旅游和工业化对亚热带森林地区大气环境质量及两种木本植物叶绿素荧光特性的影响

研究了旅游、工业化等不同类型的人类活动对亚热带森林大气ＣＯ２、ＳＯ２、ＮＯｘ浓度及两种木本植物———木荷（ＳｃｈｉｍａｓｕｐｅｒｂａＧａｒｄｎ．ｅｔＣｈａｍｐ．）和马尾松（ＰｉｎｕｓｍａｓｏｎｉａｎａＬａｍｂ．）叶绿素荧光特性的影响。结果表明,不同形式人类活动使森林中大气ＣＯ２浓度上升了１７～３０μｍｏｌ·ｍｏｌ－１,ＮＯｘ化合物的浓度上升了５～２０ｎｍｏｌ·ｍｏｌ－１,ＳＯ２浓度上升了２～１９ｎｍｏｌ·ｍｏｌ－１。森林大气中ＣＯ２、ＮＯｘ、ＳＯ２浓度随着人类活动的加强而升高。木荷和马尾松叶片Ｆｖ／Ｆｍ、ΦＰＳⅡ和稳态下的ｑＰ随人类活动加强而下降,其下降趋势与ＣＯ２、ＳＯ２、ＮＯｘ的上升趋势相一致。     

硝酸钾缓解氯化钠胁迫蓝藻Anabaena 7120固氮的生理基础

营养液中添加适量ＫＮＯ３可在一定程度上缓解ＮａＣｌ对鱼腥藻固氮活性的抑制作用。暗处理或加光合抑制剂时,ＫＮＯ３对ＮａＣｌ胁迫的缓解作用便消失。供给外源蔗糖、提高ＣＯ２浓度、同时供给ＣＯ２和Ｎ２时,ＫＮＯ３对缓解ＮａＣｌ胁迫的作用则增高．同时供给Ｏ２和Ｈ２对ＫＮＯ３的缓解作用增高影响较小,而在厌氧（Ａｒ或Ｎ２中）或单加氧下,ＫＮＯ３的缓解效应则明显减弱或消失．     

钙对蓝藻固氮受氯化钠胁迫的缓解效应及其与生理条件的关系

氯化钠胁迫导致蓝藻固氮活性的下降,可因加人适当浓度的氯化钠而有一定程度的缓解．在光合作用受抑（暗处理或添加光合抑制剂）、厌氧（Ａｒ或Ｎ２中）和有分子氧的情况下,此种缓解作用减弱．光合作用、需氧代谢（通气）和羟化反应（同时供给氢和氧）正常进行以及碳架（添加外源蔗糖或提高ＣＯ２浓度）供应良好时,钙对氯化钠胁迫的缓解效应增大．改善合成固氮酶的物质基础供应（同时供应ＣＯ２和Ｎ２）对此也有一定的正效应．     

不同CO2浓度与温度条件下马铃薯叶片的淀粉浓度与比叶重和矿质…

三个马铃薯品种在５００,１０００,１５００,２０００μｍｏｌ．ｍｏｌ＾－１ＣＯ２浓度与１６,２０℃空气温度下生长３５ｄ测定了植株叶片的比叶重,淀粉浓度及主要养分Ｎ,Ｐ,Ｋ,Ｃａ,Ｍｇ的浓度。在１６℃和２５℃下,叶片淀粉浓度随ＣＯ２浓度的增加而增加,且１６℃下的测定值高于２０℃下的测定值,比叶重与以叶面积或干重为基础的叶片淀粉浓度成正相关。     

分子氢和氧对受高温胁迫蓝藻固氮活性的影响

Ａｎａｂａｅｎａ７１２０经高温处理后,固氮活性下降,对氧的敏感度增大,增大程度随氧浓度增高而递增。高温胁迫下,分子氢与对正常条件下生长的蓝藻一样可以削弱或消除氧对固氮的伤害,氢的此种行为在光照下和黑暗中表现相似,其良好作用比正常生长蓝藻显著,添加光合抑制剂。ＣＯ２或Ｎ２时亦如何。有外源蔗糖时,氢的良好作用不表现。经ＣＯ或Ｃ２Ｈ２处理的蓝藻,氢在其固氮活性受氧伤害时的良好作用消失。     

