ライフサイエンスコーパス: oxidative stress

1 y genes (e.g. placental proteins, markers of oxidative stress).

2 susceptibility and apoptotic cell death with oxidative stress.

3 ng NADPH oxidase, leading to cerebrovascular oxidative stress.

4 phenotype is enhanced glucose metabolism and oxidative stress.

5 the absence of mitochondrial dysfunction and oxidative stress.

6 an contribute to alleviating radical-induced oxidative stress.

7 o predict the molecular responses of PTPs to oxidative stress.

8 e driven by chronic exogenous and endogenous oxidative stress.

9 l of free fatty acid (FFA) palmitate-induced oxidative stress.

10 al damage via Akt/eNOS signaling and reduced oxidative stress.

11 fragmentation, mitochondrial dysfunction and oxidative stress.

12 pplementation and, therefore, are exposed to oxidative stress.

13 h endothelial dysfunction that is induced by oxidative stress.

14 and human hepatocytes more resistant against oxidative stress.

15 ns resulting from RNA polymerase mutants and oxidative stress.

16 , dependency on cysteine, and sensitivity to oxidative stress.

17 exposed to hydrogen peroxide (H2O2)-induced oxidative stress.

18 posure during pregnancy and preterm birth by oxidative stress.

19 ce of energy and lipid metabolism as well as oxidative stress.

20 total antioxidant capacity to encounter with oxidative stress.

21 xidants for prevention of diseases caused by oxidative stress.

22 ontributes to organ dysfunction by promoting oxidative stress.

23 xa and may protect cells against hypoxia and oxidative stress.

24 ed muscle energetics, and protection against oxidative stress.

25 e in renal Klotho expression and/or reducing oxidative stress.

26 d in mitochondria from wild-type mice during oxidative stress.

27 s was negatively associated with a marker of oxidative stress.

28 alth disorder that is increasingly linked to oxidative stress.

29 that diminishes mitochondrial and cytosolic oxidative stress.

30 rtal inflammation, and accompanied by marked oxidative stress.

31 dismutase (SOD1), which protects cells from oxidative stress.

32 mplement activation and cellular response to oxidative stress.

33 l proliferation but protects astrocytes from oxidative stress.

34 THI must be able to mitigate toxic levels of oxidative stress.

35 ro and in vivo, and protects osteocytes from oxidative stress.

36 n, augmented matrix metalloproteineases, and oxidative stress.

37 formed Htt aggregates under the condition of oxidative stress.

38 ity to environmental impacts known to induce oxidative stress.

39 r to counter protein damage originating from oxidative stress.

40 catalase activity and were hypersensitive to oxidative stress.

41 mmon to these exposures is radiation-induced oxidative stress.

42 rotect ECs against hydrogen peroxide-induced oxidative stress.

43 variety of chronic diseases associated with oxidative stress.

44 in respiratory function, and an increase in oxidative stress.

45 Psychosocial stress contributes to placental oxidative stress.

46 mmature mouse oocytes from damages caused by oxidative stress.

47 er-enclosed vesicles produced by cells under oxidative stress.

48 her the expression of human AID or increased oxidative stress.

49 uorogenic probe for the detection of general oxidative stress.

50 g source of compounds with potential against oxidative stress.

51 l dysfunction and consequent exacerbation of oxidative stress.

52 Oxidative stress, a state in which intra- or extracellul

53 Since oxidative stress activates protein kinase D1 (PKD1) in t

54 biological functions, including response to oxidative stress, addictive behaviour, and regulatory fu

55 Plasma oxidative stress (advanced oxidative protein product) wa

56 ed albuminuria is linked to increases in the oxidative stress-advanced glycation end products (AGEs)

57 er molecular hydrogen (H2) is able to reduce oxidative stress after corneal damage induced by UVB irr

58 -regulation of Mcl-1 and chronic adaption to oxidative stress alter mitochondrial metabolism and micr

59 Gene expression profiling of 84 oxidative stress and 249 inflammation-associated human g

60 2(-)) supplementation limits hypoxia-induced oxidative stress and activates the alternate NO pathway

61 Upon oxidative stress and aging, Nrf2 (NFE2-related factor2)

62 ebrafish could be associated with Se-induced oxidative stress and altered dopaminergic neurotransmiss

63 earning was associated with the induction of oxidative stress and altered mRNA expression of dopamine

64 ridoxal) (PAr), a marker of inflammation and oxidative stress and an inverse marker of vitamin B-6 st

65 transcriptional cascades, ultimately evoked oxidative stress and apoptosis in HpeG2 cells.

