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1 , varying in a manner that directly mirrored superoxide production.
2 persal and cell death, likely by stimulating superoxide production.
3 ge are thus potent regulators of excitotoxic superoxide production.
4 treated rats showed reduced NADPH-stimulated superoxide production.
5 ther attenuation of NO and greatly increased superoxide production.
6 ochondrial membrane potential (Deltapsi) and superoxide production.
7 pears to be a side reaction of extracellular superoxide production.
8 uce inflammatory responses) did not increase superoxide production.
9  of fMLF-induced p47phox phosphorylation and superoxide production.
10 ect of BH4 treatment on vascular function or superoxide production.
11 nduced and synaptically evoked mitochondrial superoxide production.
12 ecreased effector function in the absence of superoxide production.
13 ber of mitochondria are in the state of high superoxide production.
14 ted nitric oxide release and zymosan-induced superoxide production.
15 n also affects semiquinone concentration and superoxide production.
16 e adenine dinucleotide phosphate oxidase and superoxide production.
17 pocket and might not directly participate in superoxide production.
18 uately delivered to the subcellular sites of superoxide production.
19 (Ang II) increased endothelial mitochondrial superoxide production.
20 sion-induced cell spreading or activation of superoxide production.
21 xidase as the primary source of NMDA-induced superoxide production.
22 plasmic enzyme NADPH oxidase in NMDA-induced superoxide production.
23 ) mice had a 40% reduction in PHOX-dependent superoxide production.
24 f the PHOX complex that results in decreased superoxide production.
25 ant activity and inhibition of NADPH oxidase superoxide production.
26  cytochrome oxidases, causing an increase in superoxide production.
27 MI-1) was a potent antagonist of Nox-derived superoxide production.
28 ity of the ligand with respect to neutrophil superoxide production.
29 inal domain of TSP2 also stimulates monocyte superoxide production.
30     Dihydroethidium (DHE) was used to detect superoxide production.
31 e, we addressed whether GTPase loss affected superoxide production.
32 ere the semiquinone is destabilized to limit superoxide production.
33  is the elusive intermediate responsible for superoxide production.
34 xpression of NADPH oxidase and intracellular superoxide production.
35 the dominant inhibitory effect of p40R57Q on superoxide production.
36 helial function, eNOS coupling, and vascular superoxide production.
37  reducing equivalents accumulate and promote superoxide production.
38 ly of the neuronal NADPH oxidase complex and superoxide production.
39 -dependent hypertension and decreased aortic superoxide production.
40 dase activation, as demonstrated by enhanced superoxide production.
41 lting in bioenergetics defects and increased superoxide production.
42 ote mitochondrial ATP synthesis and suppress superoxide production.
43 ed p-38 mitogen-activated protein kinase and superoxide production.
44 ite a strong candidate for being a center of superoxide production.
45 s was generally in those with lower residual superoxide production.
46 DNA restores mitochondrial Ca(2+) uptake and superoxide production.
47 m with concomitant increase in mitochondrial superoxide production.
48 phorylate subunits of the oxidase leading to superoxide production.
49 on after hypoxia by decreasing mitochondrial superoxide production.
50 oupling between NMDA receptor activation and superoxide production.
51 hox), NOX1 and -4), NAD(P)H oxidase-mediated superoxide production, 26S proteasome activity, IkappaBa
52 phox), NOX1 to -4), NAD(P)H oxidase-mediated superoxide production, 26S proteasome activity, IkappaBa
53                                Extracellular superoxide production, a phenomenon well established to
54 ne properties, and provide a vital source of superoxide production across many different cell types.
55 F MDMs demonstrate a nearly 60% reduction in superoxide production after PMA stimulation compared wit
56 shed NO production and elevated eNOS-derived superoxide production, along with a concomitant reductio
57 tide, SS-31, or Bendavia) in restoring renal superoxide production and ameliorating DKD.
58 c reticulum (ER)-mitochondria communication, superoxide production and apoptosis were evaluated in fi
59  potential changed the relationships between superoxide production and b(566) reduction and between b
60                             Diabetes-induced superoxide production and cardiac fibrosis were partiall
61             In neuron cultures, postischemic superoxide production and cell death were completely pre
62 aling axis and was associated with increased superoxide production and cell death.