高原鼠兔氧比传导特征的实验研究

本实验采用国外新近提出的一项能综合评价机体气体交换系统中各氧降阶差时运氧能力的适应水平高低的重要指标──氧比传导（ＭＯ２－ＳＣ）,研究了高原鼠兔气体交换系统运氧能力的低氧适应特征及规律。结果表明,对照条件下,在吸入气（Ｉ）至肺泡气（Ａ）（Ｉ→Ａ）、Ａ至动脉血（ａ）（Ａ→ａ）、ａ至混合静脉血（ｖ）（ａ→ｖ）及Ｉ→ｖ各阶差中,以Ａ→ａ的ＭＯ２－ＳＣ运氧能力最大。低氧１５ｍｍ后,Ｉ→Ａ及ａ→ｖ的ＭＯ２－ＳＣ均显著升高,并以Ｉ→Ａ增加最为显著,该水平运氧能力是对照的２倍,增长１２０．９％;而Ａ→ａ及Ｉ→ｖＭＯ２－ＳＣ变化无显著性差异。低氧３０ｍｉｎ时,Ｉ→Ａ的ＭＯ２－ＳＣ继续显著增长,运氧能力是对照的２．７倍,增长１７０．７％,其余３个氧降阶差的ＭＯ２－ＳＣ无显著性改变。以上结果表明,高原鼠兔低氧代偿贮备较大,尤以肺泡气至动脉血阶差最为重要,而通气氧传导能力的增强也是高原鼠兔低氧适应的主要原因。     

CO2和温度升高及干旱对小麦叶片化学成分的影响

研究了ＣＯ２浓度升高、高温和干旱对干旱区小麦叶片化学成分的影响,结果表明：ＣＯ２浓度升高时各化学成分之间的差异只有在４０％田间持水量时才表现显著,说明未来ＣＯ２浓度升高对干旱区小麦化学成分的影响可能大于在非干旱区的影响;ＣＯ２浓度升高可减小因为土壤水分不同而造成的小麦化学成分之间的差异;高温对小麦化学成分的主要影响是引起Ｎ含量的显著降低;ＣＯ２浓度升高、高温和干旱三因子对干旱区小麦化学成分的复合影     

氢醌和双氰胺对种稻土壤N2O和CH4排放的影响

通过盆栽试验,研究了脲酶抑制剂氢醌（ＨＱ）、硝化抑制剂双氰胺（ＤＣＤ）及二者的组合（ＨＱ＋ＤＣＤ）对种稻土壤Ｎ２Ｏ和ＣＨ４排放的影响．结果表明,在未施麦秸粉时,所有施抑制剂的处理均较单施尿素的能显著减少水稻生长期供试土壤Ｎ２Ｏ和ＣＨ４的排放．特别是ＨＱ＋ＤＣＤ处理,其Ｎ２Ｏ和ＣＨ４排放总量分别约为对照的１／３和１／２．而在施麦秸粉后,该处理的Ｎ２Ｏ排放总量为对照的１／２,但ＣＨ４排放总量却较少差别．不论是Ｎ２Ｏ还是ＣＨ４的排放总量,施麦秸粉的都比未施的高出１倍和更多．因此,单从土壤源温室气体排放的角度看,将未腐熟的有机物料与尿素共施,并不是一种适宜的施肥制度．供试土壤的Ｎ２Ｏ排放通量,与水稻植株的ＮＯ－３Ｎ含量和土表水层中的矿质Ｎ量分别呈显著的指数正相关和线性正相关;ＣＨ４的排放通量则与水稻植株的生长量和土表水层中的矿质Ｎ量呈显著的线性负相关．在Ｎ２Ｏ与ＣＨ４的排放间,未施麦秸粉时存在着定量的相互消长关系;施麦秸粉后,虽同样存在所述关系,但难以定量化．     

