ライフサイエンスコーパス: oxidative damage

1 r acetotrophic growth and (ii) resilience to oxidative damage.

2 plast electron transport chain, resulting in oxidative damage.

3 protected retina against progressive retinal oxidative damage.

4 highly susceptible to, and major targets of, oxidative damage.

5 glycation, is quantitatively as important as oxidative damage.

6 o-2, SHSY-5Y and K562) against t-BHP-induced oxidative damage.

7 RCA1(5382insC) impact the cell's response to oxidative damage.

8 important therapeutic targets, are prone to oxidative damage.

9 well as sensitive enzymes from intracellular oxidative damage.

10 dicating a role of TAG in protection against oxidative damage.

11 ogenase mutants with increased resistance to oxidative damage.

12 telomeres highly susceptible to ROS-induced oxidative damage.

13 s from undergoing ferroptosis in response to oxidative damage.

14 ST-derived H2S protects chromosomal DNA from oxidative damage.

15 uces intracellular ROS formation, leading to oxidative damage.

16 xposure to oxygen compared to other forms of oxidative damage.

17 hain aliphatic aldehydes to prevent cellular oxidative damage.

18 translocation, epithelial inflammation, and oxidative damage.

19 tial to embed mutations during the repair of oxidative damage.

20 uman oocytes is caused, at least in part, by oxidative damage.

21 within a protein shell to protect cells from oxidative damage.

22 correct nucleotide excision repair following oxidative damage.

23 to (although slightly affected retention at) oxidative damage.

24 nce of the enzyme in protecting tissues from oxidative damage.

25 s MT, the primary site and primary target of oxidative damage.

26 water comes along with its vulnerability to oxidative damage.

27 g consistent with replication errors and not oxidative damage.

28 ndividual muscle fiber size while decreasing oxidative damage.

29 ase, most probably through the generation of oxidative damage.

30 d Purple Haze cultivars against H2O2-induced oxidative damage.

31 induced obesity at the cost of moderate skin oxidative damage.

32 ating pathological conditions resulting from oxidative damage.

33 ation, and the latter a mimic of age-related oxidative damage.

34 , causing in consequence the accumulation of oxidative damage.

35 l lesions of Nrf2(-/-) mice, indicating high oxidative damage.

36 sponse in the hippocampus, which counteracts oxidative damage.

37 permeability and salt passage as a result of oxidative damage.

38 ration is a prerequisite to the CM15-induced oxidative damage.

39 m Miracle Fruit leaves (AML) on mutation and oxidative damage.

40 ng of mycothiol and accumulation of cellular oxidative damage.

41 on to suppress ROS and to protect cells from oxidative damage.

42 eactive oxygen species (ROS), and ultimately oxidative damage.

43 w intriguing protective properties to resist oxidative damage.

44 he photosynthetic machinery in great risk of oxidative damage.

45 id synthesis, apoptosis, and protection from oxidative damage.

46 strogens have neuroprotective effect against oxidative damage.

47 umulation and thus may be protective against oxidative damage.

48 s and through double-stranded DNA containing oxidative damage.

49 A and proteins from Fenton's reagent-induced oxidative damage.

50 ortant for the real-time evaluation of mtDNA oxidative damage.

51 m of cell death that relies on iron-mediated oxidative damage.

52 uences highly vulnerable to NO(3)(*)-induced oxidative damage.

53 edox-active cofactors for preventing protein oxidative damage.

54 ntiated RPE cells and enhances resistance to oxidative damage.

55 ion and degradation to protect cells against oxidative damage.

56 h age from slowed translation and cumulative oxidative damage.

57 lating with female sex and microvascular and oxidative damages.

58 flozin in isoprenaline (ISO)-induced cardiac oxidative damage-a model mimicking sympathetic nervous s

59 Indeed, products of oxidative damage accumulate in skeletal muscle during ag

60 cid synthesis and structure, protection from oxidative damage, activity of ion channels, cell prolife

61 It protects hearts from oxidative damage after ischaemia-reperfusion or hypoxia-

62 ts of their consumption on the prevention of oxidative damage along the gut.

