ライフサイエンスコーパス: reactive oxygen species

1 ial function trigger release of DNA damaging reactive oxygen species.

2 r but through a mechanism that produce fewer reactive oxygen species.

3 euronal metabolism and detoxify ammonium and reactive oxygen species.

4 functional mitochondria, producing excessive reactive oxygen species.

5 nted for light penetration and scavenging of reactive oxygen species.

6 nt delivery of current without production of reactive oxygen species.

7 urthermore, EBS is an excellent scavenger of reactive oxygen species.

8 cle, the byproducts of which are deleterious reactive oxygen species.

9 alternative, (17)O-enriched sources such as reactive oxygen species.

10 n cellular redox homeostasis and detoxifying reactive oxygen species.

11 ased the propensity of CeO(2) NPs to produce reactive oxygen species.

12 ductive pathways including the production of reactive oxygen species.

13 protection adjustment against water loss and reactive oxygen species.

14 col/vegetable glycerin ratio, carbonyls, and reactive oxygen species.

15 air of double-strand breaks (DSBs) caused by reactive oxygen species.

16 ools, thereby allowing toxic accumulation of reactive oxygen species.

17 and fusion of mitochondria and production of reactive oxygen species.

18 s, reduced aerobic respiration and increased reactive oxygen species.

19 s poor photosensitizers for (1)O(2) or other reactive oxygen species.

20 NA can be damaged by spontaneous hydrolysis, reactive oxygen species, aberrant cellular metabolism or

21 hypothesized that an increase in calcium and reactive oxygen species activate a large conductance cha

22 lular calcium concentration, or formation of reactive oxygen species, all of which have been associat

23 ith an increased generation of mitochondrial reactive oxygen species along with increased prevalence

24 ndings underscore prolific marine sources of reactive oxygen species and a complex and dynamic oxygen

25 sis factor and interleukin-1alpha stimulated reactive oxygen species and a large repertoire of cytoki

26 ed early PTI responses such as generation of reactive oxygen species and activation of mitogen-activa

27 Mechanistically, enhanced production of reactive oxygen species and activation of NF-kappaB are

28 n in HFD-fed mice through neutrophil-derived reactive oxygen species and activation of stress kinases

29 Immediately following IR, reactive oxygen species and apoptotic markers were signi

30 uncovered that chitin-induced production of reactive oxygen species and callose depends on specific

31 energy as heat and limits the production of reactive oxygen species and cellular damage.

32 cts of alphaSyn that form in the presence of reactive oxygen species and cytochrome c, a proapoptotic

33 citation, the myocardium exhibited increased reactive oxygen species and evidence of mitochondrial in

34 ial cell division, and trigger production of reactive oxygen species and increased abundance of oxida

35 anoplastics induced a higher accumulation of reactive oxygen species and inhibited plant growth and s

36 dation of the substrates, which is caused by reactive oxygen species and leads to a mixture of produc

37 and resulted in generation of mitochondrial reactive oxygen species and p38 MAPK-dependent upregulat

38 cell maintenance, defence against excessive reactive oxygen species and protection from chemotherapy

39 Importantly, the production of reactive oxygen species and the subsequent stress respon

40 The inter-relationship between epithelial reactive oxygen species and tumor-promoting microbiota r

41 y kills resistant cells via intrinsic lethal reactive oxygen species and unresolved DNA damage and li

42 sed into the environment through exposure to reactive oxygen species and/or ultraviolet irradiation.

43 nactivated antioxidative pathways, increased reactive oxygen species, and apoptosis were observed in

44 nerative diseases, including neural fibrils, reactive oxygen species, and cofilin-actin rods, present

45 fects, decreased survival factors, increased reactive oxygen species, and excessive neuroinflammation

46 rs in the tumor microenvironment (acidic pH, reactive oxygen species, and glutathione).

47 ATRA)-induced differentiation, generation of reactive oxygen species, and mitochondrial dysfunction.

48 levels mitigated allergen-induced apoptosis, reactive oxygen species, and neutrophil infiltration.

49 mitochondrial depolarization, generation of reactive oxygen species, and PARP cleavage.