66 or rescued cells from high-glucose triggered oxidative stress and apoptosis.

67 Reactive oxygen species (ROS) can induce oxidative stress and are associated with cell death and

68 associated volumetric reductions: apoptosis, oxidative stress and autophagy.

69 vels, suggesting that iron overload promotes oxidative stress and cardiac hypertrophy.

70 gered gene expression pathways responsive to oxidative stress and cell death.

71 ffects of PFOS exposure on lipid metabolism, oxidative stress and cell junction signaling in testes.

72 relationship between membrane permeability, oxidative stress and chlorophyll allomers (oxidation pro

73 PerR senses oxidative stress and coordinates the regulation of genes

74 ammatory cell enrollment as well as prevents oxidative stress and cytokine production after MI.

75 Indeed, genetic deletion of Sirt3 increased oxidative stress and decreased the membrane potential of

76 ants and metalloproteinases) contributing to oxidative stress and development of the intracorneal inf

77 nce of p66Shc lysine acetylation in vascular oxidative stress and diabetic vascular pathophysiology.

78 ; response to stress, ultraviolet radiation, oxidative stress and DNA damage repair; activation of im

79 HFD-islets demonstrated evidence of oxidative stress and DNA damage, as well as activation o

80 Mdr1 mitigated oxidative stress and enforced homeostasis in Teff cells

81 ion to improve life-quality is misleading as oxidative stress and exacerbation occur when oxidant foo

82 rom TDP-43Q331K mice, indicative of elevated oxidative stress and failure of some upregulated antioxi

83 proteins indicating increased iron content, oxidative stress and higher expression of CSC markers in

84 Therefore, prevention of vascular oxidative stress and improvement of endothelial NO produ

85 Further, TLR4 deficiency reduced oxidative stress and increased antioxidant capacity (MnS

86 such as inflammation, can induce persistent oxidative stress and increased LPO, resulting in the acc

87 e risk of chronic diseases via regulation of oxidative stress and inflammation (OSI).

88 Oxidative stress and inflammation are considered to play

89 albumin acts as a pro-oxidant; this promotes oxidative stress and inflammation in SAH patients throug

90 /Zi supplementation modulates genes involved oxidative stress and inflammation including NF-kappaB an

91 lipid profile, protein genes associated with oxidative stress and inflammation pathways in the obesit

92 condary mechanisms of injury in TBI, such as oxidative stress and inflammation, are points at which i

93 ay provide a cellular memory of exposures to oxidative stress and inflammation.

94 tor receptor 2 signaling, and a reduction in oxidative stress and inflammation.

95 metabolism, which further leads to systemic oxidative stress and inflammation.

96 a activity, Acot1 knockdown enhanced hepatic oxidative stress and inflammation.

97 ation/activation are facilitated by vascular oxidative stress and inhibited by endothelial NO.

98 lavonoids at protecting neural cells against oxidative stress and is capable of rescuing damaged cell

99 hat enables cells to successfully counteract oxidative stress and is not a prerequisite or consequenc

100 ting the accumulation of lipids that lead to oxidative stress and mitochondrial dysfunction.

101 However, the connection between oxidative stress and mitogenic signals remains obscure.

102 mer, that allows assessment of mitochondrial oxidative stress and mitophagy in vivo, and were precede

103 Since oxidative stress and Nrf2 are linked to several diseases

104 in that promotes mycobacterial resistance to oxidative stress and reacts with free mycothiol and myco

105 hat these sites are associated with enhanced oxidative stress and reduced endothelial NO production i

106 ments with FTD astrocytes revealed increased oxidative stress and robust changes in whole genome expr

107 fluorescence dye assays documented increased oxidative stress and senescence in ZDHHC3-ablated cells.

108 The latter was associated with increased oxidative stress and significant ultrastructural impairm

109 f chemotherapeutics, including reductions in oxidative stress and simultaneous attenuation of ROS-dep

110 plaque SMCs, and this effect correlated with oxidative stress and SMC apoptosis.