63  iodonium chloride), enzymes responsible for superoxide production and cell differentiation in fungi.
64                                              Superoxide production and content of the oxidative stres
65                   In murine stroke, neuronal superoxide production and death were decreased by the gl
66 -silenced RAW macrophages depicted increased superoxide production and decreased parasite survival.
67 f mfpr1 resulted in abrogation of neutrophil superoxide production and degranulation in response to f
68  cytoskeleton prevents Pseudomonas-initiated superoxide production and DNA release.
69 es showed a pH-dependent correlation between superoxide production and enhanced sperm motility.
70 e, safinamide potently suppressed microglial superoxide production and enhanced the production of the
71 ctron donor for reperfusion-induced neuronal superoxide production and establish a previously unrecog
72 ion of mitoribosomes, elevated mitochondrial superoxide production and eventual loss of OXPHOS comple
73  these changes, we independently manipulated superoxide production and GSH metabolism during reperfus
74 8 with SB203580 or JNK with SP600125 reduced superoxide production and improved shear stress-induced
75 sistance and deletion of Nox2 showed reduced superoxide production and improved vascular function.
76 hosphate (GTP)-bound RAC2 including enhanced superoxide production and increased membrane ruffling.
77 ; (v) the engulfed Hb-Hp aggregates activate superoxide production and induce intracellular oxidative
78 d nitric oxide production and dampened renal superoxide production and inflammatory cell infiltration
79 erations in transcripts involved in heme and superoxide production and insulin signaling.
80 Thus, dietary Bbetaglucans inhibit leukocyte superoxide production and leukocyte, renal and aortic AD
81 ominant inhibitory effect on agonist-induced superoxide production and membrane translocation of p47(
82 l biogenesis and activation of AMPK enhances superoxide production and mitochondrial function while r
83 on of the p47(phox) subunit blocked neuronal superoxide production and negated the deleterious effect
84                                              Superoxide production and neuronal death were also block
85            In cultured neurons, NMDA-induced superoxide production and neuronal death were prevented
86 re in high glucose conditions led to reduced superoxide production and NOX4 expression.
87 s in total and mitochondria-derived arterial superoxide production and oxidative stress (nitrotyrosin
88 ellular ATP underpins increased myeloid cell superoxide production and phagocytosis associated with i
89               PBM inhibited diabetes-induced superoxide production and preserved MnSOD expression in
90            Fenofibrate significantly reduced superoxide production and protein oxidation in the ische
91 trophil adhesion and migration, and augments superoxide production and proteolytic enzyme degranulati
92 minant-negative transcript that can modulate superoxide production and provides an example of genetic
93                       These mechanisms limit superoxide production and short circuiting of the Q-cycl
94 the cell membrane potentiate haem-associated superoxide production and subsequent oxidative damage.
95 f NGB attenuated ocular hypertension-induced superoxide production and the associated decrease in ATP
96       These results establish a link between superoxide production and trans-sulfuration pathway sele
97                      AICAR treatment induced superoxide production and was linked with glomerular mat
98  I activity, impaired respiration, increased superoxide production, and a reduction in membrane poten
99 kinase (Hck), and induced cellular adhesion, superoxide production, and degranulation of eosinophils.
100 s of neutrophils, including phagocytosis and superoxide production, and did not inhibit neutrophils f
101 proliferation, migration, monocyte adhesion, superoxide production, and gene expression assays.
102  High fat feeding increased Nox2 expression, superoxide production, and impaired insulin signaling in
103  mitochondrial membrane potential, increased superoxide production, and increased expression of a glu
104  inhibited nitric oxide production, promoted superoxide production, and increased vascular cell adhes
105 (OXPHOS) efficiency, increased mitochondrial superoxide production, and mtDNA depletion as well as ab
106 reduced ischemia-induced zinc translocation, superoxide production, and neuron death.
107 purposing of the electron transport chain to superoxide production, and NF-kappaB activation.