50 w activated the NLRP3 inflammasome through a reactive oxygen species- and/or cathepsin-dependent mech

51 lar processes related to endothelial damage (reactive oxygen species, apoptosis, and senescence) and

52 Reactive oxygen species are centrally involved in the pa

53 Hyperglycemia -induced reactive oxygen species are key mediators of cardiac dys

54 Reactive oxygen species are key players in biotic and ab

55 Reactive oxygen species are linked to the induction of o

56 Our data indicate that reactive oxygen species are the key mediators of the bac

57 lism and ATP production, such as calcium and reactive oxygen species, are also key regulators of mito

58 ial dysfunction, especially in mitochondrial reactive oxygen species-associated oxidative stress, rem

59 C(18)-SMe(2)(+)), also induces production of reactive oxygen species at the level of respiratory comp

60 epend on MKK1 for suppression of PTI-induced reactive oxygen species burst, while the full virulence

61 ynergistically with doxorubicin by producing reactive oxygen species but also provide catechol moieti

62 f the antioxidant alpha-tocopherol decreased reactive oxygen species but had no significant effects o

63 720 decreased phagocytosis and production of reactive oxygen species by macrophages, a phenotype reca

64 s in metabolite levels and the generation of reactive oxygen species by mitochondria.

65 ulates OXPHOS function and the production of reactive oxygen species by modulating the fluidity of th

66 via invasive cerebrospinal fluid assays, and reactive oxygen species can be fleeting and challenging

67 lent (an H atom), such that a water-soluble "reactive oxygen species" can be used to quench a lipid-s

68 Production of reactive oxygen species caused by dysregulated endotheli

69 tolerance, low adiponectin levels, increased reactive oxygen species damage, and elevated GDF15 and F

70 ATC CM-induced NET production occurred in a reactive oxygen species-dependent and cell death-indepen

71 ionic homeostasis, osmotic homeostasis, and reactive oxygen species detoxification.

72 Relative amounts of apoplastic reactive oxygen species differed between lignified cell

73 e in response to the increased generation of reactive oxygen species during contraction.

74 ibitor TH588 potentiates the accumulation of reactive oxygen species during mitosis in cancer by dist

75 collagen produces radicals and subsequently reactive oxygen species, essential biological signaling

76 NA photosensitizer can controllably generate reactive oxygen species for targeted cell regulation.

77 oplasts remains oxidized, which can suppress reactive oxygen species formation.

78 port chain, also becomes altered, generating reactive oxygen species from Complexes I and III.

79 s a selective modulator of the production of reactive oxygen species from mitochondrial complex I tha

80 Reactive oxygen species generate the genotoxic 8-oxoguan

81 Reactive oxygen species generated by respiratory burst a

82 was not due to MANF-mediated protection from reactive oxygen species generated during reperfusion.

83 site IQ electron leak, decreased myocardial reactive oxygen species generation and improved postcard

84 ive damage promoted by glutamate, decreasing reactive oxygen species generation and preserving cell r

85 ial injury, specifically reperfusion-induced reactive oxygen species generation at electron transport

86 also negatively regulates pathways governing reactive oxygen species generation by neutrophil NOX2 NA

87 ron leak, which inhibits complex I-dependent reactive oxygen species generation by suppression of sit

88 rgen challenge contributes to the apoptosis, reactive oxygen species generation, and neutrophilic inf

89 substrate/product/substrate) associated with reactive oxygen species generation.

90 tered mitochondrial respiratory function and reactive oxygen species generation.

91 ic reprogramming, mitochondrial dysfunction, reactive-oxygen species generation, and DNA-replicative

92 lysis revealed that cellular uptake and ROS (reactive oxygen species) generation efficiency of water-

93 ate accumulation and increased production of reactive oxygen species, highlighting fumarate as an onc

94 LBL favored reactive oxygen species homeostasis and metabolic activi

95 was employed to easily synthesize the highly reactive oxygen species (hROS)- and trypsin-responsive 1

96 The reactive oxygen species hydrogen peroxide and the polyun

97 trolyte decomposition through reactions with reactive oxygen species identified through this work hav

98 n and membrane potential, and an increase of reactive oxygen species in A549 cells and fibroblasts, b

99 and function resulting in elevated levels of reactive oxygen species in glia in flies and murine Schw

100 bitor CB-839 resulted in robust induction of reactive oxygen species in high GLS-expressing but not i

101 y apoptosis and also significantly increased reactive oxygen species in the lung.

