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1.
Nitrogen dioxide (NO 2•) is a key biological oxidant. It can be derived from peroxynitrite via the interaction of nitric oxide with superoxide, from nitrite with peroxidases, or from autoxidation of nitric oxide. In this study, submicromolar concentrations of NO 2• were generated in < 1 μs using pulse radiolysis, and the kinetics of scavenging NO 2• by glutathione, cysteine, or uric acid were monitored by spectrophotometry. The formation of the urate radical was observed directly, while the production of the oxidizing radical obtained on reaction of NO 2• with the thiols (the thiyl radical) was monitored via oxidation of 2,2′-azino-bis-(3-ethylthiazoline-6-sulfonic acid). At pH 7.4, rate constants for reaction of NO 2• with glutathione, cysteine, and urate were estimated as 2 × 10 7, 5 × 10 7, and 2 × 10 7 M −1 s −1, respectively. The variation of these rate constants with pH indicated that thiolate reacted much faster than undissociated thiol. The dissociation of urate also accelerated reaction with NO 2• at pH > 8. The thiyl radical from GSH reacted with urate with a rate constant of 3 × 10 7 M −1 s −1. The implications of these values are: (i) the lifetime of NO 2• in cytosol is < 10 μs; (ii) thiols are the dominant ‘sink’ for NO 2• in cells/tissue, whereas urate is also a major scavenger in plasma; (iii) the diffusion distance of NO 2• is 0.2 μm in the cytoplasm and < 0.8 μm in plasma; (iv) urate protects GSH against depletion on oxidative challenge from NO 2•; and (v) reactions between NO 2• and thiols/urate severely limit the likelihood of reaction of NO 2• with NO• to form N 2O 3 in the cytoplasm. 相似文献
2.
It has been proposed that the C-phenyl- N-tert-butylnitrone/trichloromethyl radical adduct (PBN/ •CCl 3) is metabolized to either the C-phenyl- N-tert-butylnitrone/carbon dioxide anion radical adduct (PBN/ •CO 2−) or the glutathione (GSH) and CCl 4-dependent PBN radical adduct (PBN/[GSH- •CCl 3]). Inclusion of PBN/ •CCl 3 in microsomal incubations containing GSH, nicotinamide adenine dinucleotide phosphate (NADPH), or GSH plus NADPH produced no electron spin resonance (ESR) spectral data indicative of the formation of either the PBN/[GSH- •CCl 3] or PBN/ •CO 2− radical adducts. Microsomes alone or with GSH had no effect on the PBN/ •CCl 3 radical adduct. Addition of NADPH to a microsomal system containing PBN/ •CCl 3 presumably reduced the radical adduct to its ESR-silent hydroxylamine because no ESR signal was observed. The Folch extract of this system produced an ESR spectrum that was a composite of two radicals, one of which had hyperfine coupling constants identical to those of PBN/ •CCl 3. We conclude that PBN/ •CCl 3 is not metabolized into either PBN/[GSH- •CCl 3] or PBN/ •CO 2− in microsomal systems. 相似文献
3.
