硝酸根胁迫对黄瓜幼苗叶片光合速率、PSⅡ光化学效率及光能分配的影响

研究了不同浓度NO₃^-胁迫对黄瓜幼苗叶片光合速率、PSⅡ光化学效率及光能分配的影响.结果表明,当NO₃^-浓度较低时（14～98 mmol·L^-1）,适当增加NO₃^-浓度,可增强黄瓜幼苗叶片对光的捕获能力,促进光合作用.随着NO₃^-浓度的进一步增加（140～182 mmol·L^-1）,PSⅡ光化学效率降低,电子传递受到抑制,净光合速率降低;吸收的光能中,通过天线色素的热耗散增加,用于光化学反应的能量降低,光化学效率下降.140和182 mmol·L^-1 NO₃^-处理黄瓜幼苗叶片6 d后净光合速率(P_n)极显著下降,分别比对照降低了35%和78%;PSⅡ最大光化学效率(F_v/F_m)、天线转化效率(F_v’/F_m’)、实际光化学效率(Φ_PSⅡ)、光化学猝灭系数(q_P)均低于对照,非光化学猝灭(NPQ)高于对照,激发能在两个光系统间的分配不平衡性(β/α-1)增大.高浓度NO₃^-处理的黄瓜幼苗叶片各荧光参数变化幅度比低浓度大.当光照增强时,高浓度NO₃^-胁迫下黄瓜幼苗叶片吸收的光能中应用于光化学反应的份额(P) 显著降低,天线热耗散的份额(D)显著增加. 天线热耗散是耗散过剩能量的主要途径.     

上海地区大气氮湿沉降及其对湿地水环境的影响

根据1998～2003年上海地区雨水中NO₃^--N、NH₄⁺-N浓度,采用单因子评估模式评价了降雨对湿地水环境的影响,并结合降雨量数据,研究了大气湿沉降氮通量.结果表明,上海地区雨水中氮浓度较高,6年雨水平均硝态氮浓度为259 mg·L^-1,铵态氮浓度为2.16 mg·L^-1,总无机氮（TIN）浓度474 mg·L^-1,远大于水体富营养水中氮浓度阀值（0.2 mg·L^-1）,依据降水中的氮浓度,降水已达到地表水V类、劣V类水平.6年湿沉降氮通量平均值为58.1 kg·hm^-2·yr^-1,其中NO₃^--N占54%.大气氮沉降对湿地水体富营养化影响值得关注.     

苯噻草胺抑制旱地杂草DNA复制的研究

证实了苯噻草胺通过嵌入旱地植物DNA双螺旋中,使DNA变性而抑制DNA复制的旱地除草新机理。杂草不同,BTMPA的药效浓度不同,用苯噻草胺杀除早熟禾时,药效浓度为3.0×10-5mol/L~6.0×10-5mol/L,最宜施药期为芽期至三叶期,最宜施药温度为15℃~30℃,旱地双子叶作物黄豆对苯噻草胺有解毒作用。     

氮磷营养因子对赤潮异弯藻生长的影响

研究了N、P营养浓度对赤潮异弯藻(Heterosigma akashiwo)生长的影响.结果表明,该藻的生长速率与N、P营养因子浓度的关系符合Monod公式.在NO₃^--N浓度达到7.5 mg·L^-1时,赤潮异弯藻开始生长;浓度为3.75～75 mg·L^-1时,赤潮异弯藻的比生长速率与NO₃^--N浓度成正比关系.N营养充足时,赤潮异弯藻的最大生长速率μ_m-n=0.3475·d^-1,K_s-n=18.91 mg·L^-1.PO₄^--P浓度为0～1.0 mg·L^-1时,赤潮异弯藻的比生长速率与P浓度成正比关系;P营养充足时,赤潮异弯藻的最大生长速率μ_m-p=0.3024·d^-1,K_s-p=0.4086 mg·L^-1.N/P达到25后藻细胞浓度达到最大,表明N/P为25时最适合赤潮异弯藻生长.赤潮异弯藻最适合在N 37.5～225.0 mg·L^-1、P 5.0～50.0 mg·L^-1、N/P=25条件下生长.     