111 ximal neurotoxins involved in early neuronal oxidative stress and synapse damage, ultimately leading

112 eurons and prevented AbetaO-induced neuronal oxidative stress and synapse loss.

113 n gene expression and the ability to control oxidative stress and the phenotypic severity of SCD.

114 ants by preventing food oxidation as well as oxidative stress and various disorders in the body.

115 UCP2 can regulate oxidative stress and/or energetic metabolism.

116 nifested by reduced inflammation, steatosis, oxidative stress, and apoptosis and increased mitochondr

117 elevated levels of markers of inflammation, oxidative stress, and cell death, and transcriptomic ana

118 platelet hyperreactivity-high blood glucose, oxidative stress, and elevated vascular shear forces-coe

119 ttery of genes related to biotransformation, oxidative stress, and endocrine disruption were also mea

120 d ischemia reperfusion injury, inflammation, oxidative stress, and endothelial dysfunction, all of wh

121 nse to multiple stimuli, such as DNA damage, oxidative stress, and heat shock.

122 trategy for treatment of liver inflammation, oxidative stress, and injury.

123 HRI is activated by heme deficiency and oxidative stress, and it phosphorylates eIF2alpha (eIF2a

124 adapt to changing conditions and to control oxidative stress, and its dysfunction can lead to hypoxi

125 Fatty liver, oxidative stress, and mitochondrial dysfunction are key

126 Mitochondria are particularly susceptible to oxidative stress, and mitochondrial-dependent apoptosis

127 The db/db mice developed hyperglycemia, oxidative stress, and nephropathy at age 20 weeks compar

128 clear Nrf2 in islet cells, reduced beta-cell oxidative stress, and preservation of beta-cell mass.

129 species production, increased mitochondrial oxidative stress, and promoted nitrosative stress.

130 RX1 results in increased oxygen consumption, oxidative stress, and subsequently apoptosis in epitheli

131 the phthalate-preterm birth relationship by oxidative stress, and the utility of complex regression

132 oung flies by constant exposure to exogenous oxidative stress, and this upregulation is CLOCK-depende

133 changes in gene expression with relevance to oxidative stress, apoptosis, and ion transport.

134 In these corneas the oxidative stress appeared, followed by the excessive inf

135 rous studies have shown that proteolysis and oxidative stress are among the major effectors of ventil

136 ion exceeds endogenous antioxidant capacity, oxidative stress arises.

137 basis of published and new data, we propose oxidative stress as a common pathological mechanism lead

138 profile of the injured nociceptors revealed oxidative stress as a key biological process.

139 utic agents targeting induction of host cell oxidative stress as a mechanism for killing T. gondii.

140 thological protein TDP43 under the effect of oxidative stress as modeled in vitro.

141 d-beta levels, amyloid-associated pathology, oxidative stress, as well as mitochondrial and synaptic

142 e to the pathogenesis of the disease through oxidative stress associated with a reduced antioxidant c

143 metabolism attenuates HCV infection and the oxidative stress associated with HCV infection.

144 In male Krt16(-/-) mice, oxidative stress associated with impaired glutathione sy

145 retinal pigment epithelium (RPE), increased oxidative stress, augmented complement activation and sl

146 Phthalate metabolites and 8-isoprostane, an oxidative stress biomarker, were measured in urine from

147 In contrast, FRD enhanced oxidative stress but not apoptosis in FRD-SR-AIP mice, i

148 ween Spx and genes typically associated with oxidative stress, but also identified novel genes and me

149 325.0] U; P = .01) consistent with increased oxidative stress, but differences in high-density antiox

150 ultiplex SILAC by case study of responses to oxidative stress by hypochlorite.

151 metabolic CO2 Glandular trichomes cope with oxidative stress by producing high levels of polyunsatur

152 p < 0.05) confirmed lipotoxic conditions and oxidative stress by showing an activation of glutathione

153 thelial cells, stimulation by fluvoxamine or oxidative stress caused the sigma1-receptor to transloca

154 Oxidative stress causes significant increases in both ch

155 Concordantly, Merlin loss increased oxidative stress causing aberrant activation of Hedgehog

156 ed in endothelial dysfunction, mitochondrial oxidative stress, chromatin remodeling, and genomic inst

157 tem cell-derived primary human neurons under oxidative stress conditions in an aromatase inhibitor-de

158 e in the cellular antioxidant response under oxidative stress conditions.