低渗膨胀对菠菜完整叶绿体光合作用的影响

菠菜离体完整叶绿体需要合适的介质渗透压（约０．９ＭＰａ）以保持其较高的光合作用速率。当渗透压因降低介质中山梨醇浓度（从０．３３ｍｏｌ／Ｌ至０．１７ｍｏｌ／Ｌ）而降低时,叶绿体的完整率保持不变。低于临界渗透压（约０．５ＭＰａ）,叶绿体被膜就发生破裂．并丧失ＣＯ２同化能力。在轻度低渗条件下,虽然叶绿体被膜未破,但依赖ＣＯ２的放氧速率已受抑制。渗透压在０．９ＭＰａ与０．５ＭＰａ之间,叶绿体依赖ＰＧＡ的放氧抑制,可由加入山梨醇至正常浓度（０．３３ｍｏｌ／Ｌ）而解除。膨涨叶绿体的ＡＴＰ合成水平与正常叶绿体相同,而ＮＡＤＰＨ形成速率则明显降低。利用能透过被膜的不同电子受体ＮＣ２、ＰＧＡ和ＯＡＡ发现,在膨胀叶绿体中,ＮＯ２的还原不受形响,而ＰＧＡ及ＯＡＡ的还原明显被抑制。我们推测,低渗膨胀叶绿体中光合作用的抑制,至少有一个原因是Ｆｄ－ＮＡＤＰ氧化还原酶作用的受阻。     

CO2浓度倍增对小麦生育性状和产量构成的影响

ＣＯ_２浓度倍增对小麦生育性状和产量构成的影响王修兰,徐师华,李佑祥（中国农业科学院农业气象研究所,北京,１０００８１）ＴＨＥＥＦＦＥＣＴＳＯＦＣＯ_２ＤＯＵＢＬＩＮＧＯＮＧＲＯＷＩＮＧＡＮＤＤＥＶＥＬＯＰＩＮＧＣＨＡＲＡＣＴＥＲＳＡＮＤＹＩＥＬＤＦＯ...     

Hypercapnia induces injury to alveolar epithelial cells via a nitric oxide-dependent pathway

Ventilator strategies allowing for increases in carbon dioxide (CO(2)) tensions (hypercapnia) are being emphasized to ameliorate the consequences of inflammatory-mediated lung injury. Inflammatory responses lead to the generation of reactive species including superoxide (O(2)(-)), nitric oxide (.NO), and their product peroxynitrite (ONOO(-)). The reaction of CO(2) and ONOO(-) can yield the nitrosoperoxocarbonate adduct ONOOCO(2)(-), a more potent nitrating species than ONOO(-). Based on these premises, monolayers of fetal rat alveolar epithelial cells were utilized to investigate whether hypercapnia would modify pathways of.NO production and reactivity that impact pulmonary metabolism and function. Stimulated cells exposed to 15% CO(2) (hypercapnia) revealed a significant increase in.NO production and nitric oxide synthase (NOS) activity. Cell 3-nitrotyrosine content as measured by both HPLC and immunofluorescence staining also increased when exposed to these same conditions. Hypercapnia significantly enhanced cell injury as evidenced by impairment of monolayer barrier function and increased induction of apoptosis. These results were attenuated by the NOS inhibitor N-monomethyl-L-arginine. Our studies reveal that hypercapnia modifies.NO-dependent pathways to amplify cell injury. These results affirm the underlying role of.NO in tissue inflammatory reactions and reveal the impact of hypercapnia on inflammatory reactions and its potential detrimental influences.     

Gas-phase oxidation of nitric oxide: chemical kinetics and rate constant.

Inhaled nitric oxide (NO) is gaining popularity as a selective pulmonary vasodilator. Because of the potential toxicity of NO and its oxidizing product nitrogen dioxide (NO2), any system for the delivery of inhaled NO must aim at predictable and reproducible levels of NO and at as low concentrations of NO2 as possible. This review describes the chemical kinetics and rate constant values k for the reaction 2NO + O2 = 2NO2. This reaction has been well established as a third-order homogeneous reaction. Published data support two equally plausible two-step mechanisms for the reaction between NO and O2 over a wide range of temperature and pressure. The Arrhenius equation k (L2 x mol(-2) x s(-1)) = 1.2 x 10(3) e(530/T) (=1.2 x 10(3) x 10(230/T)) gives the best fit to the experimental values of the rate constant thus far reported in a temperature range of 273 to 600 K. Using the reaction mechanism and the rate constant k, one can make reliable predictions about NO2 formation in any set of NO inhalation therapy conditions. It is also pointed out that NO3, the intermediate of one of the two mechanisms, deserves serious attention in NO inhalation therapy.     