102 NADPH oxidase that produces highly oxidizing reactive oxygen species in the lysosome combined with a

103 R1-like), which triggers the accumulation of reactive oxygen species in tobacco phloem, thereby suppr

104 Hydrogen peroxide (H(2)O(2)) is a major reactive oxygen species in unicellular and multicellular

105 d aPS contributed to efficient generation of reactive oxygen species including singlet oxygen and sup

106 iation, Zr-TBB efficiently generates various reactive oxygen species, including singlet oxygen, super

107 On the other hand, a reactive oxygen species-induced photoinhibitory NPQ comp

108 eased immune cell infiltration, synthesis of reactive oxygen species, inflammatory chemokines, cytoki

109 the inherited ability of TiO(2) to generate reactive oxygen species is used as a strategy to avoid a

110 ependent calcium entry and the production of reactive oxygen species, leading to activation of caspas

111 trophil and monocyte activation can generate reactive oxygen species, leading to host tissue damage.

112 ial, adenosine 5'-triphosphate contents, and reactive oxygen species levels in hepatoma cells (Hepa1-

113 enine dinucleotide phosphate levels, reduced reactive oxygen species levels, improved mitochondrial d

114 s to prevent the generation of mitochondrial reactive oxygen species (mROS): hexokinases I and II and

115 myotubes to IL-6 increased the mitochondrial reactive oxygen species (mtROS) production and oxygen co

116 ell subsets, bacterial uptake and clearance, reactive oxygen species, nitrite production, autophagy,

117 dation at C674 would modulate the effects of reactive oxygen species on mitochondrial calcium and mit

118 ligate anaerobiosis is imposed by endogenous reactive oxygen species or by molecular oxygen itself.

119 out the mediation of singlet oxygen or other reactive oxygen species, phototoxicity within the deeper

120 n inside-to-outside oxidation pathway, where reactive oxygen species played an important role.

121 hanistically, our data strongly suggest that reactive oxygen species produced by NQO1-dependent redox

122 Therefore, we provide evidence that reactive oxygen species produced by the photosynthetic a

123 (FAP-alpha) were able to block CD44-mediated reactive oxygen species production and cell death, but n

124 Dual inhibition resulted in reduced cellular reactive oxygen species production compared with negativ

125 precipitates cardiomyocyte apoptosis through reactive oxygen species production in an aryl hydrocarbo

126 we observed a gene-dose-specific increase in reactive oxygen species production in G2435R-RYR1 muscle

127 e cell fluorescent imaging, cellular ATP and reactive oxygen species production quantification.

128 accumulated more Ca(2+) and showed increased reactive oxygen species production when compared with in

129 in neutrophil extracellular trap formation, reactive oxygen species production, and released human n

130 mal acidification and enhanced intracellular reactive oxygen species production, consequently limitin

131 g on ectotherm ageing through its effects on reactive oxygen species production, oxidative damage, an

132 showed lower fungal clearance and defective reactive oxygen species production.

133 ivation, as well as downstream intracellular reactive oxygen species production.

134 manner and was associated with mitochondrial reactive oxygen species production; the NETs contained m

135 oton extrusion, pH regulation, production of reactive oxygen species, proliferation of cancer cells,

136 ne or antimycin A, making the involvement of reactive oxygen species rather unlikely.

137 cell lysates, where relative amounts of free reactive oxygen species, rather than cytochrome c, are r

138 nuclear factor kappaB-dependent induction of reactive oxygen species, reactive nitrogen species, and

139 These OH precursors include reactive oxygen species, reactive nitrogen species, and

140 rtantly, blocking glycogen synthesis permits reactive oxygen species (ROS) accumulation and AMPK acti

141 Contrary to common belief, reactive oxygen species (ROS) accumulation did not appea

142 s at high levels, and mitochondrial NADH and reactive oxygen species (ROS) accumulation during hypoxi

143 nsity and increased DNA damage suggestive of reactive oxygen species (ROS) activity.

144 eceptor pathway controls the distribution of reactive oxygen species (ROS) along the developmental zo

145 t sleep deprivation leads to accumulation of reactive oxygen species (ROS) and consequent oxidative s

146 describe a correlation between generation of reactive oxygen species (ROS) and damage of the basement

147 sinophils was dependent on the production of reactive oxygen species (ROS) and downstream phosphoryla

148 tyl partially suppresses plant production of reactive oxygen species (ROS) and enhances symbiont colo

149 Because they can react with oxygen to form reactive oxygen species (ROS) and inflict cellular damag

150 t proceeds, numerous gene pathways linked to reactive oxygen species (ROS) and oxidative stress exhib

151 Elevated reactive oxygen species (ROS) and oxidative stress have

152 taBbOhmm cells and affected by intracellular reactive oxygen species (ROS) and oxygen levels.