The oxidation of melatonin (MEL) using the Cu(II) + H 2O 2 + HO − (the Fenton-like reaction) system was investigated by chemiluminescence (CL), fluorescence, spectrophotometric, and EPR spin trapping techniques. The reaction exhibits CL in the 400–730 nm region. The light emission from the Fenton-like reaction was greatly enhanced in the presence of MEL and was strongly dependent on its concentration. The spectrum measured with cut-off filters revealed maxima at around 460, 500, 580–590, 640–650, and 690–700 nm. The band at 460 nm may be due to the excited cleavage product, N 1-acetyl-N 2-formyl-5-methoxykynuramine, whereas the bands at 500, 580–590, 640–650, and 700 nm were similar to those observed for singlet molecular oxygen ( 1O 2). The effect of reactive oxygen species (ROS) scavengers on the light emission was studied. The CL was strongly inhibited by the 1O 2 scavengers in a dose-dependent manner; at concentration 1 mM the potency of 1O 2 scavenging was 5,5-dimethylcyclohexandione-1,3 > methionine > histidine > hydroquinone. The potency of HO • scavenging by thiourea, tryptophan, cysteine at concentration 5 mM was 79–94%, by 1 mM glutathione and trolox 75 and 94%, respectively, and by 10 mM cimetidine 18%. Specific acceptors of O 2•− such as p-nitroblue tetrazolium chloride and 4,5-dihydroxy-1,3-benzene disulfonic acid (tiron) at concentration 5 mM decreased the CL by 51 and 95%, respectively, whereas superoxide dismutase (SOD) does not reduce the emission at concentration 2.8 U/ml. At higher concentration SOD substantially enhanced the light emission. Addition of 1360 U/ml catalase and 100 μM desferrioxamine strongly inhibited CL (96 and 90%, respectively). The increased generation of 1O 2 from the Cu/H 2O 2 system in the presence of MEL was confirmed using the spectrophotometric method based on the bleaching of p-nitrosodimethylaniline and by trapping experiments with 2,2,6,6-tetramethylpiperidine (TEMP) and subsequent electron paramagnetic (EPR) spectroscopy. These findings suggest the increased production of reactive oxygen species (O 2•−, HO •, 1O 2) from the Fenton-like reaction in the presence of MEL. This means that the hormone is not able to act as classical chain-breaking antioxidant even at low concentration, and may show clear prooxidant activity at higher concentrations. In addition, long-lived carbonyl product of the MEL transformation in the triplet state can also be toxic by transferring its energy to organelles and causing a photochemical process. 相似文献
5.
In the present study, using the technique of EPR spin trapping with DMPO a spin trap, we demonstrated formation of thiyl radicals from thiol-containing angiotensin converting enzyme (ACE) inhibitor captopril (CAP) and from its stereoisomer epicaptopril (EPICAP), a non-ACE inhibitor, in the process of .OH radical scavenging. Splitting constants of DMPO/thiyl radical adducts were identical for both thiols and were a N = 15.3 G, and a H = 16.2 G. Bimolecular rate constants for the reaction of CAP and EPICAP with .OH radicals were close to a diffusion-controlled rate (≈ 2 × 10 10 M −1s −1). Our data also show that both CAP and EPICAP reduce Fe(III) ions and that their respective thiyl radicals are formed in this reaction. In the presence of Fe(III), H 2O 2, and CAP, or EPICAP, .OH radicals were produced by a thiol-driven Fenton mechanism. Copper(II) ions were also reduced by these thiols, but no thiyl radicals could be detected in these reactions, and no .OH or other Fenton oxidants were observed in the presence of H 2O 2. Our data show direct evidence that thiol groups of CAP and EPICAP are involved in scavenging of .OH radicals. The direct .OH radical scavenging, together with the reductive “repair” of other sites of .OH radical attack, may contribute to the known protective effect of CAP against ischemia/reperfusion-induced arrhythmias. The formation of reactive thiyl radicals in the reactions of the studied compounds with .OH radicals and with Fe(III) ions may play a role in some of the known adverse effects of CAP. 相似文献
6.
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
7.
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
8.
5-Aminolevulinic acid (ALA), a heme precursor that accumulates in acute intermittent porphyria (AIP) and lead poisoning, undergoes enolization and subsequent iron-catalyzed oxidation at neutral pH. Iron is released from horse spleen ferritin (HoSF) by both ALA-generated O 2•− and enoyl radical (ALA√), which amplifies the chain of ALA oxidation (autocatalysis). Iron chelators such as EDTA, ATP, but not citrate, and phosphate accelerate this process and ALA-promoted iron release from HoSF is faster in horse spleen isoferritins containing larger amounts of phosphate in the core. ALA (+0.377 V versus standard hydrogen electrode) is less effective in releasing iron from ferritin than are thioglycollic acid, 6-hydroxydopamine, and N,N,N′,N′-tetramethyl- p-phenylenediamine. During electrochemical one electron oxidation of ALA in a nitrogen atmosphere, spin trapping experiments with 3,5-dibromo-4-nitrosobenzenesulfonic acid demonstrated the formation of a spin adduct characterized by a six line signal, indicating a secondary carbon-centered radical and attributed to a resonant ALA√ radical. Iron is also released in such anaerobic electrochemical oxidations of ALA in the presence of ferritin, suggesting that, in addition to O 2•−, ALA√ can promote iron mobilization from ferritin. Hence, ALA√ may amplify the metal-catalyzed oxidation of ALA, damaging ALA-accumulating cells and possibly contributing to the symptoms of porphyria. 相似文献
9.
