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L-ascorbic acid potentiates endothelial nitric oxide synthesis via a chemical stabilization of tetrahydrobiopterin

JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第1期276卷 40-47页

作者： Heller, R Unbehaun, A Schellenberg, B Mayer, B Werner-Felmayer, G Werner, ER Univ Jena Ctr Vasc Biol & Med D-99089 Erfurt Germany Karl Franzens Univ Graz Inst Pharmacol & Toxicol A-8010 Graz Austria Univ Innsbruck Inst Med Chem & Biochem A-6020 Innsbruck Austria

Ascorbic acid has been shown to stimulate endothelial nitric oxide (NO) synthesis in a time- and concentration-dependent fashion without affecting NO synthase (NOS) expression or L-arginine uptake. The present study investigates if the underlying mechanism is related to the NOS cofactor tetrahydrobiopterin, Pretreatment of human umbilical vein endothelial cells with ascorbate (1 muM to 1 mM, 24 h) led to an up to 3-fold increase of intracellular tetrahydrobiopterin levels that was concentration-dependent and saturable at 100 mum. Accordingly, the effect of ascorbic acid on Ca2+-dependent formation of citrulline (co-product of NO) and cGMP (product of the NO-activated soluble guanylate cyclase) was abolished when intracellular tetrahydrobiopterin levels were increased by coincubation of endothelial cells with sepiapterin (0.001-100 muM, 24 h), In contrast, ascorbic acid did not modify the pterin affinity of endothelial NOS, which was measured in assays with purified tetrahydrobiopterin-free enzyme. The ascorbate-induced increase of endothelial tetrahydrobiopterin was not due to an enhanced synthesis of the compound. Neither the mRNA expression of the rate-limiting enzyme in tetrahydrobiopterin biosynthesis, GTP cyclohydrolase I, nor the activities of either GTP cyclohydrolase I or 6-pyruvoyl-tetrahydropterin synthase, the second enzyme in the de novo synthesis pathway, were altered by ascorbate, Our data demonstrate that ascorbic acid leads to a chemical stabilization of tetrahydrobiopterin, This was evident as an increase in the half-life of tetrahydrobiopterin in aqueous solution. Furthermore, the increase of tetrahydrobiopterin levels in intact endothelial cells coincubated with cytokines and ascorbate was associated with a decrease of more oxidized biopterin derivatives (7,8-dihydrobiopterin and biopterin) in cells and cell supernatants, The present study suggests that saturated ascorbic acid levels in endothelial cells are necessary to protect tetrahydrobiopteri

关键词：抗坏血酸/药理学生物蝶呤/类似物和衍生物生物蝶呤/代谢细胞培养的瓜氨酸/代谢环GMP/代谢内皮血管/药物作用内皮血管/酶学内皮血管/代谢酶激活/药物作用 GTP环化水解酶/拮抗剂和抑制剂 GTP环化水解酶/遗传学 GTP环化水解酶/代谢次黄嘌呤类/药理学一氧化氮/代谢一氧化氮合酶/代谢磷氧裂合酶类/代谢蝶啶类/药理学蝶呤类 RNA 信使/遗传学 RNA 信使/代谢溶液脐带人类

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A kinetic simulation model that describes catalysis and regulation in nitric-oxide synthase

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第2期276卷 1233-1243页

作者： Santolini, J Adak, S Curran, CML Stuehr, DJ Cleveland Clin Fdn Lerner Res Inst Dept Immunol Cleveland OH 44195 USA