63 EPA significantly attenuated IND-induced oxidative damage and apoptosis.

64 tential of this compound against UVA-induced oxidative damage and cell death was evaluated in culture

65 Photo-induced oxidative damage and cell death were drastically reduced

66 ta and Tau accumulation through increases in oxidative damage and cellular energy deficits; these, in

67 Increased oxidative damage and decreased capacity of intracellular

68 ns and that this was paralleled by increased oxidative damage and deficits in cognition and memory.

69 ssion of SODA also resulted in mitochondrial oxidative damage and failure of SODA/DeltasodA promastig

70 id and its ability to adapt to and cope with oxidative damage and immune clearance.

71 les including photoprotection, regulation of oxidative damage and immune responses.

72 uman macula, where they protect the eye from oxidative damage and improve visual performance.

73 N-acetylcysteine (NAC) reduces oxidative damage and increases cone function/survival in

74 ce, and this was associated with hippocampal oxidative damage and inflammation despite an enhanced ex

75 ulted in a significant prevention of cardiac oxidative damage and inflammation.

76 dogenous Na(+) and K(+) contents, regulating oxidative damage and key genes and modulating endogenous

77 Considerable evidence indicates that oxidative damage and mitochondrial dysfunction contribut

78 SS31 is associated with some improvements in oxidative damage and mitophagy in muscles of old mice.

79 consumption were evaluated on biomarkers of oxidative damage and on aging-associated reductions in m

80 en species accumulation, limiting downstream oxidative damage and preserving mitochondrial function.

81 dd45, that act to both "shield" tissues from oxidative damage and promote efficient damage repair.

82 evolved as a radical sponge against mechano-oxidative damage and proposes a mechanism for exercise-i

83 However, the positive relationship between oxidative damage and survival emphasises the need to inv

84 ed AML cells to AraC treatment by triggering oxidative damage and sustaining oxidative stress, partic

85 AT1 has potential to protect the retina from oxidative damage and to prevent or slow down diabetic re

86 ve developed strategies to protect PSII from oxidative damage and to repair damaged PSII.

87 onents of salinity stress along with reduced oxidative damage and upregulation of stress-responsive g

88 hemodynamic changes, reducing inflammation, oxidative damage, and fibrosis in the experimental model

89 Mitochondria are susceptible to oxidative damage, and healthy mitochondrial populations

90 f antioxidant genes in their skin, more skin oxidative damage, and increased epidermal thickness and

91 xpression, loss of ATF4 resulted in enhanced oxidative damage, and increased free cholesterol in live

92 ht increased adenosine triphosphate, reduced oxidative damage, and increased median life spans, witho

93 is causes an increase of intravascular heme, oxidative damage, and inflammation in which macrophages

94 fects on reactive oxygen species production, oxidative damage, and telomere shortening, at the indivi

95 ates employ distinct mechanisms to remediate oxidative damage, and that carbon source affected the is

96 Many organisms seem to tolerate oxidative damage, and the extension of health span and l

97 enesis, the mutation spectrum shifted toward oxidative damage, and the mutation rate increased.

98 iciency makes red cells highly vulnerable to oxidative damage, and therefore susceptible to hemolysis

99 Mitochondrial dysfunction and oxidative damage are commonly associated with early stag

100 Levels of ROS and the risk for oxidative damage are dictated by the balance between ROS

101 acid oxidation in mitochondria and increased oxidative damage are features of non-alcoholic fatty liv

102 acid oxidation in mitochondria and increased oxidative damage are features of non-alcoholic fatty liv

103 e oocytes and granulosa cells, indicative of oxidative damage as a crucial factor in ovarian function

104 y of JAK2-deficient livers, which diminished oxidative damage as compared to GH(tg)STAT5(Deltahep) mi

105 endent mechanism and are not as sensitive to oxidative damage as previously thought.

106 ession markedly sensitizes cells to telomere oxidative damage as well as XRCC1 inhibition.

107 ses in PPARG coactivator 1beta could prevent oxidative damage associated with complete loss of PGC1A

108 plantation, and autoimmunity, and preventing oxidative damage associated with inflammation.

109 ized role for mitochondrial cyclin B1 in the oxidative damage associated with neurological disorders.