Steady-state measurement of NO and CO lung diffusing capacity on moderate exercise in men.

Using a rapidly responding nitric oxide (NO) analyzer, we measured the steady-state NO diffusing capacity (DL(NO)) from end-tidal NO. The diffusing capacity of the alveolar capillary membrane and pulmonary capillary blood volume were calculated from the steady-state diffusing capacity for CO (measured simultaneously) and the specific transfer conductance of blood per milliliter for NO and for CO. Nine men were studied bicycling at an average O(2) consumption of 1.3 +/- 0.2 l/min (mean +/- SD). DL(NO) was 202.7 +/- 71.2 ml. min(-1). Torr(-1) and steady-state diffusing capacity for CO, calculated from end-tidal (assumed alveolar) CO(2), mixed expired CO(2), and mixed expired CO, was 46.9 +/- 12.8 ml. min(-1). Torr(-1). NO dead space = (VT x FE(NO) - VT x FA(NO))/(FI(NO) - FA(NO)) = 209 +/- 88 ml, where VT is tidal volume and FE(NO), FI(NO), and FA(NO) are mixed exhaled, inhaled, and alveolar NO concentrations, respectively. We used the Bohr equation to estimate CO(2) dead space from mixed exhaled and end-tidal (assumed alveolar) CO(2) = 430 +/- 136 ml. Predicted anatomic dead space = 199 +/- 22 ml. Membrane diffusing capacity was 333 and 166 ml. min(-1). Torr(-1) for NO and CO, respectively, and pulmonary capillary blood volume was 140 ml. Inhalation of repeated breaths of NO over 80 s did not alter DL(NO) at the concentrations used.     

Low levels of nitric oxide and carbon monoxide in alpha 1-antitrypsin deficiency.

Quantitations of exhaled nitric oxide (NO) and carbon monoxide (CO) have been proposed as noninvasive markers of airway inflammation. We hypothesized that exhaled CO is increased in individuals with alpha(1)-antitrypsin (AT) deficiency, who have lung inflammation and injury related to oxidative and proteolytic processes. Nineteen individuals with alpha(1)-AT deficiency, 22 healthy controls, and 12 patients with non-alpha(1)-AT-deficient chronic obstructive pulmonary disease (COPD) had NO, CO, CO(2), and O(2) measured in exhaled breath. Individuals with alpha(1)-AT deficiency had lower levels of NO and CO than control or COPD individuals. Alpha(1)-AT-deficient and COPD patients had lower exhaled CO(2) than controls, although only alpha(1)-AT-deficient patients had higher exhaled O(2) than healthy controls. NO was correlated inversely with exhaled O(2) and directly with exhaled CO(2), supporting a role for NO in regulation of gas exchange. Exhaled gases were not significantly related to corticosteroid use or lung function. Demonstration of lower than normal CO and NO levels may be useful as an additional noninvasive method to evaluate alpha(1)-AT deficiency in individuals with a severe, early onset of obstructive lung disease.     

A technique to estimate the rate of whole body nitric oxide formation in conscious mice.

OBJECTIVE: We have established a technique to estimate the total rate of nitric oxide (NO) formation in mice, based on inhalation of a stable oxygen isotope (18O(2)). Changes of NO production with age were also studied. METHODS: The experiments were performed in eight-week- (n=6) and eight-month-old (n=6-7), respectively, female (C57/Bl6xCBAca) mice. Pairs of conscious mice were kept in an air-tight closed system allowing breathing of a mixture containing 18O(2). The 18O(2)-technique was validated by L-NAME (10mg/kg) and lipopolysaccharide (LPS, 8 mg/kg) administration. The concentrations of O(2) and CO(2) in the system were controlled and plasma nitrate analyzed by GC/MS technique. RESULTS: NO formation was similar in young and old mice (young=7.68+/-1.47 vs. old = 6.25+/-1.49 micromol/kg/h, n.s.). Total NO production was reduced after L-NAME treatment in young animals by 91% and in old animals by 71% (p<0.05 for both), whereas LPS administration increased NO production (114+/-17%, p<0.05).Conclusion. NO formation is unaltered with age in mice. The 18O(2)-technique is a valid and specific technique to estimate whole body NO production in conscious mice.     