蚯蚓和秸秆对铜污染土壤微生物类群和活性的影响

试验设置4个Cu浓度水平：0、100、200和400 mg·kg^-1 Cu²⁺,每个Cu浓度水平设置4个处理：对照(CK)、表施秸秆(M)、接种蚯蚓(E)、同时加入蚯蚓和秸秆(ME),研究了在Cu污染土壤中加入蚯蚓和秸秆对土壤微生物数量及活性的影响.结果表明：Cu污染、秸秆和蚯蚓均明显影响土壤微生物类群; Cu污染对细菌、放线菌具有抑制作用,而对真菌没有影响;秸秆显著提高了真菌数量;蚯蚓使土壤细菌、放线菌数量显著增加,而对真菌数量影响不大.Cu污染浓度＞200 mg·kg^-1处理对微生物量碳具有抑制作用;加入秸秆或蚯蚓,可显著提高土壤微生物量碳,而且同时加蚯蚓和秸秆处理土壤微生物量碳增加最显著.加入蚯蚓和秸秆后,土壤呼吸值显著增高.Cu<200 mg·kg^-1时,蚯蚓处理土壤呼吸值最大,平均比对照高3.06～5.58倍;Cu≥200mg·kg^-1时,蚯蚓、秸秆同时加入处理土壤呼吸值最高.4个处理土壤代谢商大小顺序为：ME>E>M>CK.蚯蚓和秸秆处理对土壤NH₄⁺-N没有影响,而对土壤NO₃^--N影响各异.接种蚯蚓,可显著提高土壤NO₃^--N含量;加入秸秆,可显著降低土壤NO₃^--N含量;同时加入蚯蚓和秸秆处理NO₃^--N含量最低.相关分析表明,土壤有效态Cu(DTPA-Cu)与土壤放线菌、细菌呈显著负相关,而与土壤呼吸、土壤NO₃^--N、NH₄⁺-N含量呈显著正相关.引入秸秆和蚯蚓,可在一定程度上减缓Cu污染对微生物数量和活性的影响.     

不同渗漏计对稻田氮素渗漏量的测定差异

采用直管型和弯管型渗漏计,对不同施氮水平下水稻生育期间渗漏水中的铵态氮、硝态氮和全氮浓度进行测定分析.结果表明：2007年直管与弯管渗漏计中渗漏水的铵态氮浓度变化范围均在0～8 mg·L^-1,高于2006年0～4 mg·L^-1的铵态氮浓度变化范围;2007年直管渗漏计中渗漏水的硝态氮浓度主要集中在0～4 mg·L^-1,与2006年基本一致,而弯管渗漏计中渗漏水的硝态氮浓度变化较大,其变动范围主要集中在0～20 mg·L^-1,高于2006年的硝态氮浓度;2007年渗漏水中的全氮浓度变化范围为0～60 mg·L^-1,远高于2006年0～16 mg·L^-1的全氮浓度变化范围.稻田渗漏水中的氮素以硝态氮为主.2007年直管型渗漏计中总氮(TN)渗漏流失负荷为15.81 kg·hm^-2,NO₃^--N为9.33 kg·hm^-2,弯管型渗漏计中TN渗漏流失负荷为7.21 kg·hm^-2,NO₃^--N为4.25 kg·hm^-2.稻田渗漏水中铵态氮和硝态氮的渗漏流失途径不同,应当采用不同的计算方法估算直管型及弯管型渗漏计中的氮素渗漏量,采用直管型渗漏计对氮素渗漏量的估算较接近于用测坑试验测定的氮素渗漏负荷.     

丁草胺在不同类型水中的光化学降解

研究了除草剂丁草胺在氙灯、高压汞灯光照下的光解动态。结果表明,丁草胺在氙灯光照作用下,其光解速率为纯水>河水>塘水>稻田水;丁草胺在氙灯光源下的光解速度比高压汞灯下低;其光解率与浓度(剂量)呈反相关;充N₂脱O₂使丁草胺的光解速度减缓。     

苯噻草胺与水稻DNA和稗草DNA作用的谱学研究

提出了苯噻草胺用于水田除草的新除草机理 ,BTMPA在DNA和RNA分子表面堆积 ,抑制DNA复制 ,阻止RNA参与植物体内的蛋白质合成 ,造成稗草等杂草细胞不能分裂 ,从而杀除杂草。发现水稻DNA对BTMPA有解毒作用。用苯噻草胺除草时 ,在植物体内的有效浓度为 1 7× 10 - 5mol L - 5 1× 10 - 5mol L ,最宜施药期为芽期至三叶期 ,最宜施药温度为 2 0℃ - 2 5℃。     

