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1.
We examined, by using a specific PGE receptor subtype EP4 agonist and antagonist, the involvement of EP4 receptors in duodenal HCO(3)(-) secretion induced by PGE(2) and mucosal acidification in rats. Mucosal acidification was achieved by exposing a duodenal loop to 10 mM HCl for 10 min, and various EP agonists were given intravenously 10 min before the acidification. Secretion of HCO(3)(-) was dose-dependently stimulated by AE1-329 (EP4 agonist), the maximal response being equivalent to that induced by sulprostone (EP1/EP3 agonist) or PGE(2). The stimulatory action of AE1-329 and PGE(2) but not sulprostone was attenuated by AE3-208, a specific EP4 antagonist. This antagonist also significantly mitigated the acid-induced HCO(3)(-) secretion. Coadministration of sulprostone and AE1-329 caused a greater secretory response than either agent alone. IBMX potentiated the stimulatory action of both sulprostone and AE1-329, whereas verapamil mitigated the effect of sulprostone but not AE1-329. Chemical ablation of capsaicin-sensitive afferent neurons did not affect the response to any of the EP agonists used. We conclude that EP4 receptors are involved in the duodenal HCO(3)(-) response induced by PGE(2) or acidification in addition to EP3 receptors. The process by which HCO(3)(-) is secreted through these receptors differs regarding second-messenger coupling. Stimulation through EP4 receptors is mediated by cAMP, whereas that through EP3 receptors is regulated by both cAMP and Ca(2+); yet there is cooperation between the actions mediated by these two receptors. The neuronal reflex pathway is not involved in stimulatory actions of these prostanoids. 相似文献
2.
The effect of Cl −, HCO 3−, Br −, acetazolamide, thiocyanate and amiloride on urine formation in Locusta migratoria Malpighian tubules have been determined. The rate of fluid secretion depends markedly on the concentration of Cl − in the bathing solution with concentrations less than 90 mM resulting in reduced fluid secretion. Substitution of Br − for Cl − had no significant effect on the rate of the fluid secretion. Replacement of NaHCO 3 with NaCl in Hepes buffered Ringer solution reduced the rate of urine production by 23%. Fluid secretions were reduced in the presence of 10 −4–10 −2 M acetazolamide, a carbonic anhydrase inhibitor. The combined effect of acetazolamide in the absence of HCO 3− appears to be additive. A 1 mM concentration of thiocyanate, an ionic inhibitor, reduced fluid secretion by 35%. Amiloride interferes with the electrogenic entry of Na + into the cell and a 1 mM solution reduced fluid secretion by 94% with secretion completely inhibited in 80% of the tubules tested. 相似文献
3.
Radioactive labelling techniques show that isolated broken chloroplasts can take up HCO 3− in the dark. There are two pools of binding sites for this ion on, or within, the thylakoid membranes. A smaller, high affinity pool exists at a concentration of one HCO 3− bound per 380–400 chlorophyll molecules. Removal of HCO 3− bound in this pool requires special conditions and results in greater than 90% inhibition of oxygen evolution. The inhibition is fully reversed when HCO 3− is added back. HCO 3− bound in the small pool does not necessarily exchange with free HCO 3− in the dark or in light. Evidence presented suggests that this site is very near the site of action of 3-(3,4-dichlorophenyl)-1,1-dimethyl urea. A second, much larger, pool of HCO 3− binding sites also exists in a concentration approaching that of the bulk chlorophyll. These sites have a much lower affinity for HCO 3−, and their function has not yet been determined. 相似文献
4.
We investigated the cyclooxygenase (COX) isoforms as well as prostaglandin E receptor EP subtypes responsible for acid-induced gastric HCO(3)(-) secretion in rats and EP receptor-knockout (-/-) mice. Under urethane anesthesia, a chambered stomach (in the presence of omeprazole) was perfused with saline, and HCO(3)(-) secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Mucosal acidification was achieved by exposing the stomach for 10 min to 50 or 100 mM HCl. Acidification of the mucosa increased the secretion of HCO(3)(-) in the stomach of both rats and WT mice, in an indomethacin-inhibitable manner. The acid-induced gastric HCO(3)(-) secretion was inhibited by prior administration of indomethacin and SC-560 but not rofecoxib in rats and mice. Acidification increased the PGE(2) content of the rat stomach, and this response was significantly attenuated by indomethacin and SC-560 but not rofecoxib. This response was also attenuated by ONO-8711 (EP1 antagonist) but not AE3-208 (EP4 antagonist) in rats and disappeared in EP1 (-/-) but not EP3 (-/-) mice. PGE(2) increased gastric HCO(3)(-) secretion in both rats and WT mice, and this action was inhibited by ONO-8711 and disappeared in EP1 (-/-) but not EP3 (-/-) mice. These results support a mediator role for endogenous PGs in the gastric response induced by mucosal acidification and clearly indicate that the enzyme responsible for production of PGs in this process is COX-1. They further show that the presence of EP1 receptors is essential for the increase in the secretion of HCO(3)(-) in response to mucosal acidification in the stomach. 相似文献
5.