153 Ps) which include intracellular formation of reactive oxygen species (ROS) and surface exposure of ca

154 hich compartmentalize pathways that generate reactive oxygen species (ROS) and thus protect against c

155 es during infection result in an increase in reactive oxygen species (ROS) and toxic by-products of e

156 Clearance and adaptation to reactive oxygen species (ROS) are crucial for cell survi

157 poxic tumors since lower levels of cytotoxic reactive oxygen species (ROS) are generated in regions o

158 Increased levels of intracellular reactive oxygen species (ROS) are linked to proliferatio

159 Reactive oxygen species (ROS) are physiological mediator

160 tative RT-PCR, promoter-reporter assays, and reactive oxygen species (ROS) assays, we demonstrate tha

161 ion up-regulates the intracellular levels of reactive oxygen species (ROS) by inhibiting ROS scavengi

162 t this may play a role in the development of reactive oxygen species (ROS) damage caused by nutrient

163 ay represent an attractive target to exploit reactive oxygen species (ROS) elevation in cancer.

164 d endothelium-dependent vasodilation through reactive oxygen species (ROS) formation.

165 consumption relative to mammals, increasing reactive oxygen species (ROS) formation.

166 nsin II (Ang II)-induced AAA by facilitating reactive oxygen species (ROS) formation.

167 Here, we show that reactive oxygen species (ROS) function as signaling mole

168 autophagy and metabolic reprogramming during reactive oxygen species (ROS) generation, and how ROS pr

169 eakage from the bacterial cells by virtue of reactive oxygen species (ROS) generation.

170 dynamic therapy (CDT), resulting in enhanced reactive oxygen species (ROS) generation.

171 Oxygen and reactive oxygen species (ROS) have been co-opted during

172 It is becoming increasingly evident that reactive oxygen species (ROS) have critical roles as "se

173 Mac1p additionally controls reactive oxygen species (ROS) homeostasis by repressing

174 eaks and functions as an important sensor of reactive oxygen species (ROS) in human cells.

175 Mitochondria are the main source of reactive oxygen species (ROS) in neurons and they contro

176 induce endoplasmic reticulum (ER) stress by reactive oxygen species (ROS) in PCa cells.

177 enzymes (NOXs), namely NOX1, and NOX-derived reactive oxygen species (ROS) in radiation-induced GEnC

178 Here, we show that conditions that generate reactive oxygen species (ROS) in the chloroplast, includ

179 to neurons and a rapid increase in levels of reactive oxygen species (ROS) in the larval brain.

180 e structure helped in the photogeneration of reactive oxygen species (ROS) in water.

181 Reactive oxygen species (ROS) increased in human donor l

182 biological evaluation of a quinazolinedione reactive oxygen species (ROS) inducer, QD394, with signi

183 Reactive oxygen species (ROS) inflict multiple types of

184 Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution

185 xidation of cysteine thiols by physiological reactive oxygen species (ROS) initiates thermogenesis in

186 Excessive production of reactive oxygen species (ROS) is considered a principal

187 Production of reactive oxygen species (ROS) is critical for successful

188 Since reactive oxygen species (ROS) is vitally involved in tis

189 udy, we demonstrate that the accumulation of reactive oxygen species (ROS) late after DENV infection

190 ls, vs. non-cancer cells, elevates levels of reactive oxygen species (ROS) leading to higher oxidativ

191 s in ischemic cells produces high amounts of reactive oxygen species (ROS) leading to myocardial tiss

192 IFN)-gamma expression in mouse BM, decreased reactive oxygen species (ROS) level in the irradiated mo

193 om a PBMT-mediated increase of intracellular reactive oxygen species (ROS) levels and Src protein pho

194 fects are mediated by reducing mitochondrial reactive oxygen species (ROS) levels and upregulating au

195 As results, cellular ATP and reactive oxygen species (ROS) levels are elevated, mTOR

196 methyl Methylene Blue increased by 5000% the reactive oxygen species (ROS) levels in N. caninum tachy

197 eterious effects of protein carbonylation by reactive oxygen species (ROS) make understanding molecul

198 Reactive oxygen species (ROS) oxidize nucleotide triphos

199 Reactive oxygen species (ROS) play a pivotal role in man

200 Reactive oxygen species (ROS) play important roles in ti

201 We are exposed to endogenous reactive oxygen species (ROS) produced during normal aer

202 Singlet oxygen ((1)O(2)), the major reactive oxygen species (ROS) produced in chloroplasts,

203 d tumor cells, thereby resulting in enhanced reactive oxygen species (ROS) production and downstream