159 Oxidative stress contributes to both intraocular pressur

160 Oxidative stress-dependent inflammatory diseases represe

161 ral cardiovascular risk factors in promoting oxidative stress: diabetes, obesity, smoking, and excess

162 Here, we report that arsenite-induced oxidative stress differs from thapsigargin- or tunicamyc

163 xygen limitation, high metabolic demand, and oxidative stress, disturb the protein-folding capacity o

164 ore, a subset of 34 DMRs related to impaired oxidative stress, DNA repair, and inflammatory pathways

165 However, when mineralization was induced via oxidative stress, DRP1 inhibition attenuated mouse and h

166 ch as altered calcium handling and increased oxidative stress due to mitochondrial dysfunction.

167 ence-associated beta-galactosidase activity, oxidative stress, early phosphorylation of mitogen-activ

168 osure of 13-HODE to Hepa-1c1c7 cells induced oxidative stress, ER stress and apoptosis.

169 , including hypoxia, cold shock, heat shock, oxidative stress, exercise-induced adaptation, caloric r

170 Cancer cells experience higher oxidative stress from reactive oxygen species (ROS) than

171 H2S in vivo and as a line of defense against oxidative stress, from which it is clear that RSSH are m

172 s consistent with a role in defenses against oxidative stress generated during host immune responses

173 stress regulon and expand the repertoire of oxidative stress genes in S. mutans, shedding new light

174 mutans - SpxA1 was the primary activator of oxidative stress genes whereas SpxA2 served a backup rol

175 atagen and hair growth inhibition induced by oxidative stress (H2O2 or menadione), significantly amel

176 induced nephrotoxicity is multifactorial but oxidative stress has a critical role in this process.

177 Oxidative stress has pervasive effects on cells but how

178 ed to reestablish 'normal' BiP activity post-oxidative stress has remained unknown.

179 In the absence of oxidative stress, HPbetaCD addition induces a paradoxica

180 FRD mice showed an increase in oxidative stress, hypertrophy and systolic dysfunction.

181 not fully understood, although mitochondrial oxidative stress in alveolar macrophages is critical for

182 rt 1 of a 3-part series covering the role of oxidative stress in cardiovascular disease.

183 tern-style diet (WD) increases steatosis and oxidative stress in fetal liver and is associated with l

184 creased susceptibility to chronic CS-induced oxidative stress in Hhip haploinsufficiency states.

185 then tested the hypothesis that PQS induces oxidative stress in host cells by determining the abilit

186 reserved mitochondrial structure and reduced oxidative stress in injured kidneys.

187 maging of prodromal hippocampus CA1 subfield oxidative stress in models of Alzheimer disease and Ange

188 e carbonyls, which are often used to monitor oxidative stress in organisms.

189 es in cell metabolism, energy production and oxidative stress in others.

190 se findings indicate a role for reduction of oxidative stress in preserving the gut microbiota and it

191 orted the role of copper, zinc and iron, and oxidative stress in several neurodegenerative diseases l

192 t circulating tumour cells (CTCs) experience oxidative stress in the bloodstream, but their survival

193 Next, we analyzed the oxidative stress in the pancreata.

194 These hypothyroid mice displayed oxidative stress in the thyroid, but not in the brown ad

195 y confined to the detection of intracellular oxidative stress in vitro.

196 mote erythroid differentiation and to reduce oxidative stress in vivo during ID.

197 rt the study of the roles of replication and oxidative stresses in mediating cellular senescence in c

198 ion of 4-hydroxynonenal (4-HNE), a marker of oxidative stress, in podocytes and increased the phospho

199 otective capacity against excitotoxicity and oxidative stress including reduced taurine and glutathio

200 adverse effects on birth outcomes, including oxidative stress, increased blood viscosity, and impaire

201 se a rapid attenuation of protein synthesis: oxidative stress induced by hydrogen peroxide and nutrie

202 Oxidative stress induced higher numbers of microfracture

203 cytoprotection against ectoplasmic reticulum/oxidative stress-induced apoptosis both in vitro and in

204 ival phosphatase preventing both thermal and oxidative stress-induced cell death, whereas studies in

205 mal systemic glucose homeostasis and prevent oxidative stress-induced endothelial dysfunction.