110 A gold-standard oxidative damage biomarker [heme oxidase 1 (HO-1)] suppo

111 ne levels, total reactive oxygen species and oxidative damage biomarker levels, and of serum IgE leve

112 ly, PS significantly decreased the levels of oxidative damage biomarkers, malondialdehyde (MDA), 4-hy

113 The heart is sensitive to oxidative damage but a global view on how the cardiac pr

114 his increased ROS production not only causes oxidative damage but also ultimately induces an oxidativ

115 sms evolved to protect against iron-mediated oxidative damage, but the molecular details of these pro

116 tein haptoglobin (Hp) protects the host from oxidative damage by clearing hemoglobin that has leaked

117 f 3-bromotyrosine as a specific biomarker of oxidative damage by HOBr warrants further investigation

118 SA counteracted the alkaline stress-induced oxidative damage by lowering the accumulation of reactiv

119 ing a mechanism for protection against photo-oxidative damage by minimizing the tissue exposure to de

120 ly increased Caco-2 cells resistance towards oxidative damage by recovering the cell viability and in

121 (FFA) levels (P < 0.001) and ameliorated the oxidative damage by reducing malondialdehyde (MDA) conce

122 Repair of virally induced oxidative damage by the DNA MMR pathway not only allowed

123 ings indicate that a strain's sensitivity to oxidative damage can be elucidated from the structural p

124 w other proteins with only mild or localized oxidative damage can be targeted for degradation without

125 e, loss of estrogen signaling contributes to oxidative damage caused by low levels of PGC1A in liver,

126 ne hallmark of aging cells is an increase in oxidative damage caused by reactive oxygen species (ROS)

127 Oxidative damage caused by reactive oxygen species has b

128 ectarivores use nectar sugar to mitigate the oxidative damage caused by the muscular demands of fligh

129 The labile iron-mediated oxidative damage caused by UVA to mitochondria leads to

130 The effect of apple phenolics on the oxidative damage caused to myofibrillar proteins by an i

131 on of TRIM21 in mice confers protection from oxidative damages caused by arsenic-induced liver insult

132 Interestingly, infected chub exhibited lower oxidative damage compared to uninfected fish, irrespecti

133 PrimPol to study lesion bypass synthesis on oxidative damage-containing DNA templates.

134 data are consistent with the hypothesis that oxidative damage contributes to chemotherapy-associated

135 nescence in vitro and accumulate products of oxidative damage, despite activation of the redox respon

136 Evidence of subsequent oxidative damage due to chronic exposure was found throu

137 likely coordinate photosynthesis and prevent oxidative damage during cold exposure.

138 chlorophyll synthesis genes to prevent photo-oxidative damage during de-etiolation.

139 breed contain candidate genes for combating oxidative damage during exercise, and within the "Straig

140 decreases in flavonol pigments, which reduce oxidative damage during extremes of abiotic stress, a pa

141 n complexes in biological fluids that resist oxidative damage during heme-driven inflammation.

142 nd thereby shielding protection of UFAs from oxidative damage during microencapsulation process.

143 ycosylases protect mitochondrial DNA against oxidative damage during neural crest differentiation.

144 in the gelation media allowed decreasing the oxidative damage during storage in comparison to the fre

145 valuable tool for the quantification of ROS oxidative damage during winemaking.

146 results suggest that, with the exception of oxidative damage, endogenously induced DNA damage does n

147 xercise appear to be a transient increase in oxidative damage followed by redox-sensitive adaptations

148 olony health and productivity, and levels of oxidative damage for individual bees.

149 al and fungal pathogens against H2O2-induced oxidative damage from host immune responses.

150 , suggesting that ALT activation may prevent oxidative damage from reaching levels that threaten cell

151 rganic pollutants (POPs) in the induction of oxidative damage in cell structures, this issue has been

152 nstrate the utility of CAP to model membrane oxidative damage in cells and characterise a previously

153 deficient primary glial cultures exacerbated oxidative damage in cultured neurons.

154 dynamics, immune defences, antioxidants and oxidative damage in different tissues vary along the urb

155 long period and was paralleled by decreased oxidative damage in fat and liver.