204 ination inhibited autophagic flux, increased reactive oxygen species (ROS) production and mitochondri

205 the DWF or BZR1 genes altered the timing of reactive oxygen species (ROS) production and programmed

206 stically, Kras(G12D)-RAC1 activation induces reactive oxygen species (ROS) production causing NLRP3 i

207 shifting glycolytic pathways and inhibiting reactive oxygen species (ROS) production in PM-activated

208 rradiation of mouse corneas with UVA induced reactive oxygen species (ROS) production in the aqueous

209 n in mice; however, K. pneumoniae-stimulated reactive oxygen species (ROS) production in vitro was ab

210 integrity and molecular mechanisms involving reactive oxygen species (ROS) production, and lipid and

211 hagocytosis, degranulation, leukotriene, and reactive oxygen species (ROS) production, rendering ORAI

212 on transition, which also influences ATP and reactive oxygen species (ROS) production.

213 UVC also induced reactive oxygen species (ROS) productions at immediate (

214 al adenocarcinoma (PDAC) model, we show that reactive oxygen species (ROS) regulation by TIGAR suppor

215 oxidase assembly inhibitor apocynin, and the reactive oxygen species (ROS) scavenger N-acetylcysteine

216 Metabolites associated with reactive oxygen species (ROS) scavenging including malon

217 have used to analyze differences between the reactive oxygen species (ROS) sensitivity of the proteom

218 We previously identified that reactive oxygen species (ROS) signal to SI-PCD.

219 Recent studies highlighted a key role for reactive oxygen species (ROS) signaling in mediating sys

220 how fast and efficient they induce systemic reactive oxygen species (ROS) signals; transcriptomic, h

221 The NADPH oxidase complex (NOX) produces reactive oxygen species (ROS) that are among the key mar

222 Hydrogen peroxide (H(2)O(2)) is a reactive oxygen species (ROS) that mediates essential si

223 LDHA binds to NADH and promotes reactive oxygen species (ROS) to induce catabolic change

224 rst time, we show that TiO(2) can accumulate reactive oxygen species (ROS) under daylight irradiation

225 ers and then oxidized to death by generating reactive oxygen species (ROS) under light irradiation.

226 ycolysis, and intracellular concentration of reactive oxygen species (ROS) were reduced by ganoderic

227 rowth, dye-decolorizing peroxidase (DyP) and reactive oxygen species (ROS) were significantly correla

228 g clones both deployed a lower production of reactive oxygen species (ROS) when exposed to As salts a

229 lutamine catabolism from generating damaging reactive oxygen species (ROS) when TCA cycle activity ex

230 n, TMNP causes the accelerated generation of reactive oxygen species (ROS) which subsequently damages

231 regulation, calcium signaling, generation of reactive oxygen species (ROS), and additional determinan

232 nd reduced intracellular lipid peroxidation, reactive oxygen species (ROS), and cytokine release (P <

233 n that together with low pH, high amounts of reactive oxygen species (ROS), and increased adenosine l

234 tochondria are known to be a major source of reactive oxygen species (ROS), and oxidative stress is t

235 l role in cellular metabolism, generation of reactive oxygen species (ROS), and the initiation of apo

236 dria, the consequent increased production of reactive oxygen species (ROS), and ultimately oxidative

237 Previously, we showed that overproduction of reactive oxygen species (ROS), arising from constitutive

238 including increased activated caspase-3 and reactive oxygen species (ROS), autophagy dysfunction, an

239 age caused by glial and neuronally generated reactive oxygen species (ROS), but that in later life th

240 Reactive oxygen species (ROS), cellular triglyceride (TG

241 on of N-acetylcysteine (NAC), a scavenger of reactive oxygen species (ROS), diminished the morphologi

242 These include calcium, reactive oxygen species (ROS), hydraulic and electric wa

243 Diverse stresses, including reactive oxygen species (ROS), ionizing radiation, and c

244 ide anion (O(2) (.-) ), the primary cellular reactive oxygen species (ROS), is implicated in various

245 n attributed to the AMP sensitizing cells to reactive oxygen species (ROS), making them more suscepti

246 Reactive oxygen species (ROS), mitochondrial dysfunction

247 drial membrane potential and accumulation of reactive oxygen species (ROS), resulting in the differen

248 neration of NADPH oxidase 2 (NOX2)-dependent reactive oxygen species (ROS), signals we term X-ROS.