After initiating NO synthesis a majority of neuronal NO synthase (nNOS) quickly partitions into a ferrous heme-NO complex. This down-regulates activity and increases enzyme K-m,K-O2. To understand this process, we developed a 10-step kinetic model in which the ferric heme-NO enzyme forms as the immediate product of catalysis, and then partitions between NO dissociation versus reduction to a ferrous heme-NO complex. Rate constants used for the model were derived from recent literature or were determined here. Computer simulations of the model precisely described both pre-steady and steady-state features of nNOS catalysis, including NADPH consumption and NO production, buildup of a heme-NO complex, changes between pre-steady and steady-state rates, and the change in enzyme K-m,K-O2 in the presence or absence of NO synthesis. The model also correctly simulated the catalytic features of nNOS mutants W409F and W409Y, which are hyperactive and display less heme-NO complex formation in the steady state. Model simulations showed how the rate of heme reduction influences several features of nNOS catalysis, including populations of NO-bound versus NO-free enzyme in the steady state and the rate of NO synthesis. The simulation predicts that there is an optimum rate of heme reduction that is close to the measured rate in nNOS, Ratio between NADPH consumption and NO synthesis is also predicted to increase with faster heme reduction. Our kinetic model is an accurate and versatile tool for understanding catalytic behavior and will provide new perspectives on NOS regulation.

关键词：氨基酸取代结合部位催化作用瓜氨酸/代谢克隆分子大肠杆菌血红素/代谢动力学模型化学模型理论诱变定点 NADP/代谢一氧化氮/代谢一氧化氮合酶/化学一氧化氮合酶/代谢一氧化氮合酶Ⅰ型重组蛋白质类/化学重组蛋白质类/代谢

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Characterization of the roles of the 594-645 region in human endothelial nitric-oxide synthase in regulating calmodulin binding and electron transfer

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第17期275卷 13155-13163页

作者： Chen, PF Wu, KK Univ Texas Hlth Sci Ctr Sch Med Dept Internal MedDiv Hematol Houston TX 77225 USA Univ Texas Hlth Sci Ctr Dept Internal Med Vasc Biol Res Ctr Houston TX 77225 USA

It has been postulated that a segment (residues 594-645) inserted in the FMN subdomain of human endothelial nitric oxide synthase (eNOS) plays a crucial role in controlling Ca2+-dependent CaM binding for eNOS activity. To investigate its functions, we expressed human eNOS in a baculovirus system with deletion of a 45-residue segment from this region (residues 594-606 and 614-645, designated as Delta 45eNOS), and characterized the purified mutant enzyme. In contrast with wild-type eNOS, Delta 45eNOS exhibited characteristics resembling inducible NOS (NOS). It contained an endogenously bound CaM, which was essential in folding and stabilizing this mutant enzyme, and retained 60% of L-citrulline formation in 5 mM EGTA. We also produced four N-terminally truncated reductase domains with or without the 45-residue segment, and either including or excluding the CaM-binding sequence. Basal cytochrome c reductase activity of reductase domains without the 45-residue segment was up to 20 fold greater than that of corresponding insert-containing domains, and higher than CaM-stimulated activity of the wild-type enzyme. A series of mutants with smaller fragment deletion in this region such as Delta 594-604, Delta 605-612, Delta 613-625, Delta 626-634, Delta 632-639, and Delta 640-645 mutants were further characterized. The crude lysate of mutants Delta 613-625 and Delta 632-639 did not show activity in the presence of Ca2+/CaM, while other four mutants had activity comparable to that of WTeNOS. The purified Delta 594-604 and Delta 605-612 proteins had a 3-5-fold higher affinity for Ca2+/CaM, but their L-citrulline forming activity was still 80% dependent upon the addition of Ca2+/CaM. Both mutants exhibited a low level of the cytochrome c and ferricyanide reductase activities, which either did not respond to (Delta 594-604) or slightly enhanced by (Delta 605-612) the exogenous CaM, In contrast, activities of Delta 626-634 and Delta 640-645 like those of WTeNOS were largely Ca2+/C

关键词：氨基酸序列钙/代谢钙调蛋白/化学钙调蛋白/代谢催化作用细胞系瓜氨酸/代谢剂量效应关系药物电子转运大肠杆菌/代谢同工酶类动力学分子序列数据诱变 NADH脱氢酶/代谢硝酸盐类/代谢一氧化氮合酶/化学一氧化氮合酶/遗传学一氧化氮合酶/代谢一氧化氮合酶Ⅲ型亚硝酸盐类/代谢蛋白质结合序列同源性氨基酸动物人类

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Kinetics of the arginine metabolism of malolactic wine lactic acid bacteria Lactobacillus buchneri CUC-3 and Oenococcus oeni Lo111

