ライフサイエンスコーパス: rotenone

1 of substrates and by the complex I inhibitor rotenone.

2 ex I activity from the inhibitory effects of rotenone.

3 tly protected RGCs against 24 hours of 1 muM rotenone.

4 ochondria exposed to the complex I inhibitor rotenone.

5 in activity, also antagonized this action of rotenone.

6 lices were superfused for 30 min with 100 nM rotenone.

7 the induction of this pathway in response to rotenone.

8 st injury from mitochondrial poisons such as rotenone.

9 e in mitochondrial biogenesis in response to rotenone.

10 effect was blocked by NAD(+), forskolin, or rotenone.

11 ation in response to the mitochondrial toxin rotenone.

12 NAD state similar to Complex 1 inhibition by rotenone.

13 dopaminergic neurons were more sensitive to rotenone.

14 sal root ganglion (DRG) neurons treated with rotenone.

15 cells from death as induced by etoposide and rotenone.

16 redox potential high even in the presence of rotenone.

17 50 muM EGCG potentiated the cytotoxicity of rotenone.

18 membrane potential after depolarization with rotenone.

19 and protects against the complex I inhibitor rotenone.

20 e, was substantial but markedly inhibited by rotenone.

21 ce of the mitochondrial complex I inhibitor, rotenone.

22 ns showing a loss of only 13 +/- 4% at 20 nM rotenone.

23 romoter of cyclin D1 was inhibited by NAC or rotenone.

24 , including diphenyleneiodonium chloride and rotenone.

25 ith mitochondrial toxins, such as MPP(+) and rotenone.

26 ved caspase-3 in mice treated with 6-OHDA or rotenone.

27 sed to the mitochondrial complex I inhibitor rotenone.

28 pMLC but only when combined with 2DG and/or rotenone.

29 role in response to complex I inhibition by rotenone.

30 when mitochondrial complex I is inhibited by rotenone.

31 ng mutated alpha-Syn and chronic exposure to rotenone.

32 tress induced by the mitochondrial inhibitor rotenone.

33 sm in SH-SY5Y neuroblastoma cells exposed to rotenone.

34 nvironmental pesticides paraquat, maneb, and rotenone.

35 of PD, we observed that a short exposure to rotenone (0.5 muM) resulted in impaired autophagic flux

36 Treatment of these dopaminergic cells with rotenone (1-50 muM) alone or EGCG (25 or 50 muM) alone c

37 Similarly, larvae chronically exposed to rotenone (10 muM in food) showed age-dependent decline i

38 dministration of the mitochondrial inhibitor rotenone (2 mg/kg/d, 7d, s.c.) induced a marked decrease

39 they 1) occur in the presence of cyanide or rotenone, 2) are suppressed by iodoacetate, 3) are accom

40 partially inhibited by low concentrations of rotenone (25-50 nmol/l).

41 h and was moderately neuroprotective against rotenone (3 muM).

42 ected cells from mitochondrial inhibition by rotenone, 3-nitropropionic acid, antimycin A, and sodium

43 Mitochondrial inhibitors, rotenone, 3-NPA, antimycin, KCN, and oligomycin, exhibit

44 ure to the mitochondrial complex I inhibitor rotenone (30-100 nM; 30 min) causes concentration-depend

45 lysis of ATP, we found that coapplication of rotenone (50 nM), a mitochondrial complex I inhibitor, a

46 carboxamide-1-beta-4-ribofuranoside (AICAR), rotenone (a Complex I inhibitor), dinitrophenol (a mitoc

47 of FAO), but was only partially inhibited by rotenone (a complex I inhibitor).

48 In the present report using rotenone, a complex I inhibitor that causes mitochondria

49 protected cells against toxicity mediated by rotenone, a complex I inhibitor.

50 ructurally similar to CPC, and the pesticide rotenone, a known complex 1 inhibitor, also showed mitoc

51 eived single bilateral intravitreal doses of rotenone, a mitochondrial complex I inhibitor, or roteno

52 ion cell layer (GCL) degeneration induced by rotenone, a mitochondrial complex I inhibitor.

53 determined the capacity of chronic low-dose rotenone, a mitochondrial respiratory chain complex I in

54 We find that rotenone, a pesticide associated with Parkinson's diseas

55 Using rotenone, a potent inhibitor of the mitochondrial enzyme

56 for oxidative phosphorylation on succinate + rotenone, a resistance that is absent in mammalian mitoc

57 inally tagged AIF and AMID were sensitive to rotenone, a well known complex I inhibitor.