Hydrogen peroxide, produced by inflammatory and vascular cells, induces oxidative stress that may contribute to endothelial dysfunction. In smooth muscle cells, H 2O 2 induces production of O 2− by activating NADPH oxidase. However, the mechanisms whereby H 2O 2 induces oxidative stress in endothelial cells are poorly understood. We examined the effects of H 2O 2 on O 2− levels on porcine aortic endothelial cells (PAEC). Treatment with 60 μmol/L H 2O 2 markedly increased intracellular O 2− levels (determined by conversion of dihydroethidium to hydroxyethidium) and produced cytotoxicity (determined by propidium iodide staining) in PAEC. Overexpression of human manganese superoxide dismutase in PAEC reduced O 2− levels and attenuated cytotoxicity resulting from treatment with H 2O 2. L-NAME, an inhibitor of nitric oxide synthase (NOS), and apocynin, an inhibitor of NADPH oxidase, reduced O 2− levels in PAEC treated with H 2O 2, suggesting that both NOS and NADPH oxidase contribute to H 2O 2-induced O 2− in PAEC. Inhibition of NADPH oxidase using apocynin and NOS rescue with L-sepiapterin together reduced O 2− levels in PAEC treated with H 2O 2 to control levels. This suggests interaction-distinct NOS and NADPH oxidase pathways to superoxide. We conclude that H 2O 2 produces oxidative stress in endothelial cells by increasing intracellular O 2− levels through NOS and NADPH oxidase. These findings suggest a complex interaction between H 2O 2 and oxidant-generating enzymes that may contribute to endothelial dysfunction. 相似文献
6.
The amine/ammonium materials were prepared by cross-linking of starch (S) with epichlorohydrin (E→SE) in the presence of ammonia (A→SEA) or choline (C→SEC–HO −) or with 1,3-bis-(3-chloro-2-hydroxypropyl)imidazolium hydrogensulphate (BCHIHS→SHI–HO −) and transfered into the acid/salt forms with HCl (SEA–HCl, SEC–Cl −, or SHI–Cl −), H 2SO 4 (SEA–H 2SO 4, SEC–HSO 4−, or SHI–HSO 4−), and H 3PO 4 (SEA–H 3PO 4, SEC–H 2PO 4−, or SHI–H 2PO 4−) and analyzed with thermogravimetry (TG) under dynamic and isothermal conditions in nitrogen or oxygen environment. According to the values of thermooxidation maxima (TM) calculated from the maximal difference of measured residues on the dynamic TG curves run in nitrogen and oxygen environments the order of decreasing thermooxidation resistance is: S>SEA–H 3PO 4>SHI–H 2PO 4−>SHI–HSO 4−>SEA–H 2SO 4>SEC–HSO 4−>SEC–HO −>SEA–HCl>HCl–Cl −> SEC–Cl −>SHI–HO −>SEA>SEC–H 2PO 4−>SE. The first-order rate constants calculated by the linear regression method (regression coefficient R>0.95) represented the initial rate constants for residue formation ( kr's) and gasification ( kg's). All the derivatives had greater values of rate constants than S and the kg's were about 1000 times greater than kr's. The values obtained in nitrogen were smaller than those calculated from runs in oxygen environment with the exception of S. Most of the salt forms had greater values of kg's in oxygen environment. The activation energies ( E's) were usually greater in nitrogen than in oxygen as well as for residue formation than for gasification. The SHI–HO − sample had high kg's and low Eg's in oxygen environment while for SHI–H 2SO 4− the opposite was true. This we consider as two extremes for labile and resistant samples for gasification. 相似文献
7.