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JOURNAL OF APPLIED MICROBIOLOGY 2000年第3期89卷 547-552页

作者： Mira de Orduña, R Liu, SQ Patchett, ML Pilone, GJ Massey Univ Inst Mol Biosci Palmerston North New Zealand New Zealand Dairy Res Inst Palmerston North New Zealand

The excretion of citrulline, a precursor of carcinogenic ethyl carbamate, formed from arginine degradation by malolactic bacteria in wine is of toxicological concern. The arginine metabolism of resting cells of Lactobacillus buchneri CUC-3 and Oenococcus oeni Lo111 was examined. The citrulline excretion rate was found to be linearly correlated to the arginine degradation rate. It was possible to calculate an arginine to citrulline conversion ratio which could be used to predict the amount of citrulline expected after the degradation of a known quantity of arginine. The conversion ratios determined in this study were similar to data calculated from other authors for fermentations in wine and ranged between 4.0% and 7.7%. Ribose, fructose and glucose inhibited the degradation of arginine in Lact. buchneri CUC-3, and inhibition of arginine degradation by glucose correlated with higher arginine to citrulline conversion ratios. The work presents new results of arginine metabolism in malolactic bacteria and gives starting points for investigations in wine.

关键词：精氨酸瓜氨酸/代谢发酵果糖葡萄糖革兰氏阳性球菌/生长和发育革兰氏阳性球菌/代谢动力学明串珠菌属/生长和发育明串珠菌属/代谢核糖葡萄酒/微生物学

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Modulation of nitric-oxide synthase by nicotine

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期295卷 601-606页

作者： Tonnessen, BH Severson, SR Hurt, RD Miller, VM Mayo Clin & Mayo Fdn Dept Surg Rochester MN 55905 USA Mayo Clin & Mayo Fdn Dept Internal Med Rochester MN 55905 USA Mayo Clin & Mayo Fdn Nicotine Res Ctr Rochester MN 55905 USA Mayo Clin & Mayo Fdn Dept Physiol & Biophys Rochester MN 55905 USA

Effects of nicotine on arterial endothelium-dependent relaxations mediated by nitric oxide are controversial. Experiments were designed to test the hypothesis that nicotine can directly alter activity of endothelial nitric-oxide synthase (eNOS). NOS from aortic endothelial cells of untreated dogs and recombinant eNOS, neuronal NOS, and inducible NOS were used for these experiments. NOS activity was determined as conversion of L-[H-3] arginine to L-[H-3] citrulline in the absence or presence of nicotine (10(-7)-10(-3) M) in vitro. In separate assays, concentrations of cofactors NADPH, FAD, and tetrahydrobioprotein were reduced by half to assess for possible interaction with nicotine. With enzyme from aortic endothelial cells, total and calcium-dependent accumulation of citrulline increased by 30% in the presence of 10(-5) M nicotine. Nicotine dose dependently also increased citrulline accumulation by recombinant eNOS and neuronal NOS but not inducible NOS. Effects of nicotine on accumulation of citrulline by isolated eNOS and recombinant eNOS were further modulated by changes in the concentration of NADPH in the incubation solution. Our data demonstrate a significant effect of nicotine on eNOS-mediated citrulline accumulation. These results suggest that effects of nicotine on production of nitric oxide may depend on NADPH or oxygen radical interactions with NOS and thus may explain, in part, inconsistent findings of changes in production of endothelium-derived nitric oxide with nicotine administration.

关键词：主动脉胸/酶学精氨酸/代谢生物蝶呤/类似物和衍生物生物蝶呤/代谢生物蝶呤/药理学瓜氨酸/代谢内皮血管/酶学黄素腺嘌呤二核苷酸/代谢黄素腺嘌呤二核苷酸/药理学 NADP/代谢 NADP/药理学尼古丁/药理学一氧化氮合酶/分离和提纯一氧化氮合酶/代谢一氧化氮合酶Ⅰ型一氧化氮合酶Ⅱ型一氧化氮合酶Ⅲ型重组蛋白质类/代谢动物狗男(雄)性