108 ice also had significantly less leukostasis, superoxide production, and nuclear factor-kappaB (NF-kap
109 s suppressed fMLP-stimulated Rac activation, superoxide production, and PI3-kinase activation in diff
110 uced TNF-alpha-stimulated p65 translocation, superoxide production, and proinflammatory gene expressi
111 proliferation, migration, monocyte adhesion, superoxide production, and proinflammatory gene expressi
112  activity, restore physiologic mitochondrial superoxide production, and promote organ healing.
113  flux through the enzyme, different rates of superoxide production are attained when the enzyme is di
114     In addition, HHcy accelerated HG-induced superoxide production as determined by dihydroethidium a
115 om Rap1a-/- mice had reduced fMLP-stimulated superoxide production as well as a weaker initial respon
116 yphal morphology and size, and mitochondrial superoxide production as well as development.
117   Acute infusion of ascorbic acid to inhibit superoxide production associated with a nonsignificant t
118 e mouse neutrophil chemotaxis at 1-10 nM and superoxide production at 10-100 nM, similar to the poten
119                                        Thus, superoxide production at Q(o) depends on the reduction s
120 ve force of the reaction rate, and simulates superoxide production at the Qo-site.
121 e p40(phox) or PI3 kinase activity, although superoxide production before and after phagosome sealing
122 eficiency, BCNU exposure further exacerbates superoxide production, BH4 oxidation, and eNOS activity.
123 /gp91(phox) protein expression, decreased NO/superoxide production, blocked peroxynitrite formation,
124              The effects of hyperglycemia on superoxide production, blood-brain barrier disruption, i
125 ctase inhibition abolished the difference in superoxide production but did not affect myocardial func
126 on of Mn(II) oxidation by NADH oxidase-based superoxide production by a common marine bacterium (Rose
127                                              Superoxide production by a model bacterium within the ub
128                                    Phagocyte superoxide production by a multicomponent NADPH oxidase
129                                              Superoxide production by brain mitochondria isolated fro
130        In addition, indirect measurements of superoxide production by cells and isolated mitochondria
131 mational changes and NADPH oxidase-dependent superoxide production by cells.
132 or of site IQ electron leak, an inhibitor of superoxide production by complex I of the mitochondrial
133 on the mechanisms of energy transduction and superoxide production by complex I, discusses contempora
134 se electron transport and rotenone-sensitive superoxide production by complex I.
135 tor in regulating the balance between NO and superoxide production by endothelial NOS (eNOS coupling)
136 ey role for Trp-447 in determining NO versus superoxide production by eNOS, by effects on BH4-depende
137         Here we show that dark extracellular superoxide production by marine microbes represents a pr
138 ts clarify the maximum rate and mechanism of superoxide production by mGPDH.
139                                              Superoxide production by NADPH oxidase is a requisite ev
140 rglycemia is mediated through an increase in superoxide production by NADPH oxidase.
141                           Here, we evaluated superoxide production by neuronal nicotinamide adenine d
142  studies, apocynin was administered to block superoxide production by nicotinamide adenine dinucleoti
143 h inhibition of Nf-kappaB, and inhibition of superoxide production by phagocytes.
144  inflammation, we suggest that the decreased superoxide production by PHOX in p66Shc-deficient mice c
145 sion studies, we found that H(2)O(2)-induced superoxide production by primary sperm cells was mediate
146 inflammation, results from loss of phagocyte superoxide production by recessive mutations in any 1 of
147 ermatozoa motility, was required for optimal superoxide production by spermatozoa.
148 ial permeability transition pore stimulating superoxide production by the ETC.
149 phenylene iodonium-sensitive NADPH-dependent superoxide production by the liver following I/R.
150  the mechanism and function of extracellular superoxide production by the marine diatom Thalassiosira
151 ranulation responses but a profound block in superoxide production by the phagocyte oxidase.