A procedure is described for preparing particles from cells of Micrococcus denitrificans which were broken osmotically after treatment with lysozyme. 1. 1. The preparations catalysed ATP synthesis coupled to O2 uptake or NO3− reduction. With NADH or succinate as the electron donors the P:O ratios were about 1.5 and 0.5, respectively; and the P:NO3− ratios were about 0.9 and 0.06, respectively. 2. 2. Addition of ADP or Pi to the reaction mixture increased the rates of NADH-dependent O2 uptake and NO3− reduction. Addition of 1 mM 2,4-dinitrophenol, which inhibited phosphorylation by 50–60%, increased the basal rates of electron transport. 3. 3. Evidence derived from spectrophotometry and from the differential inhibition by antimycin A of O2 and NO3− reduction leads to the conclusion that the nitrate reductase interacted with the respiratory chain in the region of the b-type cytochrome, and that the c-type cytochrome present was not involved in the reduction of NO3− to NO2−.
Abbreviations: TMPD; tetramethyl-p-phenylenediamine 相似文献
8.
Previously, we showed that oxidation of tryptophan-32 (Trp-32) residue was crucial for H 2O 2/bicarbonate (HCO 3−)-dependent covalent aggregation of human Cu,Zn SOD1 (hSOD1). The carbonate anion radical (CO 3−)-induced oxidation of Trp-32 to kynurenine-type oxidation products was proposed to cause the aggregation of hSOD1. Here we used the matrix-assisted laser desorption ionization–time of flight mass spectroscopy, high-performance liquid chromatography–electrospray ionization mass spectroscopy, and liquid chromatography mass spectroscopy methods to characterize products. Results show that a peptide region (31–36) of hSOD1 containing the Trp-32 residue (VWGSIK) is oxidatively modified to the N-formylkynurenine (NFK)- and kynurenine (Kyn)-containing peptides (V(NFK)GSIK) and (V(Kyn)GSIK) during HCO −-dependent peroxidase activity of hSOD1. Also, UV photolysis of a cobalt complex that generates authentic CO 3− radical induced a similar product profile from hSOD1. Similar products were obtained using a synthetic peptide with the same amino acid sequence ( i.e., VWGSIK). We propose a mechanism involving a tryptophanyl radical for CO 3−-induced oxidation of Trp-32 residue (VWGSIK) in hSOD1 to V(NFK)GSIK and V(Kyn)GSIK. 相似文献
9.
The survival of Leishmania, which encounter drastic changes of environment during their life-cycle, requires regulation and control of ionic concentrations within the cell. We analysed the influence of growth stage, ionic composition of the medium, heat and acidic stress on 86Rb + influx in L. infantum promastigetes. Proliferating promastigotes exibited faster and higher 86Rb + uptake than stationary cells. Cl − anion did not have any effect, but in the presence of physiological concentration of HCO 3−, 86Rb + uptake was significantly increased. This enhancing effect was only partially inhibited by N,N′-dicyclohexylcarbodiimide (DCCD), a blocker of ion-translocating ATPases. 86Rb + influx was abolished by N-ethylmaleimide (NEM), indicating a major contribution of plasma membrane transporters. Heat shock and acidic shock notably decreased 86Rb + influx. Our data provide indirect evidence that an energy-dependent system which brings K + in, such as K +/H +-ATPase evidenced by Jiang et al. (1994), is active in Leishmania in different environments. Mechanism(s) other than ion-translocating ATPase occur, at least in the presence of HCO 3−, and their contribution to K + pathways varies in different environmental conditions. 相似文献
10.