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Unique gonococcal phenotype associated with asymptomatic infection in men and with erroneous diagnosis of nongonococcal urethritis

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JOURNAL OF INFECTIOUS DISEASES 2000年第3期181卷 1044-1048页

作者： Whittington, WLH Holmes, KK Harborview Med Ctr Div Infect Dis Seattle WA 98104 USA Univ Washington Sch Med Dept Med Seattle WA 98195 USA Univ Washington Sch Med Ctr AIDS & STD Seattle WA 98195 USA Publ Hlth Seattle & King Cty Seattle WA USA

The percentage of gonococcal isolates in King County, Washington, requiring citrulline and uracil (CU auxotype) increased from 1.6% in 1986 to 16.5% in 1997. Among men, urethral infection with the CU auxotype (n = 93), in comparison with infection by other auxotypes (n = 1211), was associated with coexisting chlamydial infection, younger age, heterosexual contact, and fewer new recent partners (P < .05). Among heterosexual men, urethral infection with the CU auxotype, compared with infection with other auxotypes, less often produced symptoms of urethral discharge (75% vs. 92%) or dysuria (47% vs. 74%) or signs of moderate or profuse urethral discharge (57% vs. 89%, P < .05 for each comparison), produced symptoms of longer duration (7.0 vs. 4.5 days, P < .01), less often resulted in urethral smears showing gram-negative intracellular diplococci (67% vs. 95%, P < .01), and thus more often was erroneously diagnosed as nongonococcal urethritis. Several mechanisms could explain reduced inflammatory response to the CU auxotype and its recent spread.

关键词：瓜氨酸/代谢误诊淋病/微生物学奈瑟球菌淋病/代谢表型尿嘧啶/代谢尿道炎/微生物学成年人人类男(雄)性

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The inhibitory potency and selectivity of arginine substrate site nitric-oxide synthase inhibitors is solely determined by their affinity toward the different isoenzymes

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MOLECULAR PHARMACOLOGY 2000年第5期58卷 1026-1034页

作者： Boer, R Ulrich, WR Klein, T Mirau, B Haas, S Baur, I Byk Gulden Lomberg GmbH D-78467 Constance Germany

We have investigated various nitric oxide (NO) synthase inhibitors for their affinity and selectivity toward the three human isoenzymes in radioligand binding experiments. Therefore, we developed the new radioligand [H-3]2-amino-4-picoline to measure binding of these compounds to the three human NO synthase (NOS) isoenzymes. Aminopicoline is a potent and nonselective inhibitor of all three isoforms. [H-3]2-amino-4-picoline bound saturably and with high affinity to human NOSs. Affinity constants (K-D values) of 59, 111, and 136 nM were obtained for the inducible, neuronal, and endothelial NOS isoforms (iNOS, nNOS, eNOS). Binding of [H-3]2-amino-4-picoline was competitive with the substrate arginine. From all the inhibitors tested, AMT (2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine hydrochloride) showed the highest affinity and no selectivity. L-NIL [L-N-6-(1-Iminoethyl) lysine hydrochloride] and aminoguanidine were moderately iNOS-selective while L-NA (N-G-nitro-L-arginine) and L-NAME (N-G-nitro-L-arginine methyl ester hydrochloride) showed selectivity toward the constitutive isoforms. High iNOS versus eNOS selectivity was found for 1400W, whereas several isothiourea derivatives and 1400W displayed moderate n- versus eNOS selectivity. To relate the affinity of these compounds to their inhibitory potency, we measured the inhibitory potency under almost identical conditions using a new microtiter plate assay. The inhibitory potency of selective and nonselective NOS inhibitors was almost exactly mirrored by their affinity toward the different isoenzymes. Highly significant correlations were obtained between the potency of enzyme inhibition and the inhibition of [H-3]2-amino-4-picoline binding for all three isoenzymes. These data show that the potency and selectivity of NOS inhibitors are solely determined by their affinity toward the different isoforms. Furthermore, these data identify the new radioligand [3H]2-amino-4-picoline as a very useful radiolabel for the investi

