ライフサイエンスコーパス: reactive oxygen species

1 and resident immune cells generate cytotoxic reactive oxygen species.

2 eurospora crassa and induces accumulation of reactive oxygen species.

3 systems to avoid the bactericidal effects of reactive oxygen species.

4 ed femoral arteries show increased levels of reactive oxygen species.

5 a highly pro-mutagenic DNA lesion formed by reactive oxygen species.

6 cells by a mechanism probably independent of reactive oxygen species.

7 ncreased intracellular albumin scavenging of reactive oxygen species.

8 SIRT3 activation, controlling mitochondrial reactive oxygen species.

9 act the effects of relatively high levels of reactive oxygen species.

10 elopment of antioxidants capable of reducing reactive oxygen species.

11 on of pro-inflammatory signaling mediated by reactive oxygen species.

12 oxidative metabolism and protection against reactive oxygen species.

13 NRAMP2 is required for the detoxification of reactive oxygen species.

14 on of red blood cells and decreased level of reactive oxygen species.

15 DPH production and consequent high levels of reactive oxygen species.

16 ex III activity, and increased production of reactive oxygen species.

17 y low membrane potential and a high level of reactive oxygen species.

18 mor necrosis factor, interleukin (IL)-6, and reactive oxygen species.

19 robust p53 activation, which is mediated by reactive oxygen species.

20 cer cells results in increased production of reactive oxygen species.

21 ence p16(INK4a) , p53, p21 and mitochondrial reactive oxygen species.

22 d DNA damage consistent with the exposure to reactive oxygen species.

23 5'-GG-3' sequence contexts after exposure to reactive oxygen species.

24 ontrol molecule, and consequent formation of reactive oxygen species.

25 ng thioredoxin-interacting protein abrogated reactive oxygen species accumulation in EZH2 suppressed

26 ling nitroxide to mitochondria could prevent reactive oxygen species accumulation, limiting downstrea

27 vascular complications are largely driven by reactive oxygen species accumulation, yet the extent to

28 t lipid overload and increased production of reactive oxygen species after reoxygenation.

29 Reactive oxygen species also regulate multiple vascular

30 al tissue overgrowth via the accumulation of reactive oxygen species and activation of the Jun kinase

31 stress, associated with the accumulation of reactive oxygen species and apoptosis.

32 This, in turn, increases the levels of reactive oxygen species and causes apoptosis of tumour c

33 activity and resulted in the accumulation of reactive oxygen species and cell death in the absence of

34 ay stimulate the production of mitochondrial reactive oxygen species and contribute to alcohol-induce

35 thelial fatty acid oxidation, an increase of reactive oxygen species and decreased angiogenesis.

36 xposure of cancer cells results in increased reactive oxygen species and decreased GSH.

37 e of a quinone-mimicking drug that generates reactive oxygen species and DNA damage, inducing cell de

38 f NPRL2 induces NOX2-dependent production of reactive oxygen species and DNA damage.

39 g cascade; and the mechanisms by which H2 S, reactive oxygen species and haem oxygenase may integrate

40 tured adipocytes increased the generation of reactive oxygen species and induction of autophagy durin

41 Reactive oxygen species and malondialdehyde in H2O2 trea

42 ession, demonstrated increased generation of reactive oxygen species and mitochondrial damage.

43 cardiac myocytes subjected to I/R increased reactive oxygen species and necrotic cell death, both of

44 t cellular buffering system that counteracts reactive oxygen species and other oxidants.

45 stress in cells can lead to accumulation of reactive oxygen species and oxidation of DNA precursors.

46 able Mn is utilized by S. aureus to detoxify reactive oxygen species and protect against neutrophil k

47 on of mitochondrial DNA along with increased reactive oxygen species and reduced superoxide dismutase

48 tocytes were analyzed for insulin signaling, reactive oxygen species, and estrogen response.

49 defective in endocytosis, scavenging of the reactive oxygen species, and in the response to endoplas

50 ing via second messengers-cytosolic calcium, reactive oxygen species, and nitric oxide.

51 ng protein POT1a inhibited the production of reactive oxygen species, and rejuvenated aged HSCs.

52 nsible for destroying invading pathogens via reactive oxygen species, antimicrobial peptides, and neu

53 Reactive oxygen species are ancient processes that prote

54 brane potentials, produce elevated levels of reactive oxygen species, are fragmented, and do not aggr

55 role in oxygen sensing by the carotid body; reactive oxygen species as key transducers in the oxygen

56 NET formation, reactive oxygen species, autophagy activation and intrac

57 he formation of cellular deposits and a host reactive oxygen species burst.