We examined the role of prostaglandin E (EP) receptor subtypes in the regulation of gastric acid secretion in the rat. Under urethane anesthesia, the stomach was superfused with saline, and the acid secretion was determined at pH 7.0 by adding 50 mM NaOH. The acid secretion was stimulated by intravenous infusion of histamine or pentagastrin. Various EP agonists were administered intravenously, whereas EP antagonists were given subcutaneously 30 min or intravenously 10 min before EP agonists. PGE(2) suppressed the acid secretion stimulated by either histamine or pentagastrin in a dose-dependent manner. The acid inhibitory effect of PGE(2) was mimicked by sulprostone (EP(1)/EP(3) agonist) but not butaprost (EP(2) agonist) or AE1-329 (EP(4) agonist). The inhibitory effect of sulprostone, which was not affected by ONO-8711 (EP(1) antagonist), was more potent against pentagastrin- (50% inhibition dose: 3.6 mug/kg) than histamine-stimulated acid secretion (50% inhibition dose: 18.0 mug/kg). Pentagastrin increased the luminal release of histamine, and this response was also inhibited by sulprostone. On the other hand, AE1-329 (EP(4) agonist) stimulated the acid secretion in vagotomized animals with a significant increase in luminal histamine. This effect of AE1-329 was totally abolished by cimetidine as well as AE3-208 (EP(4) antagonist). These results suggest that PGE(2) has a dual effect on acid secretion: inhibition mediated by EP(3) receptors and stimulation through EP(4) receptors. The former effect may be brought about by suppression at both parietal and enterochromaffin-like cells, whereas the latter effect may be mediated by histamine released from enterochromaffin-like cells. 相似文献
11.
The perchlorate (ClO 4−)-respiring organism, strain perc1ace, can grow using nitrate (NO 3−) as a terminal electron acceptor. In resting cell suspensions, NO 3− grown cells reduced ClO 4−, and ClO 4− grown cells reduced NO 3−. Activity assays showed that nitrate reductase (NR) activity was 1.31 μmol min −1 (mg protein) −1 in ClO 4− grown cells, and perchlorate reductase (PR) activity was 4.24 μmol min −1 (mg protein) −1 in NO 3− grown cells. PR activity was detected within the periplasmic space, with activities as high as 14 μmol min −1 (mg protein) −1. The NR had a pH optimum of 9.0 while the PR had an optimum of 8.0. This study suggests that separate terminal reductases are present in strain perclace to reduce NO 3− and ClO 4−. 相似文献
12.
The bioconversion of propionitrile to propionamide was catalysed by nitrile hydratase (NHase) using resting cells of Microbacterium imperiale CBS 498-74 (formerly, Brevibacterium imperiale). This microorganism, cultivated in a shake flask, at 28 °C, presented a specific NHase activity of 34.4 U mg DCW−1 (dry cell weight). The kinetic parameters, Km and Vmax, tested in 50 mM sodium phosphate buffer, pH 7.0, in the propionitrile bioconversion was evaluated in batch reactor at 10 °C and resulted 21.6 mM and 11.04 μmol min −1 mg DCW−1, respectively. The measured apparent activation energy, 25.54 kJ mol −1, indicated a partial control by mass transport, more likely through the cell wall. UF-membrane reactors were used for kinetic characterisation of the NHase catalysed reaction. The time dependence of enzyme deactivation on reaction temperature (from 5 to 25 °C), on substrate concentrations (from 100 to 800 mM), and on resting cell loading (from 1.5 to 200 μg
ml−1) indicated: lower diffusional control (Ea=37.73 kJ mol−1); and NHase irreversible damage caused by high substrate concentration. Finally, it is noteworthy that in an integral reactor continuously operating for 30 h, at 10 °C, 100% conversion of propionitrile (200 mM) was attained using 200 μg
ml−1 of resting cells, with a maximum volumetric productivity of 0.5 g l−1 h−1. 相似文献
13.
Arterial pH, PCO 2 (P aCO 2), plasma bicarbonate [HCO 3− and respiratory frequency were measured in pigeons exposed to ambient temperatures ( TaS) of 30–60°C. Acclimated, nonpanting birds regulated acid-base balance at normal levels, when exposed to Tas) between 30 and 53°C Ta. At higher Tas (55–60°C), both nonpanting and panting acclimated pigeons regulated pH at normal levels, 7.544 ± 0.011 (SD) and 7.531 ± 0.022 (SD), respectively, accompanied by a slight hypocapnia, 24.8 ± 4.0 Torr and 23.8 ± 2.49 Torr (P aCO 2), respectively. Nonacclimated birds, exposed to 50°C Ta, endured a severe hypocapnia (P aCO 2 of 9.1 ± 2.52 Torr) and alkalosis (pH of 7.702 ± 0.048). Thirteen exposures to > 50°C T a, 4–6 h a day, resulted in a significant improvement in the capacity of the panting pigeon to maintain an almost normal acid-base balance, i.e. actual and standard [HCO 3− of 22.6 ± 1.22 and 25.7 ± 1.10 mM/l, respectively, and only a slight hypocapnia (P aCO 2 of 23.6 ± 3.9 Torr) and alkalosis (pH of 7.589). The suggestion that acclimation to high Tas (50–60°C) is needed for fine adjustment between the competing needs for heat dissipation, pulmonary gas exchange, and acid-base regulation in the heat-exposed pigeon is discussed. 相似文献
14.