156 rds aberrations in complement activation and oxidative damage in IPF patients and provides haptoglobi

157 The reduced oxidative damage in JAK2-deficient livers was linked to

158 ngs showed reduced body size, high levels of oxidative damage in lipids and proteins, and a fragile j

159 AP sites to the real-time evaluation of the oxidative damage in living cells.

160 High aerobic performance is linked to oxidative damage in muscles.

161 absence of TERT increases ROS generation and oxidative damage in neurons induced by pathological tau.

162 reases mitochondrial respiration and induces oxidative damage in neurons through mammalian target of

163 eight gain, prevents neuronal death, reduces oxidative damage in neurons, suppresses the decline of m

164 Therefore, increased oxidative damage in older oocytes may be one of the fact

165 ry eicosanoids and may account for increased oxidative damage in pericentral regions in NASH.

166 de (MDA) suggests that Ga stress could cause oxidative damage in plants.

167 can reverse isoprenaline (ISO)-induced renal oxidative damage in rats, a model that mimics SNS overst

168 adiol against kanic acid-induced hippocampal oxidative damage in rats.

169 ministration failed to attenuate age-related oxidative damage in skeletal muscle of old mice or provi

170 collaborate to protect M. smegmatis against oxidative damage in stationary phase.

171 mpair the translation apparatus or may cause oxidative damage in the cell.

172 ts, kynurenine pathway mediators, TXNIP, and oxidative damage in the cerebrum and spleen, including i

173 Defective repair of such oxidative damage in the fertilized oocyte results in the

174 /-) mice had increased inflammation-mediated oxidative damage in the ipsilateral foot and ankle joint

175 o characterize the effects of spaceflight on oxidative damage in the mouse brain and its impact on bl

176 ttractiveness may be costly due to increased oxidative damage in the postmenopausal period.

177 alters gene expression profiles and induces oxidative damage in the retina.

178 of double-strand breaks in the DNA, and (2) oxidative damage in the sperm DNA.

179 dentified as a unique approach in preventing oxidative damage in these molecules, which had been link

180 on rate possibly through the accumulation of oxidative damage, in particular in the mitochondrial gen

181 ddition, rearing conditions affect levels of oxidative damage incurred as adults.

182 in cell model, increasing protection against oxidative damage induced by H(2)O(2).

183 em II (PSII) are highly susceptible to photo-oxidative damage induced by high-fluence or fluctuating

184 Besides protecting against the oxidative damage induced by paraquat treatment, our data

185 The leading cause of mutation due to oxidative damage is 8-oxo-2'-deoxyguanosine (8-oxoG) mis

186 nderstand AD aetiology and pathogenesis, but oxidative damage is a key component.

187 nsequence of ischemia-reperfusion injury and oxidative damage is a leading cause of permanent disabil

188 Our work shows that (i) blood lipid oxidative damage is associated with observable clinical

189 Oxidative damage is considered to play a central role in

190 The accumulation of oxidative damage is strongly linked to age-dependent dec

191 mitochondrial dysfunction and an increase in oxidative damage, leading to retinal ganglion cell (RGC)

192 se in endogenous antioxidant defences, while oxidative damage levels were mostly not affected or even

193 acilitates fatty acid oxidation, counteracts oxidative damage, maintains mitochondrial sirtuin activi

194 , increased 8-hydroxyguanosine abundance (an oxidative damage marker), and overexpression of the necr

195 r acellular capillaries and were stained for oxidative damage markers using nitrotyrosine immunohisto

196 analyzed immunofluorescence distribution of oxidative damage markers, and of SOD2 (superoxide dismut

197 omic-level physicochemical properties and of oxidative damage mechanisms for multiple strains in a sp

198 gh the NRF2 transcription factor, preventing oxidative damage, mitochondrial DNA release, and DNA sen

199 However, neither oxidative damage nor oxidized glutathione differed betwe

200 cardiac damage markers for fibrosis (Ctgf), oxidative damage (Nox4) and haemodynamic load (Nppa).

201 In diabetes, oxidative damage occurs when there is an imbalance betwe

202 h pathways appear to play major roles in the oxidative damage of [FeFe]-hydrogenases under electron-d

203 Oxidative damage of DNA may contribute to the pathophysi

204 phils expressing membrane PR3 may potentiate oxidative damage of endothelial cells and promote the sy

205 Our results show that oxidative damage of even single residues at the interfac

206 Here, we present the first study on oxidative damage of human telomere G-quadruplexes withou

207 esent in tobacco smoke not only cause direct oxidative damage of lung proteins, contributing to the m

208 t from external invaders or amyloid but from oxidative damage of our own genes.