152 s known to be associated with high levels of superoxide production by the sperm mitochondria; however
153           To better define the activation of superoxide production by this multisubunit enzyme comple
154          GR was also linked to extracellular superoxide production by whole cells via quenching by th
155                  Diabetes mellitus increased superoxide production, canonical Wnt antagonist expressi
156                               This increased superoxide production causes the activation of 5 major p
157                  Furthermore, an increase in superoxide production combined with an increase in p22ph
158 e decreased expression of SOD2 and increased superoxide production correlate with RPE apoptosis induc
159                       Although this enhanced superoxide production correlates with effects due to the
160 ocal microscopy, revealed that Abeta-induced superoxide production could be blunted by MitoQ, but not
161 phosphateoxidase) activity and mitochondrial superoxide production coupled with a compromised antioxi
162                                   Viability, superoxide production, cytotoxic RNA transfection effici
163               Brain death leads to increased superoxide production, decreased GPx activity, decreased
164 is the sole superoxide producer, the rate of superoxide production depends on the concentrations of g
165  by molecular modeling, to explain decreased superoxide production during alpha-tocopherol deficiency
166                                 In contrast, superoxide production during forward electron transport
167 e during reverse electron transport, its low superoxide production during forward electron transport
168 es in coordinating directional migration and superoxide production during neutrophil responses to che
169 showed a substantial defect in intracellular superoxide production during phagocytosis, whereas extra
170 portant role for NADPH oxidase (NOX)-derived superoxide production during T1D pathogenesis, as NOX-de
171 le to Hb autoxidation and to hypoxia-induced superoxide production enhanced the hypoxia-induced respo
172 increased glucose consumption, mitochondrial superoxide production, ERK and JNK phosphorylation, tyro
173 valents in activated microglia, GSH, trigger superoxide production, favor the reorganization of lipid
174                                Extracellular superoxide production followed a typical photosynthesis-
175 s responded to NMDA with a rapid increase in superoxide production, followed by neuronal death.
176                               We report that superoxide production following CB3 infection may exacer
177                                              Superoxide production from antimycin-inhibited complex I
178                                              Superoxide production from atrial samples was measured b
179 de over time, OSS time-dependently increased superoxide production from endothelial cells.
180                      The concept that excess superoxide production from mitochondria is the driving,
181 nergy-conserving NADH oxidation with minimal superoxide production from the nucleotide-free site.
182 semiquinone in the Q-binding site, the rapid superoxide production from this site during reverse elec
183                                In each case, superoxide production had a similar bell-shaped relation
184                          In support of this, superoxide production has also been found for native AO
185 he ecophysiological role(s) of extracellular superoxide production has remained elusive.
186             Despite significant reduction in superoxide production, Hv1(-/-) mice are able to clear s
187 from RAC2[E62K] patients exhibited excessive superoxide production, impaired fMLF-directed chemotaxis
188 showed that estrogen decreases mitochondrial superoxide production in a receptor-mediated manner, as
189                       Here we examined renal superoxide production in a type 2 diabetes animal model,
190 ar ROS and induced significant mitochondrial superoxide production in bronchial epithelial cells (16-
191 t Crb restricts Rac1-NADPH oxidase-dependent superoxide production in epithelia and photoreceptor cel
192  attenuation of NADPH oxidase activation and superoxide production in hippocampal CA1 pyramidal neuro
193 ent transcripts on protein translocation and superoxide production in human leukemia cells (HL-60) an
194 ing, endothelium-dependent vasodilation, and superoxide production in human vessels, whereas plasma b
195 ing and contractile performance and controls superoxide production in isolated cardiomyocytes.
196     Dihydroethidium (DHE) was used to detect superoxide production in isolated retinal arterioles.
197 use carotid arteries significantly increased superoxide production in medial VSMCs and enhanced neoin
198 hese results indicate that lack of leukocyte superoxide production in mice with chronic hyperglycemia
199 ate comparable with the other major sites of superoxide production in mitochondria, the superoxide-pr
200      The accumulation of Zn caused increased superoxide production in N. caerulescens, but inoculatio
201 ced p47(phox) phosphorylation and diminished superoxide production in neutrophils.
202 phagocytosis in monocytes and stimulation of superoxide production in neutrophils.