苯噻草胺与玉米DNA和狗尾草DNA作用的研究

提出了苯噻草胺用于旱地除草的新除草机理,BTMPA嵌入旱地植物DNA双螺旋中,使DNA变性而抑制DNA复制,造成狗尾草等杂草细胞不能分裂,从而杀除杂草。用苯噻草胺旱地除草时,在植物体内的有效浓度为5.4×10-8mol/L-5.4×10-5mol/L,最宜施药期为芽期至三叶期,最宜施药温度为20℃-30℃。     

森林和沼泽对溪流水化学特征的影响

以小兴安岭北部公别拉河上游为研究区,于2004年7～9月对森林溪流和沼泽溪流水样进行水化学特征对比分析.结果表明,森林和沼泽溪流水化学类型均为重碳酸盐类钙组Ⅰ型水(C^Ca_Ⅰ).森林溪流水的pH、矿化度、总硬度、HCO₃^-、SO₄^2-、Ca²⁺、Mg²⁺、Fe均低于沼泽溪流,而总氮、总磷、Cl^-、K⁺、Na⁺则高于沼泽溪流.森林溪流和沼泽溪流中重金属元素Fe、Mn、Cu、Zn、Cd、Hg和Pb含量较低,均未超过我国Ⅰ类地表水环境质量标准.森林溪流中总氮含量为（0.27±0.04） mg·L^-1、总磷含量为（0.040±0.005） mg·L^-1,明显高于沼泽溪流中总氮含量(（0.21±0.02） mg·L^-1)和总磷含量(（0.025±0.004） mg·L^-1),沼泽湿地对N、P有较强的储存和吸附能力,且对NH₄⁺-N的吸附作用远大于对NO₃^--N的吸附.沼泽溪流中Fe含量为（0.26±0.05） mg·L^-1,显著高于森林溪流Fe含量,沼泽湿地对Fe起到还原释放作用.     

Induction of iNOS restricts functional activity of both eNOS and nNOS in pig cerebral artery

The aim of the study was to investigate the effect of iNOS expression on eNOS and nNOS functional activity in porcine cerebral arteries. iNOS was induced in pig basilar arteries using lipopolysaccharide (LPS). Arteries expressing iNOS generated NO and relaxed when challenged with L-arginine (30 microM), an effect that was reduced by treatment with dexamethasone (coincubated with LPS) and prevented by the iNOS inhibitor 1400 W (administered 10 min prior to precontraction). eNOS was activated by A23187 and was found to be impaired in arteries that had iNOS induced (A23187 1 microM relaxation: control 110+/-8%, LPS-treated 50+/-16% ; p<0.05, N=5-6). This was due mainly to reduced formation of NO by A23187 (NO concentration in response to A23187 1 microM: control 25+/-6 nM, LPS-treated 0.8+/-1.2 nM; p<0.001, N=5-6), in addition to a small reduction in the vasodilator response to the NO-donors NOC-22 and SIN-1. Cerebral vasodilation produced by stimulation of intramural nitrergic nerves was impaired in arteries that had iNOS induced, and this was reversed by 1400 W (control 23+/-4% relaxation, LPS-treated 11+/-1% relaxation, LPS plus 1400 W 10 microM treated 25+/-2% relaxation; p<0.01 for control versus LPS, N=6). It is concluded that the induction of iNOS in cerebral arteries reduces NO-mediated vasodilation initiated by eNOS and by nNOS, primarily by modulation of NO formation.     

硝酸盐供应对玉米侧根生长的影响

以两个玉米(Zea mays L.)自交系478和Wu312为研究材料,采用琼脂培养方法,研究不同浓度NO-3对侧根生长的影响.结果表明,在外部浓度0.01～1.0mmol/L范围内,NO-3供应能显著增加侧根的长度及根生物量.但当NO-3供应超过1.0 mmo1/L后,侧根长度开始下降.当NO-3供应分别在超过5.0(Wu312)与10(478)mmol/L后,侧根密度显著下降.在10 mmol/LNO-3下,Wu312的侧根生长几乎完全被抑制.而478在20 mmol/L时,侧根密度仍可达到其最大值的30%(主根)～50%(胚根).植株地上部全氮及硝酸盐含量随NO-3供应的增加而升高,二者与侧根长度、侧根密度及冠根比的数学函数关系相同.     

Induction of filopodia by direct local elevation of intracellular calcium ion concentration.