209 metabolites and produced in large amounts by oxidative damage of the CO2 acceptor molecule ribulose 1

210 However, it did not lead to oxidative damage of the enriched batches or affect the m

211 y of 1alpha and 1beta with stability against oxidative damage of the ligand via aliphatic C-H oxidati

212 cteria by binding to the membrane, promoting oxidative damage of the lipids, which then disrupts the

213 BA or proline could alleviate stress-induced oxidative damage of the mutant and partially rescue its

214 l substrate binding leading to autocatalytic oxidative damage of these variants.

215 low density lipoprotein (LDL) oxidation and oxidative damage of vector DNA.

216 imuli, but if left unchecked, it can inflict oxidative damage on all types of biological macromolecul

217 these organelles particularly susceptible to oxidative damage on exposure to ultraviolet A (UVA, 320-

218 ssue, which switches on the early process of oxidative damages on heart rapidly through a ROS-p38 MAP

219 whether nestlings with either low levels of oxidative damage or high levels of antioxidant protectio

220 none mesylate fails to attenuate age-related oxidative damage or rescue the loss of muscle mass and f

221 ROS can cause oxidative damage particularly to proteins.

222 in itself at Lys(11) and Lys(48) rather than oxidative damage per se.

223 Both processes might contribute to prevent oxidative damage, potentially explaining the negative re

224 , it protects neuronal SH-SY5Y cells against oxidative damage promoted by glutamate, decreasing react

225 A recently proposed oxidative damage protection mechanism in proteins relies

226 Here, we measured oxidative damage (protein carbonyls, 8-OHdG) and antioxi

227 tDNA mutations are not the results of direct oxidative damage, rather are caused, at least in part, b

228 The thousands of mutations caused by oxidative damage recovered across the entire genome reve

229 ed decreased antioxidant activity, increased oxidative damage, reduced longevity, and oxidative stres

230 le of 8-oxo-dG and 8-oxo-dA in AMD and other oxidative damage-related diseases in humans.

231 ent cells, mitochondrial common deletion and oxidative damage repair capacity in U2OS cells were foun

232 , biocatalysis, and signaling as well as for oxidative damage repair.

233 et radiation (UVR) and radiation-independent oxidative damage, requires specific DNA-damage response

234 ncreased insulin production and protect from oxidative damage, respectively.

235 echanism is insufficient to prevent neuronal oxidative damage, resulting in chronic deficits in worki

236 Among these factors, oxidative damage seems to initiate the injury.

237 stingly, deletion of CSB's UBD gives rise to oxidative damage sensitivity as well, while CSB DeltaUBD

238 rategies to enhance respiration and initiate oxidative damage should improve tuberculosis chemotherap

239 Instead, Neil-deficiency results in oxidative damage specific to mitochondrial DNA, which tr

240 to become sensitized to agents that increase oxidative damage such as ionizing radiation.

241 1 provides protection against H2 O2 -induced oxidative damage, suggesting potential future applicatio

242 dox balance and increases RPE sensitivity to oxidative damage, suggesting that deficiencies of reduct

243 fatty acid accumulated in NAFLD, causes more oxidative damage than other free fatty acids such as pal

244 asthmatic lungs displayed three hallmarks of oxidative damage that render it NO-insensitive, and iden

245 ve burst and to protect Caco-2 cells against oxidative damage, the peel extract being the most effici

246 s unprotected peptides from Cu(II) -mediated oxidative damage through the formation of an insoluble C

247 apparatus to the client proteins preventing oxidative damage to [4Fe-4S] clusters.

248 essive reactive oxygen species (ROS) induces oxidative damage to cellular constituents, ultimately le

249 Compared with the CD, the PD reduced oxidative damage to DNA (mean: -3.5%; 95% CI: -8.07%, 1.

250 Chronic pistachio consumption reduces oxidative damage to DNA and increases the gene expressio

251 Lessening oxidative damage to DNA and telomerase expression throug

252 Lymphocytes exposed to oxidative damage to DNA at 8:00 AM display lower accumul

253 Oxidative damage to DNA is a threat to the genomic integ

254 reased, probably owing, at least in part, to oxidative damage to enzymes involved in glycolysis, the

255 lly demanding, and both factors can increase oxidative damage to essential biomolecules, accelerating

256 ective than the HRGS system in promoting the oxidative damage to food proteins.