58 Systemic administration of rotenone, a widely used pesticide, causes selective dege

59 Systemic administration of rotenone, a widely used pesticide, causes selective dege

60 Exposure to rotenone, a widely used pesticide, has been suggested to

61 The bioenergetic consequences of rotenone addition were quantified by monitoring cell res

62 Rotenone administration in animals induces neurodegenera

63 In naive animals, rotenone administration induced mPTP formation, ROS gene

64 Rotenone also induced increased glutamine utilization fo

65 The mitochondrial Complex I inhibitor rotenone also stimulated glucose transport but it inhibi

66 n inhibitor of the electron transport chain, rotenone, also effectively prevented the ISO-mediated RO

67 stresses, including the mitochondrial poison rotenone, amyloid beta-peptide, hydrogen peroxide, and h

68 In contrast, micromolar CCCP, or rotenone, an electron transport chain blocker, induced a

69 tection against mitochondrial toxins such as rotenone, an environmental PD risk factor.

70 Rotenone, an environmental PD toxin, exhibited much grea

71 ells were incubated with increasing doses of rotenone, an inhibitor of electron transport complex I.

72 rom untreated neurons and neurons exposed to rotenone, an inhibitor of mitochondrial complex I.

73 rmore, the "rescued" cells were resistant to rotenone, an inhibitor of mitochondrial respiration.

74 insensitive to complex I inhibitors such as rotenone and 1-methyl-4-phenylpyridinium ion, known as a

75 specific mitochondrial complex I inhibitors (rotenone and 1-methyl-4-phenylpyridinium or MPP(+)) on s

76 nhibits mitochondrial fission induced by NO, rotenone and Amyloid-beta peptide.

77 eater sensitivity to mitochondrial stressors rotenone and carbonyl cyanide 3-chlorophenylhydrazone, w

78 ced by prolonged treatment with menadione or rotenone and expression of genetic alterations, such as

79 ate-fueled mitochondria was not inhibited by rotenone and likely derived from semiquinone formation a

80 eated with mitochondrial inhibitors, such as rotenone and myxothiazol, provided direct evidence that

81 ited by the mitochondrial complex inhibitors rotenone and oligomycin, but not by the cytosolic phosph

82 anges induced by the Parkinsonian neurotoxin rotenone and opposed by those induced by clioquinol, a c

83 Mechanistic studies indicate that, unlike rotenone and other mitochondrial inhibitors, compound 2

84 (which is insensitive to inhibitors such as rotenone and piericidin A).

85 t with mitochondrial respiratory inhibitors, rotenone and potassium cyanide.

86 owever, the cell death mechanisms induced by rotenone and potential neuroprotective mechanisms agains

87 are resistant to the mitochondrial inhibitor rotenone and proliferate in response to lowered oxygen c

88 The effects of rotenone and sodium nitroprusside (complex inhibitors of

89 Strikingly, coapplication of rotenone and succinate also prevented glutamate-dependen

90 ffectively prevent the neurotoxic effects of rotenone and that it might be used in the treatment of n

91 ormin was mimicked by a complex 1 inhibitor (rotenone) and an uncoupler (dinitrophenol) and by overex

92 last survival, and protected both complex I (rotenone) and complex IV (azide) Danio rerio vertebrate

93 The mitochondrial poisons cyanide, rotenone, and antimycin A prevented mitochondrial- but n

94 Polyethylene glycol-catalase, rotenone, and Mito-TEMPO impaired FID in healthy adipose

95 ctive effect against oxidative toxins (H2O2, rotenone, and oligomycin-A).

96 The antiestrogenic activity of CPC, BAK, rotenone, and triclosan may be related to their mitochon

97 superoxide generation in the mitochondria of rotenone- and antimycin A-treated cells was observed and

98 ndria and upregulation of Nox4 enhanced both rotenone- and diphenyleneiodonium-sensitive O(2)(-) prod

99 In contrast, rotenone, another complex I inhibitor, causes selective

100 potential neuroprotective mechanisms against rotenone are not well defined.

101 Rotenone at 20 nM inhibited basal and carbonyl cyanide p

102 Sustained exposure to rotenone at a higher dose (10 muM) decreased mTORC1 acti

103 nhibition of mitochondria with CCCP, KCN, or rotenone blocked intracellular ATP production, ATP relea

104 g the isolation procedure completely removed rotenone bound to the mitochondria.

105 in mitochondria with NADH in the presence of rotenone but not by exogenous oxidant.