We have previously shown that crystals of calcium oxalate (COM) elicit a superoxide (O 2−) response from mitochondria. We have now investigated: (i) if other microparticles can elicit the same response, (ii) if processing of crystals is involved, and (iii) at what level of mitochondrial function oxalate acts. O 2− was measured in digitonin-permeabilized MDCK cells by lucigenin (10 μM) chemiluminescence. [ 14C]-COM dissociation was examined with or without EDTA and employing alternative chelators. Whereas mitochondrial O 2− in COM-treated cells was three- to fourfold enhanced compared to controls, other particulates (uric acid, zymosan, and latex beads) either did not increase O 2− or were much less effective (hydroxyapatite +50%, p < 0.01), with all at 28 μg/cm 2. Free oxalate (750 μM), at the level released from COM with EDTA (1 mM), increased O 2− (+50%, p < 0.01). Omitting EDTA abrogated this signal, which was restored completely by EGTA and partially by ascorbate, but not by desferrioxamine or citrate. Omission of phosphate abrogated O 2−, implicating phosphate-dependent mitochondrial dicarboxylate transport. COM caused a time-related increase in the mitochondrial membrane potential (Δψ m) measured using TMRM fluorescence and confocal microscopy. Application of COM to Fura 2-loaded cells induced rapid, large-amplitude cytosolic Ca 2+ transients, which were inhibited by thapsigargin, indicating that COM induces release of Ca 2+ from internal stores. Thus, COM-induced mitochondrial O 2− requires the release of free oxalate and contributes to a synergistic response. Intracellular dissociation of COM and the mitochondrial dicarboxylate transporter are important in O 2− production, which is probably regulated by Δψ m. 相似文献
15.
Both two-dimensional phase diagrams and mean molecular area ( A)—mole fraction(x 2π) curves have been investigated for various types of mixed monolayer systems. Two-dimensional phase diagram analysis and the behavior of A− x2π curves were found to be in good agreement with each other. From this result it was concluded that we should consider both phase diagrams and A− x2π curves of a mixed monolayer system in order to understand the behavior of the A− x2π curves. 相似文献
16.
Bacterial β-ketoacyl-ACP reductase (FabG) and the β-ketoacyl reductase domain in mammalian fatty acid synthase (FAS) have the same function and both are rendered as the novel targets for drugs. Herein we developed a convenient method, using an available compound ethyl acetoacetate (EAA) as the substitutive substrate, to measure their activities by monitoring decrease of NADPH absorbance at 340 nm. In addition to the result, ethyl 3-hydroxybutyrate (EHB) was detected by HPLC analysis in the reaction system, indicating that EAA worked effectively as the substrate of FabG and FAS since its β-keto group was reduced. Then, the detailed kinetic characteristics, such as optimal ionic strength, pH value and temperature, and kinetic parameters, for FabG and FAS with this substitutive substrate were determined. The Km and kcat values of FabG obtained for EAA were 127 mM and 0.30 s − 1, while those of this enzyme for NADPH were 10.0 μM and 0.59 s − 1, respectively. The corresponding Km and kcat values of FAS were 126 mM and 4.63 s − 1 for EAA; 8.7 μM and 4.09 s − 1 for NADPH. Additionally, the inhibitory kinetics of FabG and FAS, by a known inhibitor EGCG, was also studied. 相似文献
17.
A novel nutrient removal/waste heat utilization process was simulated using semicontinuous cultures of the thermophilic cyanobacterium Fischerella. Dissolved inorganic carbon (DIC)-enriched cultures, maintained with 10 mg l −1 daily productivity, diurnally varying temperature (from 55°C to 26–28°C), a 12:12 light cycle (200 μE sec −1 m −2) and 50% biomass recycling into heated effluent at the beginning of each light period, removed > 95% of NO 3− + NO 2−−N, 71% of NH 3-N, 82% of PO 43− −P, and 70% of total P from effluent water samples containing approximately 400 μg l −1 combined N and 60 μg l −1 P. Nutrient removal was not severely impaired by an altered temperature gradient, doubled light intensity, or DIC limitation. Recycling 75% of the biomass at the end of each light period resulted in unimpaired NO 3− + NO 2− removal, 38–45% P removal and no net NH 3 removal. Diurnally varying P removal, averaging 50–60%, and nearly constant > 80% N removal, are therefore projected for a full-scale process with continuous biomass recycling. 相似文献
18.