In neuronal growth cones, cycles of filopodial protrusion and retraction are important in growth cone translocation and steering. Alteration in intracellular calcium ion concentration has been shown by several indirect methods to be critically involved in the regulation of filopodial activity. Here, we investigate whether direct elevation of [Ca2+]i, which is restricted in time and space and is isolated from earlier steps in intracellular signaling pathways, can initiate filopodial protrusion. We raised [Ca2+]i level transiently in small areas of nascent axons near growth cones in situ by localized photolysis of caged Ca2+ compounds. After photolysis, [Ca2+]i increased from approximately 60 nM to approximately 1 microM within the illuminated zone, and then returned to resting level in approximately 10-15 s. New filopodia arose in this area within 1-5 min, and persisted for approximately 15 min. Elevation of calcium concentration within a single filopodium induced new branch filopodia. In neurons coinjected with rhodamine-phalloidin, F-actin was observed in dynamic cortical patches along nascent axons; after photolysis, new filopodia often emerged from these patches. These results indicate that local transient [Ca2+]i elevation is sufficient to induce new filopodia from nascent axons or from existing filopodia.     

Regulation of photosynthesis in isolated spinach chloroplasts during orthophosphate limitation

The stromal concentration of orthophosphate in intact spinach chloroplasts (prepared in the absence of orthophosphate or pyrophosphate but supplied with both in the reaction medium) fell from a value of approx. 20 mM in the dark to a steady-state concentration of approx. 8 mM in the light. Chloroplasts illuminated in the absence of orthophosphate or pyrophosphate showed a similar trend. However, in this situation the stromal inorganic phosphate (P_i) concentration rapidly decreased from approx. 10 mM in the dark to a constant steady-state concentration of between 1.5 and 2.5 mM in the light. This P_i concentration was not further diminished (even though CO₂-dependent O₂ evolution had ceased) and was therefore considered to be stromal orthophosphate not freely available to metabolism. In the P_i-deficient chloroplasts the rate of photosynthesis declined rapidly after 1–2 min in the light such that CO₂-dependent O₂ evolution ceased with 5 min of the onset of illumination. The decline in O₂ evolution was accompanied by an increase in the transthylakoid ΔpH (as measured by 9-aminoacridine fluorescence quenching) and in the high-energy state, non-photochemical component of chlorophyll fluorescence quenching (q_E). Measurements of stromal metabolite concentrations showed that the ATP/ADP ratio was decreased in the P_i-deficient chloroplasts relative to chloroplasts illuminated in the presence of P_i. The stromal concentration of glycerate 3-phosphate was comparable in the P_i-deficient chloroplasts and those to which P_i had been supplied. Chloroplasts which were illuminated in P_i-free media showed a large accumulation of ribulose-1,5-bisphosphate relative to those supplied with P_i, suggesting inhibition of ribulose-1,5-bisphosphate carboxylase under these conditions. When P_i was added to chloroplasts illuminated in the absence of P_i, both non-photochemical quenching (q_E), photochemical quenching (q_Q) and ΔpH increased. This suggests that electron transport was not limited by inability to discharge transthylakoid ΔpH. These observation are consistent with the hypothesis that P_i limitation results in decreased ATP production by the thylakoid ATP synthase. The data presented here show that there are multiple sites of flux control exerted by low stromal P_i in the chloroplast. At least three factors contribute to the inhibition of photosynthesis under phosphate limitation: (1) there appears to be a direct effect of P_i on the energy-transducing system; (2) there is direct inhibition of the Calvin cycle decreasing the ability of the pathway to act as a sink for ATP and NADPH; and (3) feedback inhibition of primary processes occurs either via ΔpH or the redox state of electron carriers. However, ΔpH does not appear to be a limiting factor, but rather an inability to regenerate NADP as electron acceptor is suggested. The addition of DCMU to chloroplasts during illumination in the absence of P_i for periods of up to 10 min showed that there was very little loss of variable fluorescence despite a 60% reduction in the capacity for O₂ evolution. This would suggest that photoinhibitory damage to Photosystem II was not the major cause of the inhibition of photosynthesis observed with low P_i.     