58 eir role in ATP production and generation of reactive oxygen species, but little is known about the m

59 transduction, the cell biological details of reactive oxygen species-catalyzed protein-tyrosine phosp

60 ified the modulation of phase II metabolism, reactive oxygen species clearance, the pentose phosphate

61 taxis, opsonophagocytosis, and production of reactive oxygen species, closely mimicking the defective

62 tivated by diverse stress stimuli, including reactive oxygen species, cytokines, and osmotic stress;

63 eral predictions of the model with regard to reactive oxygen species, cytosolic Ca2+ (Ca2+c), and het

64 cells upon the stress situations tested in a reactive oxygen species-dependent manner.

65 e and radiation synergistically up-regulated reactive oxygen species-dependent PBMC chemotaxis to HNS

66 accumulation, yet the extent to which excess reactive oxygen species derive from specific NADPH oxida

67 xpression of Sp-1 and MIOX and generation of reactive oxygen species derived from NADPH oxidase (NOX)

68 nsition permeability pore, and scavengers of reactive oxygen species did not attenuate capsaicin-indu

69 this harsh acidic environment which contains reactive oxygen species due to the mycobacterial genomes

70 ion of flavonols alleviated the accretion of reactive oxygen species during abiotic stress conditions

71 hat TRPA1 activation is mediated by H2O2 and reactive oxygen species, early markers of tissue damage

72 Furthermore, phalloidin staining and reactive oxygen species estimation of Wnt5a-treated macr

73 ited mitochondrial dysfunction, indicated by reactive oxygen species expression, reduced expression o

74 nanofactories protect human cells from toxic reactive oxygen species for up to a week.

75 In line with this, BCD also reduced reactive oxygen species formation caused by CC in whole

76 Reactive oxygen species generate potentially cytotoxic a

77 ubiquinone is to mitigate elevated levels of reactive oxygen species generated by LCFA degradation.

78 The reactive oxygen species-generating enzyme, NADPH oxidase

79 y and exhibited insignificant differences on reactive oxygen species generation in response to stress

80 diseases through their role in respiration, reactive oxygen species generation, and energy productio

81 aHS on high glucose-induced NOX4 expression, reactive oxygen species generation, and, matrix laminin

82 s which elicit cytotoxic effects by inducing reactive oxygen species generation.

83 Superoxide anion as a primary member of reactive oxygen species, has physiological and pathologi

84 and are essential for NADPH regeneration and reactive oxygen species homeostasis.

85 n, leads to the production of high levels of reactive oxygen species in a p38 mitogen-activated prote

86 ts chemical inhibition reduced production of reactive oxygen species in both mouse and human islets i

87 cytes constitutively generate threefold more reactive oxygen species in cell culture.

88 Phenformin induces production of reactive oxygen species in granulocytic myeloid-derived

89 d neurosteroid formation and lowers cellular reactive oxygen species in mitochondria.

90 We measured levels of reactive oxygen species in mouse livers and primary hepa

91 rial respiration and decreased production of reactive oxygen species in mutant cells, emphasizing PDH

92 They kill endocytosed pathogens by releasing reactive oxygen species in the phagosome and release neu

93 rst study to demonstrate the crucial role of reactive oxygen species in the switching expression of M

94 also attenuated anoxia-induced generation of reactive oxygen species in these cells and in normoxic c

95 tals in particulate matter (PM) can generate reactive oxygen species in vivo by redox cycling, leadin

96 Furthermore, increase in vascular reactive oxygen species induced by ER stress is mitigate

97 could reverse block in mitochondrial OCR and reactive oxygen species induced by MPP(+) in real time.

98 17F), MPL(W515L), or CALR(del52) accumulated reactive oxygen species-induced DNA double-strand breaks

99 trix keratinocyte apoptosis and reversed the reactive oxygen species-induced reduction in hair matrix

100 ydia maintain mitochondrial integrity during reactive oxygen species-induced stress that occurs natur

101 an early destructive phase, where a burst of reactive oxygen species induces loss of E-cadherin-media

102 4-induced cancer cell death was dependent on reactive oxygen species induction and was rescued by ove

103 wed increased expression of genes related to reactive oxygen species, inflammation, and proliferation

104 Compound SA-2 scavenged reactive oxygen species, inhibited proliferation and mig

105 ediated through CYP3A5-induced generation of reactive oxygen species, inhibition of neocortical proge