203 r basal conditions, angiotensin II increased superoxide production in nondiabetics and diabetics, and
204                   G. bethesdensis stimulated superoxide production in normal monocytes, but to a less
205                                              Superoxide production in ovarian, lung, colon, breast, a
206 us expression of p40(phox) markedly enhanced superoxide production in phorbol 12-myristate 13-acetate
207 creased mitochondrial proteins and increased superoxide production in PKD patient-derived renal epith
208 ting, eNOS becomes "uncoupled," resulting in superoxide production in place of NO.
209  hypoxia, increased Hb autoxidation augments superoxide production in RBCs.
210 ip2(cmo) neutrophils display highly elevated superoxide production in response to a range of stimuli.
211 capacity, Ca(2+) homeostasis, and attenuated superoxide production in response to ischemia and excito
212 lic switch from oxidative phosphorylation to superoxide production in response to its ligand, oxidize
213 p67(phox) protein expression, and subsequent superoxide production in response to TNF-alpha.
214                                Extracellular superoxide production in T. oceanica exudates was couple
215 ng showed that CRP produced TEMPOL-sensitive superoxide production in the arteriolar endothelium.
216 lows rapid agonist-induced redistribution of superoxide production in the cell.
217 R-dependent phagocytosis was associated with superoxide production in the early FCP and restricted ph
218 ll-free assay system where p47SH3AB enhanced superoxide production in the presence of a p67phox (1-21
219 glomerular damage index, and NADPH-dependent superoxide production in the renal cortex from Asm(+/+)
220 y degeneration, proinflammatory changes, and superoxide production in the retina and allodynia were i
221 JCI, my colleagues and I revealed a role for superoxide production in the vascular dysfunction associ
222 /db mice and fully preserved levels of renal superoxide production in these mice.
223 d microglia in injured WT, whereas increased superoxide production in vessels and nuclear factor (NF)
224                                       Atrial superoxide production increased significantly after repe
225 on of AT1R mRNA, c-Jun mRNA, c-fos mRNA, and superoxide production induced by Ang II.
226                              In mouse brain, superoxide production induced by NMDA injections or isch
227 eta-glucans (Bbetaglucans) reduced leukocyte superoxide production, inflammatory ADAM17, TNFalpha, nS
228 inal cells, 30-mM glucose exposure increased superoxide production, inflammatory biomarker expression
229 er, these results suggest that extracellular superoxide production is a byproduct of a transplasma me
230 nt embryos, demonstrating that limitation of superoxide production is a crucial function of Crb and t
231 -induced activation loop phosphorylation and superoxide production is also established in the differe
232            We recently reported that reduced superoxide production is associated with mitochondrial d
233 key role in host defense; however, excessive superoxide production is believed to participate to infl
234                                        Since superoxide production is one of the first indicators of
235 ent studies showed that phagocytosis-induced superoxide production is stimulated by p40(phox) and its
236 th extensive NMDAR activation, the resulting superoxide production leads to neuronal death.
237 duration and included vascular permeability, superoxide production, leukotriene generation, leukocyte
238 uce superoxide, this microbial extracellular superoxide production may play a central role in the cyc
239 E2-EA, inhibits leukotriene B4 biosynthesis, superoxide production, migration, and antimicrobial pept
240                                      Greater superoxide production, mitochondrial injury, and oligode
241 erved differential activation of endothelial superoxide production, NF-kappaB activation, and reducti
242 at IL-27 is able to enhance the potential of superoxide production not only during differentiation bu
243             We also asked: 3) if substantial superoxide production occurs during and after HI, thinki
244 , and the strong dependence of both modes of superoxide production on DeltapH.
245 esults support a two-site model of complex I superoxide production; one site in equilibrium with the
246 icantly less leukostasis (P < 0.005) but not superoxide production or NF- kappaB expression.
247          It is widely held that NMDA-induced superoxide production originates from the mitochondria,
248 icytes and increases in both leukostasis and superoxide production (P < 0.006).