Combining Nitrous Oxide with Carbon Dioxide Decreases the Time to Loss of Consciousness during Euthanasia in Mice — Refinement of Animal Welfare?

Carbon dioxide (CO(2)) is the most commonly used euthanasia agent for rodents despite potentially causing pain and distress. Nitrous oxide is used in man to speed induction of anaesthesia with volatile anaesthetics, via a mechanism referred to as the "second gas" effect. We therefore evaluated the addition of Nitrous Oxide (N(2)O) to a rising CO(2) concentration could be used as a welfare refinement of the euthanasia process in mice, by shortening the duration of conscious exposure to CO2. Firstly, to assess the effect of N(2)O on the induction of anaesthesia in mice, 12 female C57Bl/6 mice were anaesthetized in a crossover protocol with the following combinations: Isoflurane (5%)+O(2) (95%); Isoflurane (5%)+N(2)O (75%)+O(2) (25%) and N(2)O (75%)+O(2) (25%) with a total flow rate of 3 l/min (into a 7 l induction chamber). The addition of N(2)O to isoflurane reduced the time to loss of the righting reflex by 17.6%. Secondly, 18 C57Bl/6 and 18 CD1 mice were individually euthanized by gradually filling the induction chamber with either: CO(2) (20% of the chamber volume.min-1); CO(2)+N(2)O (20 and 60% of the chamber volume.min(-1) respectively); or CO(2)+Nitrogen (N(2)) (20 and 60% of the chamber volume.min-1). Arterial partial pressure (P(a)) of O(2) and CO(2) were measured as well as blood pH and lactate. When compared to the gradually rising CO(2) euthanasia, addition of a high concentration of N(2)O to CO(2) lowered the time to loss of righting reflex by 10.3% (P<0.001), lead to a lower P(a)O(2) (12.55 ± 3.67 mmHg, P<0.001), a higher lactataemia (4.64 ± 1.04 mmol.l(-1), P = 0.026), without any behaviour indicative of distress. Nitrous oxide reduces the time of conscious exposure to gradually rising CO(2) during euthanasia and hence may reduce the duration of any stress or distress to which mice are exposed during euthanasia.     

Metabolism of a liver-selective nitric oxide-releasing agent, V-PYRRO/NO, by human microsomal cytochromes P450

Endogenously generated nitric oxide (NO) mediates a host of important physiological functions, playing roles in the vascular, immunological, and neurological systems. As a result, exogenous agents that release NO have become important therapeutic interventions and research tools. O(2)-Vinyl 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO) is a prodrug designed with the hypothesis that it might release nitric oxide via epoxidation of the vinyl group by cytochrome P450, followed by enzymatic and/or spontaneous epoxide hydration to release the ultimate NO-donating moiety, 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (PYRRO/NO) ion. In this study, we investigated this hypothetical activation mechanism quantitatively for V-PYRRO/NO using cDNA-expressed human cytochrome P450 (CYP)2E1. Incubation with CYP2E1 and an NADPH-regenerating system resulted in a time-dependent decomposition of V-PYRRO/NO, with a turnover rate of 2.0 nmol/min/pmol CYP2E1. Nitrate and nitrite were detected in high yield as metabolites of NO. The predicted organic metabolites pyrrolidine and glycolaldehyde were also detected in near-quantitative yields. The enzymatic decomposition of V-PYRRO/NO was also catalyzed, albeit at lower rates, by CYP2A6 and CYP2B6. We conclude that the initial step in the metabolism of V-PYRRO/NO to NO in the liver is catalyzed efficiently but not exclusively by the alcohol-inducible form of cytochrome P450 (CYP2E1). The results confirm the proposed activation mechanism involving enzymatic oxidation of the vinyl group in V-PYRRO/NO followed by epoxide hydration and hydrolytic decomposition of the resulting PYRRO/NO ion to generate nitric oxide.     