106 s pathogenic process with endosomal-targeted reactive oxygen species inhibitors has implications for

107 the treatment of viral disease.Production of reactive oxygen species is an ancient antimicrobial mech

108 Such glycolytic flux and elevated reactive oxygen species is supported by increased antiox

109 antly, Nrf2 activation significantly reduced reactive oxygen species levels and associated lipid pero

110 Neutrophil reactive oxygen species levels and mitochondrial stress

111 Reactive oxygen species levels increase in response to c

112 The increased mitochondrial reactive oxygen species levels of atherosclerotic-MSCs p

113 n filaments in smooth muscle cells increases reactive oxygen species levels, activates nuclear factor

114 In vivo, H2S administration reduced reactive oxygen species levels, as well as PYK2 (Y402) a

115 f cardiac troponin I and elevated amounts of reactive oxygen species, lower phosphorylated extracellu

116 ly, we identified that Lactobacillus-derived reactive oxygen species may suppress host kynurenine met

117 via proteasome-dependent degradation and via reactive oxygen species mediated ERK-1/2 phosphorylation

118 l contact in epidermal keratinocytes through reactive oxygen species-mediated disassembly of adherens

119 ade the key innate host defense mechanism of reactive oxygen species-mediated killing of bacteria by

120 himurium-induced oxidative stress results in reactive oxygen species-mediated mitochondrial damage, e

121 8 mice, which are known to have deregulated reactive oxygen species metabolism and accelerated aging

122 od, we evaluate cell viability, formation of reactive oxygen species, mitochondrial health, as well a

123 is, bactericidal activity, and mitochondrial reactive oxygen species (mROS) production.

124 c response such as the rise of intracellular reactive oxygen species of two cancer cell lines to the

125 without causing an increase in intracellular reactive oxygen species or depolarization of the mitocho

126 adducts that result from diverse chemicals, reactive oxygen species or UV light.

127 ox properties in generation and/or silencing reactive oxygen species (overproduced in oxidative stres

128 us cell death as well as the accumulation of reactive oxygen species, phytoalexins, and the stress-re

129 ipid headgroups and allows 5-HT to intercept reactive oxygen species, preventing membrane oxidation.

130 sponse, salicylic acid (SA) accumulation and reactive oxygen species production .

131 icular injection of clodronate abrogates the reactive oxygen species production and cerebrovascular d

132 ent, disruption of SDP1 caused a decrease in reactive oxygen species production and hence the level o

133 e activity should be followed by analysis of reactive oxygen species production and NET formation to

134 nhibition of oxidative metabolism, decreased reactive oxygen species production and oxidative DNA dam

135 A non-ribosylatable version of Ras restores reactive oxygen species production and results in increa

136 f beta2 integrin-dependent cell adhesion and reactive oxygen species production but is required for N

137 d the exaggerated pressor reflex and reduced reactive oxygen species production in rats with ligated

138 However, in mammals reactive oxygen species production paradoxically promote

139 Interestingly, reactive oxygen species production was diminished by uri

140 ion of phosphorylated p38 protein, increased reactive oxygen species production, and decreased surviv

141 n, we assessed cytotoxicity, nitric oxide or reactive oxygen species production, and phagocytosis.

142 in terms of mitochondrial energy metabolism, reactive oxygen species production, gene expression, DNA

143 tion and growth of M. bovis BCG via enhanced reactive oxygen species production, immune cell activati

144 HDM stimulated cellular reactive oxygen species production, increased mitochondr

145 -4 agonists, which associated with decreased reactive oxygen species production, increased nuclear lo

146 ucleotide phosphate/NADPH levels, phagocytic reactive oxygen species production, neutrophil extracell

147 carbon receptor and subsequent mitochondrial reactive oxygen species production, which is known to ac

148 PGC-1alpha, UCP2 and UCP3 mRNA and decreased reactive oxygen species production.

149 We conclude that endosomal reactive oxygen species promote fundamental molecular me

150 l effect stems from a reduced number of anti-reactive oxygen species proteins coded in this taxon's g

151 of specific amino acid residues oxidized by reactive oxygen species provides insights into the mecha

152 verexpressing plants have elevated levels of reactive oxygen species, PRP may connect MAPK and oxidat

153 ellular (P=0.006) and mitochondrial (P=0.03) reactive oxygen species reflecting altered mitochondrial

154 l dynamics are achieved as a balance between reactive oxygen species-regulated effects on polymerizat

155 e and T-cell cytokine production, neutrophil reactive oxygen species release, and apoptosis.