Crystals of calcium oxalate monohydrate (COM) in the renal tubule form the basis of most kidney stones. Tubular dysfunction resulting from COM-cell interactions occurs by mechanism(s) that are incompletely understood. We examined the production of reactive oxygen intermediates (ROI) by proximal (LLC-PK1) and distal (MDCK) tubular epithelial cells after treatment with COM (25–250 μg/ml) to determine whether ROI, specifically superoxide (O 2•−), production was activated, and whether it was sufficient to induce oxidative stress. Employing inhibitors of cytosolic and mitochondrial systems, the source of ROI production was investigated. In addition, intracellular glutathione (total and oxidized), energy status (ATP), and NADH were measured. COM treatment for 1–24 h increased O 2•− production 3–6-fold as measured by both lucigenin chemiluminescence in permeabilized cells and dihydrorhodamine fluorescence in intact cells. Using selective inhibitors we found no evidence of cytosolic production. The use of mitochondrial probes, substrates, and inhibitors indicated that increased O 2•− production originated from mitochondria. Treatment with COM decreased glutathione (total and redox state), indicating a sustained oxidative insult. An increase in NADH in COM-treated cells suggested this cofactor could be responsible for elevating O 2•− generation. In conclusion, COM increased mitochondrial O 2•− production by epithelial cells, with a subsequent depletion of antioxidant status. These changes may contribute to the reported cellular transformations during the development of renal calculi. 相似文献
10.
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
11.
Rates of stepwise anation of cis-Cr(ox) 2(H 2O 2) − with SCN −/N 3−, Cr(acac) 2(H 2O) 2+ with SCN − and Cr(atda)(H 2O) 2 with SCN − have been investigated in weakly acidic aqueous solutions. Rate constants, kI and kII for the two steps in each system, are composite as kx = kx0+ kxX[X −] ( x = I, II; X − = SCN −, N 3−). These rate constants have been evaluated also as the corresponding Δ H≠ and Δ S≠ values. The results obtained and the plausible I d mechanism seem to suggest Cr---OOC bond dissociation (hence a strongly negative Δ S≠) generating the transition state in each system with outer-sphere association forming the precursor complex in the X − dependent paths. 相似文献
12.
Trehalose is known to protect membranes and macromolecules. Its accumulation has been implicated in allowing plants to tolerate stress, including heat-shock. However, under heat-shock, it is not clear whether trehalose eliminates reactive oxygen species (ROS) directly or indirectly by protecting antioxidant enzymes. In this study, we initially examined the effects of trehalose on the activities of key antioxidant enzymes, including superoxide dismutases (SODs), ascorbate catalases (CATs), and ascorbate peroxidases (APX) from wheat ( Triticum aestivum L.), and then measured the ability of trehalose to scavenge hydrogen peroxide (H 2O 2) and superoxide anions (O 2−). Our results indicated that trehalose protected SOD activity slightly. However, it inhibited CAT and APX activities under heat stress, with a little protection of CAT activity (only about 7% promotion) at 22 °C. Moreover, trehalose scavenged H 2O 2 and O 2− greatly in a concentration-dependent manner, reaching the maximal scavenging H 2O 2 rate of 95% and O 2− rate of 78%, respectively, at 50 mM trehalose. These results suggest that trehalose plays a direct role in eliminating H 2O 2 and O 2− in wheat under heat stress. 相似文献
13.