关键词：精氨酸/代谢瓜氨酸/代谢酶抑制剂/药理学同工酶类/拮抗剂和抑制剂同工酶类/代谢一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢甲基吡啶类/药理学放射配体测定底物特异性氚人类

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Interaction of endothelial and neuronal nitric-oxide synthases with the bradykinin B2 receptor: binding of an inhibitory peptide to the oxygenase domain blocks uncoupled NADPH oxidation. (vol 275, pg 5291, 2000)

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第21期275卷 16400-16400页

作者： Golser, R Gorren, ACF Leber, A Andrew, P Habisch, HJ Werner, ER Schmidt, K Venema, RC Mayer, B InstitutfürPharmakologieundToxikologie Karl-Franzens-UniversitätGrazUniversitätsplatz2A-8010GrazAustria.

Endothelial nitric-oxide synthase (type III) (eNOS) was reported to form an inhibitory complex with the bradykinin receptor B2 (B2R) from which the enzyme is released in an active form upon receptor activation (Ju, H., Venema, V. J., Marrero, M. B., and Venema, R. C. (1998) J. Biol. Chem. 273, 24025-24029). Using a synthetic peptide derived from the known inhibitory sequence of the B2R (residues 310-329) we studied the interaction of the receptor with purified eNOS and neuronal nitric-oxide synthase (type I) (nNOS). The peptide inhibited formation of L-citrulline by eNOS and nNOS with IC(50) values of 10.6 +/- 0.4 microM and 7.1 +/- 0.6 microM, respectively. Inhibition was not due to an interference of the peptide with L-arginine or tetrahydrobiopterin binding. The NADPH oxidase activity of nNOS measured in the absence of L-arginine was inhibited by the peptide with an IC(50) of 3.7 +/- 0.6 microM, but the cytochrome c reductase activity of the enzyme was much less susceptible to inhibition (IC(50) >0.1 mM). Steady-state absorbance spectra of nNOS recorded during uncoupled NADPH oxidation showed that the heme remained oxidized in the presence of the synthetic peptide consisting of amino acids 310-329 of the B2R, whereas the reduced oxyferrous heme complex was accumulated in its absence. These data suggest that binding of the B2R 310-329 peptide blocks flavin to heme electron transfer. Co-immunoprecipitation of B2R and nNOS from human embryonic kidney cells stably transfected with human nNOS suggests that the B2R may functionally interact with nNOS in vivo. This interaction of nNOS with the B2R may recruit the enzyme to allow for the effective coupling of bradykinin signaling to the nitric oxide pathway.

关键词：结合部位印迹法蛋白质细胞系瓜氨酸/代谢剂量效应关系药物内皮血管/酶学动力学神经元/酶学一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢肽类/代谢沉淀素试验蛋白质结合受体缓激肽B2 受体缓激肽/代谢重组蛋白质类/代谢时间因素动物人类大鼠

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Na⁺/Ca²⁺ exchange facilitates Ca²⁺-dependent activation of endothelial nitric-oxide synthase

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第41期274卷 29529-29535页

作者： Teubl, M Groschner, K Kohlwein, SD Mayer, B Schmidt, K Karl Franzens Univ Graz Inst Pharmakol & Toxikol A-8010 Graz Austria Graz Univ Technol Inst Biochem & Lebensmittelchem A-8010 Graz Austria