156 Mtlyk9, and Mtlyr4 mutants eliminates early reactive oxygen species responses and induction of defen

157 Although the production of reactive oxygen species (ROS) accounts for restriction o

158 ansient increases in mitochondrially-derived reactive oxygen species (ROS) activate an adaptive stres

159 y unknown how the nervous system responds to reactive oxygen species (ROS) activated by pathogenic mi

160 In cells, sensing of increased levels of reactive oxygen species (ROS) activates many defensive m

161 Most early work focused on elimination of reactive oxygen species (ROS) after radiation; however,

162 deficient muscle mitochondria produce excess reactive oxygen species (ROS) and are partially uncouple

163 Combined with UVA, FICZ generates reactive oxygen species (ROS) and induces oxidative DNA

164 ion of PAK4 in correlation with induction of reactive oxygen species (ROS) and mesenchymal transition

165 d rapid responses, such as the production of reactive oxygen species (ROS) and mitogen-activated prot

166 estricting protein translation and levels of reactive oxygen species (ROS) and Myc.

167 ia coli, inhibited PMA-induced generation of reactive oxygen species (ROS) and neutrophil extracellul

168 Liver damage, reactive oxygen species (ROS) and paracrine tumor necros

169 nse gene expression, callose deposition, and reactive oxygen species (ROS) and salicylic acid (SA) ac

170 cultures presented with elevated endogenous reactive oxygen species (ROS) and superoxide levels, as

171 Reactive oxygen species (ROS) and their associated bypro

172 so had significantly increased production of reactive oxygen species (ROS) and upregulated expression

173 It has long been hypothesized that reactive oxygen species (ROS) are responsible for the as

174 Reactive oxygen species (ROS) are toxic by-products of n

175 Cells are often subjected to the effect of reactive oxygen species (ROS) as a result of both intrac

176 Ultraviolet light (UV) is an inducer of reactive oxygen species (ROS) as well as 6-4-photoproduc

177 nd that erf74 and erf74;erf75 lines lack the reactive oxygen species (ROS) burst in the early stages

178 There was significant generation of Reactive Oxygen Species (ROS) by MCs on co-culture with

179 y (hypoxia) leads to increased production of reactive oxygen species (ROS) by the electron transport

180 Reactive oxygen species (ROS) can damage DNA, proteins,

181 Reactive oxygen species (ROS) can induce oxidative stres

182 Excess production of reactive oxygen species (ROS) caused by hyperglycemia is

183 Reactive oxygen species (ROS) contribute to the developm

184 Inhibiting xanthine oxidase, a major reactive oxygen species (ROS) contributor during acute i

185 ts dependence on oxygen to produce cytotoxic reactive oxygen species (ROS) diminishes the therapeutic

186 onally, an rpaA mutant accumulates excessive reactive oxygen species (ROS) during the day and is unab

187 reducing organic compounds and of generating reactive oxygen species (ROS) from oxygen, peroxides, or

188 rus infection, and enhances the potential of reactive oxygen species (ROS) generating activity during

189 aspase-3, and NADPH oxidase-4 expression and reactive oxygen species (ROS) generation after cisplatin

190 ocystis aeruginosa were studied by measuring reactive oxygen species (ROS) generation and redox trans

191 Life on oxygen predisposes cells to reactive oxygen species (ROS) generation by electron sli

192 palmitoyl-carnitine oxidation and increased reactive oxygen species (ROS) generation in isolated mit

193 a, a 2 log reduction and elevated amounts of reactive oxygen species (ROS) generation per colony were

194 optosis induction by YC-1 involved excessive reactive oxygen species (ROS) generation.

195 3 cell apoptosis by increasing mitochondrial reactive oxygen species (ROS) generation.

196 Reactive oxygen species (ROS) have been suggested as suc

197 We measured levels of reactive oxygen species (ROS) in bacterial cultures and

198 ors targeting the RTK/MAPK pathway increased reactive oxygen species (ROS) in cells with intact KEAP1

199 Increased intracellular reactive oxygen species (ROS) in cultured breast CTCs tr

200 e ability of PQS to induce the production of reactive oxygen species (ROS) in lung epithelial cells (

201 ibrosis (CF), despite abundant production of reactive oxygen species (ROS) in lung tissue.