Resonance Raman measurements have been performed with solutions of iodine-complexed synthetic amyloses ( DP 25–200), malto-oligomers ( DP 3–18, and -cylodextrin. Interest was focused on the minimum chain length for helical complex formation and a possible preferred length for the polyiodine chain. Four fundamental vibrations are observed at 164, 112, 52 and 24 cm −1. The 112 cm −1 Raman line was shown to arise both from free I 3− (enhanced at 363.8 nm excitation) and from bound iodine (relatively most intense at 457.9 nm excitation). The main signal of complexed iodine at 164 cm −1is enhanced at an excitation wavelength close to the long wavelength absorption maximum. This signal is observed firt with malto-octaose and -cyclodextrin. The less intense signals at 52 and 24 −1 are only detected at DP 15 and higher. Raman spectra give no evidence for a preferred length of the polyiodine chain. Significantly identical Raman spectra are obtained when using different molar ratios of I 2/KI solution or I 2 solution initially free of I − ions. The results are discussed in view of previous assignments of the Raman lines to I 2−, I 3−/I 2, and I 5− subunits. Our findings are incompatible with I 3− units as the only bound species. They are compatible with both I 3−/I 2 and I 3− subunits under certain conditions. In the case of I 2 solution used for complexation we favour the polyiodine chain model proposed previously by Cramer 35,36. The I 3− ions formed could function mainly as chain initiators, as has been suggested by Cesàro and Brant 30. 相似文献
19.
Both prostaglandins (PGs) and nitric oxide (NO) have cytoprotective and hyperemic effects in the stomach. However, the effect of NO on PG synthesis in gastric mucosal cells is unclear. We examined whether sodium nitroprusside (SNP), a releaser of NO, stimulates PG synthesis in cultured rabbit gastric mucus-producing cells. These cells did not release NO themselves. Co-incubation with SNP (2 × 10 −4, 5 × 10 −4, 10 −3 M) increased PGE 2 synthesis, and SNP (10 −3 M) increased PGI 2 synthesis in these cells. Hemoglobin, a scavenger of NO, (10 −5 M) eliminated the increase in PGE 2 synthesis by SNP, but methylene blue, an inhibitor of soluble guanylate cyclase, (5 × 10 −5 M) did not affect the increase in PGE 2 synthesis by SNP. 8-bromo guanosine 3′ : 5′-cyclic monophosphate (8-bromo cGMP), a cGMP analogue, (10 −6, 10 −5, 10 −4, 10 −3 M) did not affect PGE 2 synthesis. These findings suggest that NO increased PGE 2 and PGI 2 synthesis via a cGMP-independent pathway in cultured rabbit gastric cells. 相似文献
20.
Laboratory-scale experiments were conducted to examine the N 2O emission during the denitrification process. For each of the 6 runs carried out, synthetic effluent was fed in a 10 l batch mixed liquor to investigate the effect of nitrite on N 2O emission and Helium was continuously bubbled through the reactor at constant rate (0.12 l/min) to favour N 2O transfer and detection. An increasing COD/NO 3−-N influent ratio from 3 to 7 was firstly applied (runs 1–3). Secondly, NO 2− pulse additions were performed during run 4 and 5 (10 and 20 mg N/l, respectively). Finally, the reactor was fed with influent containing both NO 2− and NO 3−. We showed that N 2O emission was detected shortly after NO 2− accumulation, few minutes after the substrate feeding. The highest emission occurred at the lower COD/NO 3−-N ratio (=3) and at the higher NO 2− addition (20 mg N/l). In addition, the higher nitrogen conversion to N 2O gas (14.4%) was obtained with an influent containing initially both NO 2− and NO 3−. Our results suggest a direct effect of the NO 2− concentration on the N 2O emission. We have also confirmed the inhibitory effect of NO 2− concentration on N 2O reduction. 相似文献
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