249  state of cytochrome b(566), suggesting that superoxide production peaks at intermediate Q-reduction
250                               mGPDH-specific superoxide production plateaus at a rate comparable with
251 ted growth in proportion to CGD PMN residual superoxide production, providing a potential method to i
252 rst, which corresponds to an increase in the superoxide production rate by 9 +/- 3 attomoles/cell/s.
253 sign of being overreducible, and the maximum superoxide production rate correlates with mGPDH activit
254 el is capable of explaining both kinetic and superoxide production rate data.
255 uations to more periodic oscillations as the superoxide production rate increases.
256                                 However, the superoxide production rate was not uniquely related to t
257 increased oxidized biopterins, NOS-dependent superoxide production, reduced NO production, and dephos
258               We estimate that extracellular superoxide production represents a gross oxygen sink com
259 udes genes involved in phagosome maturation, superoxide production, response to vitamin D, macrophage
260 s investigated by using artificial enzymatic superoxide production revealing a sensitivity of 2235AM(
261  increased neutrophil F-actin, and excessive superoxide production seen in patients.
262 ADPH oxidase activity was blocked to prevent superoxide production showed preservation of neuronal GS
263    As the number of mitochondria in the high-superoxide-production state increases, short-lived or ab
264  When the number of mitochondria in the high-superoxide-production state reaches a critical number, r
265  burst in electron transport chain-dependent superoxide production that is coincident with a modest i
266 constriction is mediated via TRPA1-dependent superoxide production that stimulates alpha2C-adrenocept
267    TNF-alpha stimulation of PMNs resulted in superoxide production that was dependent on CD11b/CD18-m
268 ow that by eliminating macrophage and T cell superoxide production through the NADPH oxidase (NOX), T
269                                The increased superoxide production, together with the increased iron
270                  This is significant because superoxide production underlies the role of human PRODH
271                      Transient extracellular superoxide production upon stimulation was successfully
272 ys an important role in phagocytosis-induced superoxide production via a phox homology (PX) domain th
273 ctivity rather than assembly, and stimulates superoxide production via a PI3P signal that increases a
274    Restoration of mitochondrial function and superoxide production via activation of AMPK has now bee
275             To confirm whether the defect in superoxide production was a direct consequence of p66Shc
276                                              Superoxide production was also blocked by inhibiting the
277                                    Increased superoxide production was associated with increased expr
278 were seen of 58, 86, or 92%, and NOS-derived superoxide production was greatly increased.
279                                     Finally, superoxide production was higher in brain tissue from di
280                                              Superoxide production was measured by the ethidium metho
281              Further, elevated mitochondrial superoxide production was noted in tumor cells vs. non-t
282  revealed that a MPP(+)-mediated increase in superoxide production was reduced in MAC1(-/-) neuron-gl
283                         Here, we report that superoxide production was reduced in the kidneys of a st
284                                Mitochondrial superoxide production was shown to be the source of JNK-
285                                 eNOS-derived superoxide production was significantly elevated in W447
286                                       Aortic superoxide production was significantly increased in Nox
287                      NADPH oxidase-dependent superoxide production was significantly increased in ves
288 s in which TRPM2 was depleted, mitochondrial superoxide production was significantly increased, parti
289 tion, association with the cytoskeleton, and superoxide production were examined in transgenic COS-7
290 droethidine-based detection of intracellular superoxide production were used.
291 stress markers (eg, nitrotyrosine abundance, superoxide production) were also quantified.
292  component p67 (phox) , activates neutrophil superoxide production, whereas interactions with p21-act
293 ate 3 oxygen consumption rates and decreased superoxide production, whereas the opposite is seen in o
294 noelaidic acid are associated with increased superoxide production, whereas Transvaccenic acid (which
295                             We also measured superoxide production, which has been hypothesized to be
296                   Reduction of mitochondrial superoxide production with rotenone was sufficient to re
297 nzyme can also catalyze substantial rates of superoxide production, with deleterious physiological co
298 d in endothelial cells followed by increased superoxide production within 4 hours of blast.
299   Superoxide flashes are transient bursts of superoxide production within the mitochondrial matrix th
300 creased mitochondrial oxygen consumption and superoxide production without altering cellular ATP leve

 
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