202 Activation of P2X7R can generate reactive oxygen species (ROS) in macrophages and microgl

203 er found that PA increased the production of reactive oxygen species (ROS) in podocytes and that NAC

204 een shown that cryptochromes also synthesize reactive oxygen species (ROS) in response to light, sugg

205 e good GPx-mimics could reduce production of reactive oxygen species (ROS) in stimulated human mononu

206 accumulation of oxidized proteins induced by reactive oxygen species (ROS) in the cytoplasm.

207 The hypothesis that increased generation of reactive oxygen species (ROS) in vivo plays a key role i

208 tracellular ATP concentrations decreased and reactive oxygen species (ROS) increased.

209 roma-secreted growth factors, cytokines, and reactive oxygen species (ROS) influence tumor developmen

210 We provide evidence that NOX4-derived reactive oxygen species (ROS) inhibits P300/CBP-associat

211 Cellular accumulation of reactive oxygen species (ROS) is associated with a wide

212 ox)-2 component p40phox and the elevation of reactive oxygen species (ROS) is essential in apoptosis.

213 ons and oxidation of mitochondrial proteins, reactive oxygen species (ROS) leads to perturbations in

214 nd plasma catecholamine levels, and elevated reactive oxygen species (ROS) levels in the CB and adren

215 e MM cell line, MM1.S, demonstrated enhanced reactive oxygen species (ROS) levels.

216 Previous research suggested that reactive oxygen species (ROS) mediate the exaggerated EP

217 Reactive oxygen species (ROS) negatively affect myocardi

218 ormation, mutants lacking SEP4 could produce reactive oxygen species (ROS) normally.

219 ssessed as a means to disrupt the balance of reactive oxygen species (ROS) often elevated in cancer c

220 Reactive oxygen species (ROS) play a critical role in ce

221 xpression by N-acetylcysteine suggested that reactive oxygen species (ROS) play a key role in epigene

222 Reactive oxygen species (ROS) play a key role in the acc

223 Reactive oxygen species (ROS) produced by NADPH phagocyt

224 Microbial pathogens are exposed to damaging reactive oxygen species (ROS) produced from a variety of

225 ta-cells, which was accompanied by increased reactive oxygen species (ROS) production and decreased i

226 es less protein damage by rapidly decreasing reactive oxygen species (ROS) production and lend furthe

227 NADPH oxidases contribute to LPS-induced reactive oxygen species (ROS) production and modulate TL

228 ption and reverse electron transfer-mediated reactive oxygen species (ROS) production at concentratio

229 tacks on pathogens through degranulation and reactive oxygen species (ROS) production, as well as by

230 Reactive oxygen species (ROS) production, degranulation,

231 titution, which is reported to cause reduced reactive oxygen species (ROS) production, predisposes to

232 causes eosinophil apoptosis associated with reactive oxygen species (ROS) production.

233 Dysfunctional mitochondria and generation of reactive oxygen species (ROS) promote chronic diseases,

234 DJ-1 is a well-established reactive oxygen species (ROS) scavenger.

235 however, their role through accumulation of reactive oxygen species (ROS) scavenging flavonols has n

236 Here, we identify PML as a reactive oxygen species (ROS) sensor.

237 els have now demonstrated that mitochondrial reactive oxygen species (ROS) signal to support adipocyt

238 in immunity transforming Ca(2+) signals into reactive oxygen species (ROS) signaling.

239 ells experience higher oxidative stress from reactive oxygen species (ROS) than do non-malignant cell

240 ption of cruciferous vegetables and generate reactive oxygen species (ROS) that lead to the induction

241 s also combine with Cu(2+) and NADPH to form reactive oxygen species (ROS) that oxidize DNA.

242 Indirect effects from IR exposure generate reactive oxygen species (ROS) through water hydrolysis a

243 Treatments that increase reactive oxygen species (ROS) trigger TRPM7-dependent Zn

244 th electrodes, high production of endogenous reactive oxygen species (ROS) was indicative of bacteria

245 of significant enhancement in production of reactive oxygen species (ROS) when compared to controls.