The protective activity of hypotaurine (HTAU) and cysteine sulphinic acid (CSA) on peroxynitrite-mediated oxidative damage has been assessed by monitoring different target molecules, i.e. tyrosine, dihydrorhodamine-123 (DHR) and glutathione (GSH). The inhibition of tyrosine oxidation exerted by HTAU and CSA both in the presence and the absence of bicarbonate can be ascribed to their ability to scavenge hydroxyl ( •OH) and carbonate (CO 3•-) radicals. HTAU and CSA also reduce tyrosyl radicals, suggesting that this repair function of sulphinates might operate as an additional inhibiting mechanism of tyrosine oxidation. In the peroxynitrite-dependent oxidation of DHR, the inhibitory effect of HTAU was lower than that of CSA. Moreover, while HTAU and CSA competitively inhibited the direct oxidation of GSH by peroxynitrite, HTAU was again poorly effective against the oxidation of GSH mediated by peroxynitrite-derived radicals. The possible involvement of secondary reactions, which could explain the difference in antioxidant activity of HTAU and CSA, is discussed. 相似文献
14.
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
15.
1. Rate constants for reduction of paraquat ion (1,1′-dimethyl-4,4′-bipyridy-lium, PQ 2+) to paraquat radical (PQ +·) by e−aq and CO 2−· have been measured by pulse radiolysis. Reduction by e−aq is diffusion controlled ( k = 8.4·10 10 M −1·s −1) and reduction by CO 2−· is also very fast k = 1.5·10 10 M −1·s −1). 2. The reaction of paraquat radical with oxygen has been analysed to give rate constants of 7.7·108 M−1·s−1 and 6.5·108 M−1·s−1 for the reactions of paraquat radical with O2 and O2−·, respectively. The similarity in these rate constants is in marked contrast to the difference in redox potentials of O2 and O2−· (− 0.59 V and + 1.12 V, respectively). 3. These rate constants, together with that for the self-reaction of O2−·, have been used to calculate the steady-state concentration of O2−· under conditions thought to apply at the site of reduction of paraquat in the plant cell. On the basis of these calculations the decay of O2−· appears to be governed almost entirely by its self-reaction, and the concentration 5 μm away from the thylakoid is still 90% of that at the thylakoid itself. Thus, O2−· persists long enough to diffuse as far as the chloroplast envelope and tonoplast, which are the first structures to be damaged by paraquat treatment. O2−· is therefore sufficiently long-lived to be a candidate for the phytotoxic product formed by paraquat in plants. 相似文献
16.
The mechanism of the charge separation and stabilization of separated charges was studied using the femtosecond absorption spectroscopy. It was found that nuclear wavepacket motions on potential energy surface of the excited state of the primary electron donor P* leads to a coherent formation of the charge separated states P +B A−, P +H A− and P +H B− (where B A, H B and H A are the primary and secondary electron acceptors, respectively) in native, pheophytin-modified and mutant reaction centers (RCs) of Rhodobacter sphaeroides R-26 and in Chloroflexus aurantiacus RCs. The processes were studied by measurements of coherent oscillations in kinetics at 890 and 935 nm (the stimulated emission bands of P*), at 800 nm (the absorption band of B A) and at 1020 nm (the absorption band of B A−) as well as at 760 nm (the absorption band of H A) and at 750 nm (the absorption band of H B). It was found that wavepacket motion on the 130–150 cm −1 potential surface of P* is accompanied by approaches to the intercrossing region between P* and P +B A− surfaces at 120 and 380 fs delays emitting light at 935 nm (P*) and absorbing light at 1020 nm (P +B A−). In the presence of Tyr M210 ( Rb. sphaeroides) or M195 ( C. aurantiacus) the stabilization of P +B A− is observed within a few picosseconds in contrast to YM210W. At even earlier delay (40 fs) the emission at 895 nm and bleaching at 748 nm are observed in C. aurantiacus RCs showing the wavepacket approach to the intercrossing between the P* and P +H B− surfaces at that time. The 32 cm −1 rotation mode of HOH was found to modulate the electron transfer rate probably due to including of this molecule in polar chain connecting P B and B A and participating in the charge separation. The mechanism of the charge separation and stabilization of separated charges is discussed in terms of the role of nuclear motions, of polar groups connecting P and acceptors and of proton of OH group of TyrM210. 相似文献
17.