Recent evidence suggests the expression of a Na+/ Ca2+ exchanger (NCX) in vascular endothelial cells, To elucidate the functional role of endothelial NCX, we studied Ca2+ signaling and Ca2+-dependent activation of endothelial nitric-oxide synthase (eNOS) at normal, physiological Na+ gradients and after loading of endothelial cells with Na+ ions using the ionophore monensin. Monensin-induced Na+ loading markedly reduced Ca2+ entry and, thus, steady-state levels of intracellular free Ca2+ ([Ca2+](i)) in thapsigargin-stimulated endothelial cells due to membrane depolarization. Despite this reduction of overall [Ca2+](i), Ca2+-dependent activation of eNOS was facilitated as indicated by a pronounced leftward shift of the Ca2+ concentration response curve in monensin-treated cells. This facilitation of Ca2+-dependent activation of eNOS was strictly dependent on the presence of Na+ ions during treatment of the cells with monensin, Na+-induced facilitation of eNOS activation was not due to a direct effect of Na+ ions on the Ca2+ sensitivity of the enzyme. Moreover, the effect of Na+ was not related to Na+ entry-induced membrane depolarization or suppression of Ca2+ entry, since neither elevation of extracellular K+ nor the Ca2+ entry blocker 1-(beta-[3-(4-methoxyphenyl)-propoxy]-4-methoxyphenethyl)-1H-imidazole hydrochloride (SK&F 96365) mimicked the effects of Na+ loading. The effects of monensin were completely blocked by 3',4'-dichlorobenzamil, a potent and selective inhibitor of NCX, whereas the structural analog amiloride, which barely affects Na+/Ca2+ exchange, was ineffective. Consistent with a pivotal role of Na+/Ca2+ exchange in Ca2+-dependent activation of eNOS, an NCX protein was detected in caveolin-rich membrane fractions containing both eNOS and caveolin-1. These results demonstrate for the first time a crucial role of cellular Na+ gradients in regulation of eNOS activity and suggest that a tight functional interaction between endothelial NCX and eNOS may tak

关键词：阿米洛利/药理学缓激肽/药理学钙/药理学钙通道阻滞药/药理学窖蛋白1 细胞质膜微囊蛋白细胞培养的瓜氨酸/代谢内皮血管酶激活/药物作用荧光抗体技术 Fura-2/化学咪唑类/药理学膜蛋白质类/代谢莫能星/药理学一氧化氮合酶/代谢钠/药理学钠钙交换蛋白/代谢猪动物

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L-ascorbic acid potentiates nitric oxide synthesis in endothelial cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第12期274卷 8254-8260页

作者： Heller, R Münscher-Paulig, F Gräbner, R Till, U Univ Jena Ctr Vasc Biol & Med D-99089 Erfurt Germany

Ascorbic acid has been shown to enhance impaired endothelium-dependent vasodilation in patients with atherosclerosis by a mechanism that is thought to involve protection of nitric oxide (NO) from inactivation by free oxygen radicals. The present study in human endothelial cells from umbilical veins and coronary arteries investigates whether L-ascorbic acid additionally affects cellular NO synthesis. Endothelial cells were incubated for 24 h with 0.1-100 mu M ascorbic acid and were subsequently stimulated for 15 min with ionomycin (2 mu M) Or thrombin (1 unit/ml) in the absence of extracellular ascorbate. Ascorbate pretreatment led to a 3-fold increase of the cellular production of NO measured as the formation of its co-product citrulline and as the accumulation of its effector molecule cGMP. The effect was saturated at 100 mu M and followed a similar kinetics as seen for the uptake of ascorbate into the cells. The investigation of the precursor molecule L-gulonolactone and of different ascorbic acid derivatives suggests that the enediol structure of ascorbate is essential for its effect on NO synthesis. Ascorbic acid did not induce the expression of the NO synthase (NOS) protein nor enhance the uptake of the NOS substrate L-arginine into endothelial cells. The ascorbic acid effect was minimal when the citrulline formation was measured in cell lysates from ascorbate-pretreated cells in the presence of known cofactors for NOS activity. However, when the cofactor tetrahydrobiopterin was omitted from the assay, a similar potentiating effect of ascorbate pretreatment as seen in intact cells was demonstrated, suggesting that ascorbic acid may either enhance the availability of tetrahydrobiopterin or increase its affinity for the endothelial NOS. Our data suggest that intracellular ascorbic acid enhances NO synthesis in endothelial cells and that this may explain, in part, the beneficial vascular effects of ascorbic acid.

关键词：抗氧化剂/药理学抗坏血酸/药理学生物蝶呤/类似物和衍生物生物蝶呤/药理学钙/代谢细胞培养的瓜氨酸/代谢环GMP/代谢药物协同作用内皮血管/药物作用内皮血管/代谢酶诱导/药物作用自由基一氧化氮/生物合成一氧化氮合酶/生物合成一氧化氮合酶Ⅲ型人类

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