246 ofilm, neutrophils generate higher levels of reactive oxygen species (ROS) when presented with plankt

247 fects upon Caco-2 cells (MTT, cell cycle and reactive oxygen species (ROS)) were evaluated in Colombi

248 mbrane potential (DeltaPsi), cell viability, reactive oxygen species (ROS), and secretory granules we

249 PTP activity can readily be diminished by reactive oxygen species (ROS), e.g. H2O2, which oxidize

250 Reactive oxygen species (ROS), generated both endogenous

251 ling cascade, resulting in the production of reactive oxygen species (ROS), immunoinflammatory effect

252 ial biogenesis, glycolysis and production of reactive oxygen species (ROS), in a manner mediated by t

253 BMAA including: (1) localized production of reactive oxygen species (ROS), in the developing brain,

254 eural tubes (nSR-BI(-/-)) had high levels of reactive oxygen species (ROS), intermediate ROS levels b

255 luded assessment of viability, mitochondrial reactive oxygen species (ROS), membrane damage, mitochon

256 TRX1 inhibition elevates reactive oxygen species (ROS), p53 levels and cell death

257 Mink1, activated by reactive oxygen species (ROS), prevents TGF-beta activat

258 Oxidative DNA bases modified by reactive oxygen species (ROS), primarily as 7, 8-dihydro

259 d can induce the intracellular generation of reactive oxygen species (ROS), the question whether TNFa

260 mune marker gene expression but have reduced reactive oxygen species (ROS)-dependent responses such a

261 cystine/glutamate antiporter that regulates reactive oxygen species (ROS)-induced ferroptosis.

262 inc1623 in mice, in the setting of hyperoxia/reactive oxygen species (ROS)-induced lung injury.

263 this infective form and more susceptible to reactive oxygen species (ROS)-induced stress.

264 istent activation of JNK and accumulation of reactive oxygen species (ROS).

265 wnstream of NAD(P)H oxidase-4 (NOX4)-derived reactive oxygen species (ROS).

266 otential, respiratory rate and production of reactive oxygen species (ROS).

267 e the generation of intra- and extracellular reactive oxygen species (ROS).

268 nergetics, redox balance and the emission of reactive oxygen species (ROS).

269 3 ](2+) moieties to induce PDT by generating reactive oxygen species (ROS).

270 ) that is accompanied by the accumulation of reactive oxygen species (ROS).

271 Albumin is a potent scavenger of reactive oxygen species (ROS).

272 ng protein (p66Shc) is a master regulator of reactive oxygen species (ROS).

273 ibuted to excess mitochondrial production of reactive oxygen species (ROS).

274 n, synthesis of hormones, and homeostasis of reactive oxygen species (ROS).

275 utant, suggesting an increased production of reactive oxygen species (ROS).

276 phyll precursor protochlorophyllide produces reactive oxygen species (ROS).

277 ht to be major targets of receptor-activated reactive oxygen species (ROS).

278 te was found to: 1) induce the production of reactive oxygen species (ROS); 2) decrease succinate deh

279 d5, and Cybrd1, which catalyze generation of reactive oxygen species [ROS]), with concomitant higher

280 , treatment of atherosclerotic-MSCs with the reactive oxygen species scavenger N-acetyl-l-cysteine re

281 which was prevented by co-treatment with the reactive oxygen species scavenger Tempol.

282 at the SsMT2 gene plays an important role in reactive oxygen species scavenging and confers enhanced

283 -acetylcysteine (NAC) is an antioxidant with reactive oxygen species scavenging properties that also

284 miR-193b also stimulated reactive oxygen species signaling by targeting the antio

285 Mitochondria comprise the primary reactive oxygen species source and also their main effec

286 KW animals, whereas Tempol had no impact and reactive oxygen species staining was negligible in KK.

287 stigated the effects of H2O2, a prototypical reactive oxygen species that is also present at sites of

288 reactive species, the rise of intracellular reactive oxygen species, the damage on DNA and mitochond

289 ed NETs including protein kinase C, calcium, reactive oxygen species, the enzymes myeloperoxidase (MP

290 production of proinflammatory cytokines and reactive oxygen species, the reactivity of platelets, an

291 These molecules are able to interact with reactive oxygen species through singlet oxygen scavengin

292 phatase 2 phosphatase activity by scavenging reactive oxygen species, thus preventing spleen tyrosine

293 ver, FlnA negatively regulates production of reactive oxygen species upon cell activation.

294 rophils (PMN) interaction with ECs generates reactive oxygen species, we addressed the possible role

295 Peroxidized lipids, generated by reactive oxygen species, were increased in cART/HIV-1-ex

296 ted in attenuated cell invasion and elevated reactive oxygen species, whereas such phenotypes were re

297 agosomes and produce mitochondrially derived reactive oxygen species, which are necessary for microbi

298 ty, causing increased stresses, particularly reactive oxygen species, which damages DNA and reduces t

299 cell damage, QD aggregation or the level of reactive oxygen species, which have to be taken into acc

300 locally via the in-situ production of highly reactive oxygen species, which simultaneously attack var