NO介质在大鼠红藻氨酸诱导癫痫发作中的作用

目的：进一步探讨脑内一氧化氮(NO)介质(NO或NO衍生物)在复杂部分性及全身强直阵挛性癫痫发作中的作用。方法：采用红藻氨酸(KA)诱导大鼠癫痫发作,以NO合酶抑制剂L-硝基精氨酸(L-NNA)或NO前体L-精氨酸(L-Arg)予以预处理,观察其癫痫发作行为及海马结构内NO含量(NO2^-/NO3^-)的变化。结果：给予大鼠惊厥剂量KA(10mg/kg),15min时出现湿狗样抖动(WDS),1～3h出现全身痉挛;经L-NNA(50mg/kg)或L-Arg(40mg/kg)预处理的大鼠,注射相同剂量的KA后,其癫痫行为发生明显变化,L-NNA预处理的大鼠癫痫发作行为明显加重,表现为全身痉挛的潜伏期缩短、时间延长、死亡率提高;L-Arg预处理的大鼠癫痫发作行为减弱,WDS和全身痉挛的潜伏期均延长,发作程度减轻、时间缩短,观察时间内无一例死亡。KA给药后30min海马结构内的NO2^-/NO3^-含量迅速增多,7d时仍持续增高;与NS预处理组相比,经L-Arg预处理的动物,KA给药后3h及3d,其NO2^-/NO3^-浓度升高明显。结论：兴奋诱导性癫痫发作过程中内源性NO介质的变化可能具有重要的抗发作作用。     

Nitrite is an alternative source of NO in vivo

In this study, we investigated whether orally administered nitrite is changed to NO and whether nitrite attenuates hypertension in a dose-dependent manner. We utilized a stable isotope of [15N]nitrite (15NO2-) as a source of nitrite to distinguish between endogenous nitrite and that exogenously administered and measured hemoglobin (Hb)-NO as an index of circulating NO in whole blood using electron paramagnetic resonance (EPR) spectroscopy. When 1 mg/kg Na15NO2 was orally administered to rats, an apparent EPR signal derived from Hb15NO (A(Z) = 23.4 gauss) appeared in the blood. The peak blood HbNO concentration occurred at the first measurement after intake (5 min) for treatment with 1 and 3 mg/kg (HbNO: 4.93 +/- 0.52 and 10.58 +/- 0.40 microM, respectively) and at 15 min with 10 mg/kg (HbNO: 38.27 +/- 9.23 microM). In addition, coadministration of nitrite (100 mg/l drinking water) with N(omega)-nitro-L-arginine methyl ester (L-NAME; 1 g/l) for 3 wk significantly attenuated the L-NAME-induced hypertension (149 +/- 10 mmHg) compared with L-NAME alone (170 +/- 13 mmHg). Furthermore, this phenomenon was associated with an increase in circulating HbNO. Our findings clearly indicate that orally ingested nitrite can be an alternative to L-arginine as a source of NO in vivo and may explain, at least in part, the mechanism of the nitrite/nitrate-rich Dietary Approaches to Stop Hypertension diet-induced hypotensive effects.     

Exercise training and muscle microvascular oxygenation: functional role of nitric oxide

Exercise training induces multiple adaptations within skeletal muscle that may improve local O(2) delivery-utilization matching (i.e., Po(2)mv). We tested the hypothesis that increased nitric oxide (NO) function is intrinsic to improved muscle Po(2)mv kinetics from rest to contractions after exercise training. Healthy young Sprague-Dawley rats were assigned to sedentary (n = 18) or progressive treadmill exercise training (n = 10; 5 days/wk, 6-8 wk, final workload of 60 min/day at 35 m/min, -14% grade) groups. Po(2)mv was measured via phosphorescence quenching in the spinotrapezius muscle at rest and during 1-Hz twitch contractions under control (Krebs-Henseleit solution), sodium nitroprusside (SNP, NO donor; 300 μM), and N(G)-nitro-l-arginine methyl ester (l-NAME, nonspecific NO synthase blockade; 1.5 mM) superfusion conditions. Exercise-trained rats had greater peak oxygen uptake (Vo(2peak)) than their sedentary counterparts (81 ± 1 vs. 72 ± 2 ml·kg(-1)·min(-1), respectively; P < 0.05). Exercise-trained rats had significantly slower Po(2)mv fall throughout contractions (τ(1); time constant for the first component) during control (sedentary: 8.1 ± 0.6; trained: 15.2 ± 2.8 s). Compared with control, SNP slowed τ(1) to a greater extent in sedentary rats (sedentary: 38.7 ± 5.6; trained: 26.8 ± 4.1 s; P > 0.05) whereas l-NAME abolished the differences in τ(1) between sedentary and trained rats (sedentary: 12.0 ± 1.7; trained: 11.2 ± 1.4 s; P < 0.05). Our results indicate that endurance exercise training leads to greater muscle microvascular oxygenation across the metabolic transient following the onset of contractions (i.e., slower Po(2)mv kinetics) partly via increased NO-mediated function, which likely constitutes an important mechanism for training-induced metabolic adaptations.     

