group. The drugs were administered for 6 weeks. Blood pressure was measured every 2 weeks. Six weeks after treatment, all rats were sacrificed under deep anesthesia. Blood and kidney samples were collected. The level of apelin-12 in serum and kidneys was detected by ELISA. The level of Ang II in plasma and kidneys was measured by radioimmunoassay. NO level in serum was examined by nitrate reductase assay. RESULTS: Puerarin had an antihypertensive effect in a dose-dependent manner. Marked decreases in the level of serum apelin-12 in high- and middle-dose puerarin groups were observed(P<0.01). Puerarin at low dose did not cause obvious change in the content of apelin but still reached significant level (P<0.05). As the dose of puerarin went up, the level of apelin-12 in the kidneys was gradually decreased. Puerarin at high and middle doses obviously reduced the level of AngII in plasma, while purarin at low dose did not produce any significant effects. Puerarin at high and middle doses markedly increased the level of NO in serum, but puerarin at low dose did not induce any significant changes. CONCLUSION: Puerarin has an antihypertensive effect, and its mechanism may be related to inducing the changes of apelin, Ang II and NO, and regulating the balance among those factors.     

Cardioprotective effect of sevoflurane preconditioning on ROS production in rat heart with ischemia-reperfusion

AIM: To investigate the effects of sevoflurane preconditioning on the production of reactive oxygen species (ROS) and nitric oxide (NO), the activity of superoxide dismutase(SOD), glutathione peroxide(GPx) and catalase(CAT) in myocardial ischemia-reperfusion injury(IRI). METHODS: Sixty rats were randomly allocated to 8 groups. Following 2% sevoflurane preconditioning for 30 min, the left anterior descending artery was ligated for 30 min and then reperfused for 120 min in vivo. The infarction size of the hearts was measured with the staining of 2,3,5-triphenyltetrazoliumchloride. The myocardial apoptotic index was measured by the method of TUNEL. The ROS fluorescent probe dihydroethidium was used for the measurement of ROS. The myocardium was homogenized for the measurement of NO, SOD, GPx and CAT. To evaluate the effects of ROS and NO on the cardioprotection of sevoflurane preconditioning, ROS scavenger N-(2-mercaptopropionyl) glycine (2-MPG) or NOS inhibitor N^ω-nitro-L-arginine methyl ester (L-NAME) were employed to block their actions. RESULTS: Compared with control group, the production of ROS was induced by sevoflurane preconditioning before ischemia-reperfusion injury (12.0±0.8 vs 2.6±0.5, P<0.05) and decreased after ischemia-reperfusion injury (16.2 ±0.9 vs 24.9±1.3, P<0.05). 2-MPG decreased the elevation of ROS caused by sevoflurane preconditioning before ischemia-reperfusion injury (5.1±0.7 vs 12.0±0.8, P<0.05). No difference of ROS production between treating with 2-MPG+Sevo+IRI and with IRI (24.9±1.4 vs 24.9±1.3, P>0.05) was observed. Compared with control group, sevoflurane preconditioning also induced the generation of NO (34.5±3.2 vs 15.9±1.4, P<0.05) and the activity of SOD(1.5±0.5 vs 0.6±0.2, P<0.05), GPx(22.8±2.5 vs 12.7±2.2, P<0.05) and CAT(15.5±1.8 vs 11.2±1.4, P<0.05). 2-MPG blocked the increase in NO production and inhibited the activity of SOD,GPx,CAT. L-NAME also attenuated the activity of SOD,GPx,CAT. CONCLUSION: Sevoflurane preconditioning protects the rat heart against ischemia-reperfusion injury by reducing the infarction size and apoptosis. Production of ROS at sub-injury dose induced by sevoflurane preconditioning stimulates the myocardium to create SOD,GPx,CAT and NO, thus inhibiting the further formation of ROS and protecting the heart under the condition of ischemia-reperfusion.     

The effect of increased atmospheric carbon dioxide concentration on emissions of nitrous oxide, carbon dioxide and methane from a wheat field in a semi-arid environment in northern China

There are no reports on the effects of elevated carbon dioxide [CO₂] on the fluxes of N₂O, CO₂ and CH₄ from semi-arid wheat cropping systems. These three soil gas fluxes were measured using closed chambers under ambient (420 ± 18 μmol mol⁻¹) and elevated (565 ± 37 μmol mol⁻¹) at the Free-Air Carbon dioxide Enrichment experimental facility in northern China. Measurements were made over five weeks on a wheat crop (Triticum aestivum L. cv. Zhongmai 175). Elevated [CO₂] increased N₂O and CO₂ emission from soil by 60% and 15%, respectively, but had no significant effect on CH₄ flux. There was no significant interaction between [CO₂] and N application rate on these gas fluxes, probably because soil N was not limiting. At least 22% increase in C storage is required to offset the observed increase in greenhouse gas emissions under elevated [CO₂].     

外源NO对缺铁胁迫下花生生理特性的影响

为探讨外源NO对缺铁胁迫下花生生理特性的影响,采用溶液培养方法,研究了营养液中Fe(Ⅲ)-EDTA 浓度分别为0、10、100 mol/L 条件下,外施250 mol/L硝普钠（SNP, 一种NO 供体）对花生生理特性以及矿质元素含量的影响。结果表明,在相同供铁水平下,外施NO可促进花生幼苗的生长,提高根系活力、净光合速率、蒸腾速率、气孔导度和叶片抗氧化酶活性,降低胞间CO2 浓度和MDA 含量,抑制花生对P 的吸收;在Fe(Ⅲ)-EDTA 浓度分别为0、10 mol/L 条件下综合效果更显著。在0、10、100 mol/L Fe(Ⅲ)-EDTA 中施加SNP 处理20d 后,叶片活性铁含量分别比未施加SNP处理提高了130.7%、136.4%、56.1%,差异显著;同时植株全铁含量及地上部吸铁量占植株总量的百分率也显著提高。说明外源NO可促进铁从根部向植株地上部的运输以及植株体内铁的有效性,提高了铁的运输和利用效率,有效缓解缺铁胁迫的抑制。同时,外施NO还可提高花生叶片叶绿素、类胡萝卜素含量和叶绿素a/b值。在Fe(Ⅲ)-EDTA 浓度分别为0、10 mol/L 条件下,添加SNP 可以明显降低生长介质的pH,比较 1d 内生长介质中pH 变化看出,花生在14h左右分泌H+ 的能力最强。     

不同产地毛头鬼伞子实体多糖特征及其刺激巨噬细胞产生NO的活性

用水提醇沉法从6个不同产地毛头鬼伞(Coprinus comatus)子实体中获得6种粗多糖,6种粗多糖得率及多糖含量差异较大,以湖北(HB)的最高,其次为云南(YN)的;各粗多糖分子量分布相似,单糖组成均以葡萄糖为主,并含有少量半乳糖;除福建(FJ)外,其余5种粗多糖均能增强小鼠巨噬细胞RAW264.7释放NO的产量,以YN和HN的活性较好,总体来说,YN的多糖产量及活性较好.