257 ited by the excision repair protein OGG1 for oxidative damage to interact with the damage-induced bas

258 ed smaller body sizes, as well as the higher oxidative damage to lipids, contributed to the higher ch

259 tioxidant defense enzyme active in repairing oxidative damage to lipids, is a key inhibitor of ferrop

260 ular disease through direct and irreversible oxidative damage to macromolecules, as well as disruptio

261 ccinate accumulation during ischemia lead to oxidative damage to mammalian organs upon reperfusion.

262 Oxidative damage to mitochondria (MT) is a major mechani

263 Oxidative damage to mitochondrial DNA (mtDNA) in the ret

264 es in cell function, but the contribution of oxidative damage to morbidity is still debated.

265 endent form of necrotic cell death marked by oxidative damage to phospholipids(1,2).

266 This is crucial to prevent photo-oxidative damage to photosystem II (PSII) and is control

267 nment, based on known chemical mechanisms of oxidative damage to protein groups, defined by their loc

268 HDM challenge increased lung levels of oxidative damage to proteins (3-nitrotyrosine), lipids (

269 Such oxidative damage to proteins may lead to the formation o

270 d between baseline corticosterone and plasma oxidative damage to proteins.

271 Oxidative damage to renal tubular epithelial cells is a

272 w here that RPA is limiting for NER and that oxidative damage to RPA compromises NER capability.

273 Photoactivation causes oxidative damage to specific histidine residues in the k

274 UV-A exposed PG caused oxidative damage to the cell and significantly higher da

275 e pathway (PPP), resulting in a reduction in oxidative damage to the flight muscles.

276 Oxidative damage to the genome can yield the base 8-oxo-

277 sorption of too much light can lead to photo-oxidative damage to the photosynthetic apparatus and sus

278 es, as well as protective mechanisms against oxidative damage to the termite gut and its microbiota.

279 We found that sugar-fed moths had lower oxidative damage to their flight muscle membranes than u

280 During assembly of PSII, oxidative damage to vulnerable assembly intermediate com

281 nts and structural trajectories arising from oxidative damages to DNA backbone is of crucial importan

282 ory effects on the oil metabolisms to avoide oxidative damages to the imbibed seeds, and the seed she

283 ing, reading and erasing mechanism in place, oxidative 'damage' to DNA might be relabeled as 'epigene

284 the protection of C. reinhardtii from photo-oxidative damage under high light conditions, is hyperme

285 As proteins are one of the main targets of oxidative damage, understanding how the genetic changes

286 ormalities with repressed fuel oxidation and oxidative damage upon high fat diet (HFD).

287 a at low temperatures without suffering from oxidative damage upon reoxygenation, but the mechanisms

288 nerates reactive oxygen species and elevated oxidative damage was corroborated by higher malondialdeh

289 Oxidative damage was observed in livers from Ppargc1a(f/

290 ort chain activities, and persistent protein oxidative damage were evident in the muscle of survivors

291 models, mitochondrial H(2)O(2) emission and oxidative damage were greater in Taz(KD) than in wild-ty

292 together, since hippocampal inflammation and oxidative damage were partially prevented by EWH, our re

293 Levels of oxidative damage were unchanged (liver) or reduced (brai

294 ges (hypertrophy, fibrosis, inflammation and oxidative damage) were assessed by echocardiography and

295 By contrast, NDAN individuals display low oxidative damage, which is associated with high levels o

296 nuclear DNA (nDNA), mtDNA is more exposed to oxidative damage, which may result in double-strand brea

297 It predicts observed increases in cellular oxidative damage with age and provides a mechanism for t

298 Mitochondrial dysfunction and oxidative damage with age are hypothesized to increase r

299 sphorylation and the associated increment of oxidative damage, with consequent inhibition of cell act

300 etwork that combats potentially carcinogenic oxidative damage yet also protects cancer cells from oxi