249 The levels of reactive oxygen species (ROS), the epigenetic state (H3K

250 ited increased labile iron and production of reactive oxygen species (ROS), were hypersensitive to ir

251 regions by specific demethylase(s) generates reactive oxygen species (ROS), which oxidize DNA and oth

252 aracterized by inflammation and increases in reactive oxygen species (ROS), which produce a highly ox

253 these inflammatory responses is the burst of reactive oxygen species (ROS), with hydrogen peroxide (H

254 against oxidative stress while serving as a reactive oxygen species (ROS)-activated persulfide donor

255 ble poly(lactic-co-glycolic acid) (PLGA) and reactive oxygen species (ROS)-degradable poly(propylene

256 Reactive oxygen species (ROS)-dependent production of RO

257 RAD51 and RAD52 fail to localize to sites of reactive oxygen species (ROS)-induced DNA damage.

258 Reactive oxygen species (ROS)-induced oxidative stress h

259 While regenerative signaling by reactive oxygen species (ROS)-induced ROS release (RIRR)

260 a nanoparticles (MONs) containing X-ray- and reactive oxygen species (ROS)-responsive diselenide bond

261 r (EGFR), locally increases the abundance of reactive oxygen species (ROS).

262 toxic and organelle stress, and elevation of reactive oxygen species (ROS).

263 la mediates intense bactericidal activity of reactive oxygen species (ROS).

264 y pathways to manage intracellular levels of reactive oxygen species (ROS).

265 ing their ability to tolerate and metabolise reactive oxygen species (ROS).

266 re A. baumannii viability in the presence of reactive oxygen species (ROS).

267 host environments, including stress posed by reactive oxygen species (ROS).

268 modification of protein cysteine residues by reactive oxygen species (ROS).

269 from the catastrophic accumulation of lipid reactive oxygen species (ROS).

270 iolet radiation (UVA) damages human skin via reactive oxygen species (ROS).

271 hypoxia-inducible factor (HIF) signaling and reactive oxygen species (ROS).

272 ed in neuroinflammation by the generation of reactive oxygen species (ROS).

273 ectly reduce the dissolved oxygen (O(2) ) to reactive oxygen species (ROS).

274 o chilling stress with accumulation of extra reactive oxygen species (ROS).

275 'Reactive oxygen species' (ROS) is an umbrella term for a

276 tumor cell death, associated with increased reactive oxygen species, S-adenosyl-methionine depletion

277 In addition, the reactive oxygen species scavenger glutathione (GSH) was

278 egree to which normalizing mechano-activated reactive oxygen species signals can prevent calcium-depe

279 diastolic stretch to NADPH oxidase 2-derived reactive oxygen species signals that regulate calcium sp

280 domain is responsible for the Fls3-sustained reactive oxygen species, suggesting involvement of multi

281 ance is critical to prevent the formation of reactive oxygen species that can lead to cell death.

282 from its potential to catalyze formation of reactive oxygen species that, in addition to causing dam

283 chondria, which results in the production of reactive oxygen species, the activation of NF-kappaB and

284 plays an important role in the resistance to reactive oxygen species through the regulation of mangan

285 ant plants responded with elevated levels of reactive oxygen species to MAMP treatment, a negative re

286 e, we found evidence for the contribution of reactive oxygen species to NCU(IV) reoxidation.

287 nes, in stromal cells elevates production of reactive oxygen species, triggers an inflammatory respon

288 rdous, as cysteine promotes the formation of reactive oxygen species, triggers sulfide production and

289 atively regulates autophagy independently of reactive oxygen species via an unknown mechanism.

290 on of the network linked to the synthesis of reactive oxygen species was associated with the escalate

291 ing mitochondrial dysfunction in response to reactive oxygen species, we hypothesized that SERCA oxid

292 Further, reactive oxygen species were produced in both endoperoxi

293 ycolysis and the generation of mitochondrial reactive oxygen species were sufficient to induce necrop

294 ukin-1beta, tumor necrosis factor-alpha, and reactive oxygen species when compared with Sham + Sp mic

295 served that reducing serum (starved) induced reactive oxygen species which provided an early oxidativ

296 ydrogen peroxide and minimize the downstream reactive oxygen species, which are excessively produced

297 vation also caused a substantial increase in reactive oxygen species, which preceded rapid cell death

298 on requiring lipids, energy, but likely also reactive oxygen species, while PTs are especially charac

299 E-Au effectively triggered the generation of reactive oxygen species with an order-of-magnitude reduc

300 global cerebral perfusion (gCBF), increases reactive oxygen species within the brain and leads to ce