206 Apoptosis, oxidative stress, inflammation (IL-8), real-time polymer

207 n the skin and protected against UVB-induced oxidative stress, inflammation and papillomagenesis.

208 ases cardiovascular disease risk by inducing oxidative stress, inflammation, and endothelial dysfunct

209 nificantly reduced the expression of several oxidative stress/inflammatory markers and increased the

210 Endothelial cell apoptosis induced by oxidative stress is an early event in the development of

211 s an etiological factor that drives PTB, and oxidative stress is associated with PTB.

212 The ability to detect and respond to oxidative stress is crucial to the survival of living or

213 al dysfunction with increased sensitivity to oxidative stress is due to the SLC25A24 mutations.

214 DCFH2 can be targeted to other tissues where oxidative stress is important, including cancer.

215 Adaptation to oxidative stress is lost with age in both sexes.

216 Specifically, oxidative stress is negatively correlated with the integ

217 Oxidative stress is two sided: Whereas excessive oxidant

218 Age-dependent elevation in mitochondrial oxidative stress is widely posited to be a major factor

219 larly in labile forms that can contribute to oxidative stress, is connected to diseases ranging from

220 stent with a role for 12/15-LOX in promoting oxidative stress, its chemical inhibition reduced produc

221 Here, we demonstrate that oxidative stress leads to elevated O-GlcNAc levels in U2

222 high-sensitivity C-reactive protein) levels, oxidative stress markers (glutathione and cystine), and

223 hondrial respiration and increased levels of oxidative stress markers.

224 ature neurons and neuroblastoma cells during oxidative stress may denote a prosurvival role of gamma-

225 Oxidative stress may result from dysregulation of system

226 along with nuclear interaction during UV and oxidative stress may serve to modulate active DNA repair

227 argeted antioxidant enzyme to interfere with oxidative stress mechanisms in TBI and provide a proof-o

228 wer inflammation, and are thus less prone to oxidative-stress mediated diseases.

229 anscription factor, plays a critical role in oxidative stress-mediated drug resistance in mantle cell

230 ng impaired mitochondrial energy production, oxidative stress, mitochondrial DNA instability, abnorma

231 functional and structural changes including oxidative stress, neuroinflammation, and degradation of

232 alignant CD34(+) cells occurs in response to oxidative stress, NOX2 inhibition had no detectable effe

233 In the failing heart, oxidative stress occurs in the myocardium and correlates

234 dies have highlighted the positive impact of oxidative stress on chemosensitivity and prognosis of ov

235 90+/-0.78% against hydrogen peroxide-induced oxidative stress on EA.hy926, and was comparable to the

236 d can also act as a pro-oxidant that induces oxidative stress on the vascular endothelial cells, thus

237 models using mechanically induced pressure, oxidative stress, or high mobility group box 1.

238 Lenses were isolated and examined for oxidative stress parameters such as glutathione, lipid p

239 RXR, PPAR-alpha mediated lipid oxidation and oxidative stress pathways.

240 and treatment of multiple diseases in which oxidative stress plays a significant role.

241 These include adaptation to oxidative stress, polysaccharide modification and genes

242 Drug-induced reduction of oxidative stress prevented disulfide HMGB1 generation, t

243 verted into oxidized phospholipids (OxPL) by oxidative stress promoting atherosclerotic plaque format

244 Finally, in an oxidative stress-prone background, Pml(-/-) animals disp

245 vely downregulated SNPH and exhibited higher oxidative stress, reduced cell proliferation, and increa

246 This decrease sensitizes bacteria towards oxidative stress, reduces colonization and attenuates pe

247 The oxidative stress regulator Spx is ubiquitously found amo

248 the sex bias in physiological adaptation to oxidative stress remains unclear.

249 cillus subtilis homologue, and resistance to oxidative stress required the canonical CXXC redox-sensi

250 behavioral trajectories of worms subject to oxidative stress resemble trajectories observed during a

251 ial element required for central metabolism, oxidative stress resistance and replication.

252 these defences, most likely due to elevated oxidative stress resistance.