Renal ischemia induces an increase in nitric oxide levels from tissue stores

Tissue nitric oxide (NO) levels increase dramatically during ischemia, an effect that has been shown to be partially independent from NO synthases. Because NO is stored in tissues as S-nitrosothiols and because these compounds could release NO during ischemia, we evaluated the effects of buthionine sulfoximine (BSO; an intracellular glutathione depletor), light stimulation (which releases NO, decomposing S-nitrosothiols), and N-acetyl-L-cysteine (a sulfhydryl group donor that repletes S-nitrosothiols stores) on the changes in outer medullary NO concentration produced during 45 min of renal artery occlusion in anesthetized rats. Renal ischemia increased renal tissue NO concentration (+223%), and this effect was maintained along 45 min of renal arterial blockade. After reperfusion, NO concentration fell below preischemic values and remained stable for the remainder of the experiment. Pretreatment with 10 mg/kg nitro-L-arginine methyl ester (L-NAME) decreased significantly basal NO concentration before ischemia, but it did not modify the rise in NO levels observed during ischemia. In rats pretreated with 4 mmol/kg BSO and L-NAME, ischemia was followed by a transient increase in renal NO concentration that fell to preischemic values 20 min before reperfusion. A similar response was observed when the kidney was illuminated 40 min before the ischemia. The coadministration of 10 mg/kg iv N-acetyl-L-cysteine with BSO + L-NAME restored the increase in NO levels observed during renal ischemia and prevented the depletion of renal thiol groups. These results demonstrate that the increase in renal NO concentration observed during ischemia originates from thiol-dependent tissue stores.     

Diffusion of nitric oxide into low density lipoprotein.

A key early event in the development of atherosclerosis is the oxidation of low density lipoprotein (LDL) via different mechanisms including free radical reactions with both protein and lipid components. Nitric oxide (( small middle dot)NO) is capable of inhibiting LDL oxidation by scavenging radical species involved in oxidative chain propagation reactions. Herein, the diffusion of ( small middle dot)NO into LDL is studied by fluorescence quenching of pyrene derivatives. Selected probes 1-(pyrenyl)methyltrimethylammonium (PMTMA) and 1-(pyrenyl)-methyl-3-(9-octadecenoyloxy)-22,23-bisnor-5-cholenate (PMChO) were chosen so that they could be incorporated at different depths of the LDL particle. Indeed, PMTMA and PMChO were located in the surface and core of LDL, respectively, as indicated by changes in fluorescence spectra, fluorescence quenching studies with water-soluble quenchers and the lifetime values (tau(o)) of the excited probes. The apparent second order rate quenching constants of ( small middle dot)NO (k(NO)) for both probes were 2.6-3.8 x 10(10) m(-1) s(-1) and 1.2 x 10(10) m(-1) s(-1) in solution and native LDL, respectively, indicating that there is no significant barrier to the diffusion of ( small middle dot)NO to the surface and core of LDL. Nitric oxide was also capable of diffusing through oxidized LDL. Considering the preferential partitioning of ( small middle dot)NO in apolar milieu (6-8 for n-octanol:water) and therefore a larger ( small middle dot)NO concentration in LDL with respect to the aqueous phase, a corrected k(NO) value of approximately 0.2 x 10(10) m(-1) s(-1) can be determined, which still is sufficiently large and consistent with a facile diffusion of ( small middle dot)NO through LDL. Applying the Einstein-Smoluchowsky treatment, the apparent diffusion coefficient (D(')NO) of ( small middle dot)NO in native LDL is on average 2 x 10(-5) cm(2) s(-1), six times larger than that previously reported for erythrocyte plasma membrane. Thus, our observations support that ( small middle dot)NO readily traverses the LDL surface accessing the hydrophobic lipid core of the particle and affirm a role for ( small middle dot)NO as a major lipophilic antioxidant in LDL.     

Improvement of protoplast regeneration by growing yeast cells hypertonically

N2O was produced during the reduction of NO2- by resting cells of Lactobacillus lactis TS4. At an initial NO2- concentration of 69 micrograms/ml, the rate of N2O production was 1.97 nmol/min per mg of protein, and the recovery of reduced NO2- -N as N2O-N after 24 h was 77%. Higher initial NO2- concentrations decreased both the rate of production of N2O and the recovery of reduced NO2- -N. CO2 production increased during NO2- reduction.