Role of nitric oxide in hypoxic hypometabolism in rats.

Because it has been recently suggested that nitric oxide (NO) may mediate the effects of hypoxia on body temperature and ventilation, the present study was designed to assess more completely the effects of a neuronal NO synthase inhibitor (7-nitroindazole, 25 mg/kg ip), at ambient temperature of 26 and 15 degrees C, on the ventilatory (V), metabolic (O(2) consumption), and thermal changes (colonic and tail temperatures) induced by ambient hypoxia (fractional inspired O(2) of 11%) or CO hypoxia (fractional inspired CO of 0.07%) in intact, unanesthetized adult rats. At both ambient temperatures, 7-nitroindazole decreased oxygen consumption, colonic temperature, and V in normoxia. The drug reduced ambient or CO hypoxia-induced hypometabolism and ventilatory response, but the hypothermia persisted. It is concluded that NO arising from neural NO synthase plays an important role in the control of metabolism and V in normoxia. As well, it mediates, in part, the hypometabolic and the ventilatory response to hypoxia. The results are consistent with the notion that central nervous system hypoxia resets the thermoregulatory set point by decreasing brain NO.     

Synthesis, nitric oxide release, and anti-leukemic activity of glutathione-activated nitric oxide prodrugs: Structural analogues of PABA/NO, an anti-cancer lead compound

Diazeniumdiolate anions and their prodrug forms are reliable sources of nitric oxide (NO) that have generated interest as promising therapeutic agents. A number of structural analogues of O(2)-(2,4-dinitro-5-(4-(N-methylamino)benzoyloxy)phenyl) 1-(N,N-dimethylamino)diazen-1-ium-1,2-diolate (PABA/NO), an anti-cancer lead compound that is designed to release NO upon activation by glutathione, were prepared. The nitric oxide release patterns of these O(2)-(2,4-dinitrophenyl) diazeniumdiolates in the presence of glutathione were tested and it was found that in the absence of competing pathways, these compounds release nearly quantitative amounts of NO. The ability of PABA/NO and its structural analogues to inhibit human leukemia cell proliferation was determined and it was found that compounds releasing elevated amounts of NO displayed superior cytotoxic effects.     

Carbon monoxide protects against the development of experimental necrotizing enterocolitis

Necrotizing enterocolitis (NEC) is a disease of neonates that is increasing in incidence and often results in significant morbidity and mortality. Carbon monoxide (CO), a byproduct of the catabolism of heme, is known to have anti-inflammatory and antiapoptotic properties. In this study, we aimed to demonstrate that inhaled CO protects against the development of intestinal inflammation in a model of experimental NEC as well as decreases enterocyte cell death in vitro. Additionally, we also aimed to demonstrate that CO decreases enterocyte production of inducible nitric oxide synthase (iNOS) and nitric oxide (NO). Neonatal rats were exposed to intermittent hypoxia exposure and formula feeding to induce experimental NEC. Animals randomized to CO treatment were put in an environment containing 0.025% CO for 1 h/day on days 1-3 of life. All animals were killed on day 4 of life. In vitro experiments were performed with IEC-6 cells, a rat enterocyte cell line. Cells were examined for viability, iNOS production, and elaboration of NO. We found that CO diminished levels of serum inflammatory cytokines and nitrites, protected against intestinal inflammation, and decreased ileal iNOS production and protein nitration in a model of experimental NEC. In vitro, CO decreased cytokine- or hypoxia/endotoxin-induced iNOS and NO production. CO also abrogated TNF-alpha- and actinomycin D-induced apoptosis or hypoxia/endotoxin-induced cell death. In conclusion, 1 h of daily low-dose inhaled CO protected against the development of intestinal inflammation in a model of experimental NEC. iNOS and NO production were decreased by CO both in vivo and in vitro. CO may prove to be a useful clinical adjunct in the treatment of NEC.