253 cing analyses indicated that OxyR1-activated oxidative stress-resistant genes were highly expressed i

254 cludes species involved in iron utilization, oxidative stress response and oncogenic pathways.

255 Sabotaging of the oxidative stress response by an oncogenic noncoding RNA.

256 augment ER protein folding, induced numerous oxidative stress response genes not previously known to

257 tasis and transport and the up-regulation of oxidative stress response genes.

258 However, physiological links between PML and oxidative stress response in vivo remain unexplored.

259 Overall, we identify miR-500a-5p as an oxidative stress response miRNA whose activity may defin

260 oteins in cancer cells without affecting the oxidative stress response or the oncogenic pathways incl

261 We conclude that an interdependent oxidative stress response to hyperglycemia perturbs neut

262 rom multiple pathways to control metabolism, oxidative stress response, and cell cycle.

263 tion factors that have a pivotal role in the oxidative stress response, cellular homeostasis, and org

264 rate for enzymes signaling energy stress and oxidative stress response, nicotinamide adenine dinucleo

265 thways associated with the innate immune and oxidative stress response.

266 any eCig liquid resulted in the induction of oxidative stress-response genes including GCLM, GCLC, GP

267 phorylation by the MAPK Sty1 is required for oxidative stress responses in fission yeast cells by pro

268 tability and expression of genes involved in oxidative stress responses, tumor progression and chemor

269 ed metabolic alterations which may relate to oxidative stress responses.

270 RF2 interaction acts as a new checkpoint for oxidative stress responses.

271 lated proline alanine-rich kinase) and OSR1 (oxidative stress responsive kinase), which then phosphor

272 n 2; previously known as CIKS or Act1) is an oxidative stress-responsive cytoplasmic adapter molecule

273 highly modified by S-nitrosylation, and that oxidative stress-responsive genes were significantly upr

274 ein continued DNA damage owing to persistent oxidative stress results in p53 activation and a resulta

275 Cellular stress, including oxidative stress, results in increased O-GlcNAcylation o

276 ore, PAX7 target gene repression can explain oxidative stress sensitivity and epigenetic changes in F

277 Correlations between MACL and markers of oxidative stress such as urinary methionine sulfoxide we

278 kines (IL-1beta, IL-6, IL-10, TNF-alpha) and oxidative stress (superoxide dismutase, catalase, glutat

279 biomarkers related to neuronal and vascular oxidative stress (superoxide dismutase-2), neuroinflamma

280 urbations that include intermittent hypoxia, oxidative stress, sympathetic activation, and endothelia

281 -5p overexpression and downregulation of the oxidative stress targets TXNRD1 and NFE2L2.

282 uch as autism and chronic diseases involving oxidative stress that are characterized by divergent lev

283 that the LEW rat maintains inherent cellular oxidative stress that contributes to resistance to invad

284 man epigenetic markers of iron exposures and oxidative stress that could be monitored for early origi

285 of what molecular damage may be incurred by oxidative stress that is imparted by high iron status in

286 ggesting that the LEW rat maintains cellular oxidative stress that it tolerates.

287 genes are known to provide tolerance against oxidative stress, their role in plant-pathogen interacti

288 Based on the oxidative stress theory, aging derives from the accumula

289 Recent clinical studies demonstrate oxidative stress to be present early in ADPKD.

290 We found that mitochondrial dysfunction and oxidative stress trigger a niche favoring cholangiocellu

291 ell death which is mediated by RIPK1-induced oxidative stress upon caspase and necroptosis inhibition

292 Moreover, in vitro exposure to oxidative stress using H2O2 induces miR-500a-5p overexpr

293 corroborated the finding that mitochondrial oxidative stress was diminished in DMV neurons in the A5

294 equired for ISC proliferation in response to oxidative stress, we identified two regulators of cytoso

295 ithout affecting macrophage infiltration and oxidative stress, whereas TRPA1 silencing in Schwann cel

296 Mitochondria are vulnerable to oxidative stress, which can lead to changes in mitochond

297 These include oxidative stresses, which are present throughout the res

298 ted initiation by increasing CYP450-mediated oxidative stress, while loss of Arid1a within tumors dec

299 n perilesional tissues expressing gliosis or oxidative stress within days.

300 ain their increased proliferation and manage oxidative stress, yet glutamine is often depleted at tum