The reaction of peroxynitrous acid with monohydroascorbate, over the concentration range of 250 μM to 50 mM of monohydroascorbate at pH 5.8 and at 25°C, was reinvestigated and the rate constant of the reaction found to be much higher than reported earlier (Bartlett, D.; Church, D. F.; Bounds, P. L.; Koppenol, W. H. The kinetics of oxidation of L-ascorbic acid by peroxynitrite. Free Radic. Biol. Med. 18:85–92; 1995; Squadrito, G. L.; Jin, X.; Pryor, W. A. Stopped-flow kinetics of the reaction of ascorbic acid with peroxynitrite. Arch. Biochem. Biophys. 322:53–59; 1995). The new rate constants at pH 5.8 are k1 = 1 × 10 6 M −1 s −1 and k−1 = 500 s −1 for 25°C and k1 = 1.5 × 10 6 M −1 s −1 and k−1 = 1 × 10 3 s −1 for 37°C. These values indicate that even at low monohydroascorbate concentrations most of peroxynitrous acid forms an adduct with this antioxidant. The mechanism of the reaction involves formation of an intermediate, which decays to a second intermediate with an absorption maximum at 345 nm. At low monohydroascorbate concentrations, the second intermediate decays to nitrate and monohydroascorbate, while at monohydroascorbate concentrations greater than 4 mM, this second intermediate reacts with a second monohydroascorbate to form nitrite, dehydroascorbate, and monohydroascorbate. EPR experiments indicate that the yield of the ascorbyl radical is 0.24% relative to the initial peroxynitrous acid concentration, and that this small amount of ascorbyl radicals is formed concomitantly with the decrease of the absorption at 345 nm. Thus, the ascorbyl radical is not a primary reaction product. Under the conditions of these experiments, no homolysis of peroxynitrous acid to nitrogen dioxide and hydroxyl radical was observed. Aside from monohydroascorbate's ability to “repair” oxidatively modified biomolecules, it may play a role as scavenger of peroxynitrous acid. 相似文献
18.
Nitration of protein tyrosine residues by peroxynitrite (ONOO −) has been implicated in a variety of inflammatory diseases such as acute respiratory distress syndrome (ARDS). Pulmonary surfactant protein A (SP-A) has multiple functions including host defense. We report here that a mixture of hypochlorous acid (HOCl) and nitrite (NO 2−) induces nitration, oxidation, and chlorination of tyrosine residues in human SP-A and inhibits SP-A’s ability to aggregate lipids and bind mannose. Nitration and oxidation of SP-A was not altered by the presence of lipids, suggesting that proteins are preferred targets in lipid-rich mixtures such as pulmonary surfactant. Moreover, both horseradish peroxidase and myeloperoxidase (MPO) can utilize NO 2− and hydrogen peroxide (H 2O 2) as substrates to catalyze tyrosine nitration in SP-A and inhibit its lipid aggregation function. SP-A nitration and oxidation by MPO is markedly enhanced in the presence of physiological concentrations of Cl − and the lipid aggregation function of SP-A is completely abolished. Collectively, our results suggest that MPO released by activated neutrophils during inflammation utilizes physiological or pathological levels of NO 2− to nitrate proteins, and may provide an additional mechanism in addition to ONOO − formation, for tissue injury in ARDS and other inflammatory diseases associated with upregulated •NO and oxidant production. 相似文献
19.
N-acetylcysteine has been widely used as an antioxidant in vivo and in vitro. Its reaction with four oxidant species has therefore been examined. N-acetylcysteine is a powerful scavenger of hypochlorous acid (H---OCl); low concentrations are able to protect 1-antiproteinase against inactivation by HOCl. N-acetylcysteine also reacts with hydroxyl radical with a rate constant of 1.36 × 10 10 M −1s −1, as determined by pulse radiolysis. It also reacts slowly with H 2O 2, but no reaction of N-acetylcysteine with superoxide (O 2−) could be detected within the limits of our assay procedures. 相似文献
20.
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
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