106 microtubule-depolymerizing PD toxins such as rotenone by stabilizing microtubules to attenuate MAP ki

107 Blocking ROS production with rotenone by uncoupling mitochondria or by expressing the

108 nduced Bmf mRNA expression in RPTCs, whereas rotenone, catalase, diphenylene iodinium, and apocynin d

109 Rotenone caused severe dopamine depletion in the striatu

110 glucose, 2DG) and mitochondrial respiration (rotenone) caused profound actin filament loss, blocked R

111 wo models, by exposing A53T mutant larvae to rotenone, causes a much more severe PD phenotype (i.e. l

112 Microtubule destabilizers, rotenone, colchicine, and nocodazole, and the microtubul

113 TH+ neuronal loss to 25 +/- 10% at the 20-nM rotenone concentration.

114 Furthermore, incubation with rotenone decreased degranulation of effector and memory

115 Similar to E(2), the complex I inhibitor Rotenone decreased osteoclastogenesis by promoting osteo

116 CMICE-013 is a novel (123)I-labeled rotenone derivative developed for SPECT MPI.

117 Rotenone derivatives have shown promise in myocardial pe

118 ctivity of ATP13A2 was required for lowering rotenone/DFMO-induced MitoROS, whereas exogenous spermin

119 tests than wild-type mice following low oral rotenone doses given twice weekly over 50 weeks (half th

120 enhanced intracellular production of ROS by rotenone-EGCG combination may also account for the incre

121 al stress imposed by the complex I inhibitor rotenone elicited mitochondrial biogenesis, which was de

122 Pbeta from human alpha-Syn Tg mice abolishes rotenone-elicited PD pathologies and motor impairments v

123 ted previously that the mitochondrial poison rotenone enhanced currents evoked by N-methyl-D-aspartat

124 s by low ATP, we examined the involvement of rotenone-enhanced H2O2 generation.

125 The hypothesis that rotenone enhancement of neuronal cell death is attributa

126 -associated variant pS129-alpha-synuclein in rotenone-exposed mouse brains.

127 plex I inhibitor rotenone increases PD risk; rotenone-exposed rats show systemic mitochondrial defect

128 However, in rotenone-exposed rats, progressive motor deficits were s

129 Chronic rotenone exposure and commensurate reduction of metaboli

130 e findings, a clear mechanistic link between rotenone exposure and neuronal damage remains to be dete

131 Striatal H2O2 generation during rotenone exposure was examined in individual medium spin

132 TF4-CHOP-dependent stress response following rotenone exposure.

133 itochondrial complex I inhibitors, including rotenone, fenperoximate, pyridaben, or stigmatellin.

134 induce protein aggregation, such as MPP+ and rotenone, found to be associated with neurodegeneration.

135 ring RNA rendered SH-SY5Y cells resistant to rotenone, implicating BAD in rotenone-induced cell death

136 ry supplement, modulates the cytotoxicity of rotenone in human neuroblastoma SH-SY5Y cells.

137 I) and mitochondria electron chain inhibitor rotenone in the cells.

138 As little as 5 nM rotenone increased mitochondrial superoxide (O2*-) level

139 ure to the mitochondrial complex I inhibitor rotenone increases PD risk; rotenone-exposed rats show s

140 Within minutes of T cell activation, rotenone incubation decreased the production of H(2)O(2)

141 Decreased function following rotenone incubation was not restricted to naive cells, a

142 rnitine levels were increased in response to rotenone, indicating an increase in fatty acid import.

143 Rotenone induced a decrease in visual function, as deter

144 Rotenone induced a severe loss of nigral dopaminergic ne

145 Rotenone induced an increase in cell death and oxidative

146 Rotenone induced profound axonal degeneration in DRG neu

147 he loss of caspase-2 significantly inhibited rotenone-induced activation of Bid and Bax and the relea

148 Finally, rotenone-induced alpha-syn aggregates were cleared follo

149 vation, similarly to the complex I inhibitor rotenone-induced AMPK activation.

150 f Bax in mitochondria and were sensitized to rotenone-induced apoptosis as revealed by stimulated rel

151 Here we report that rotenone-induced apoptosis in human dopaminergic SH-SY5Y

152 e-2 acts upstream of mitochondria to mediate rotenone-induced apoptosis in neurons.

153 tomegalovirus infection protected cells from rotenone-induced apoptosis, a protection mediated by a 2

154 Loss of caspase-2 inhibited rotenone-induced apoptosis; however, these neurons under

155 opaminergic neurons were more susceptible to rotenone-induced ATP deficiency and cell death.

156 In vitro, inhibiting rotenone-induced autophagy in RPE cells elicits caspase-

157 ns from mesencephalon were more sensitive to rotenone-induced cell death than nondopaminergic neurons

158 ls resistant to rotenone, implicating BAD in rotenone-induced cell death.

159 Lactate accumulation in platelets due to rotenone-induced CI inhibition is reversed and rotenone-

160 iNdufs2 significantly decreased hypoxia- and rotenone-induced constriction while enhancing phenylephr

161 screen for small-molecule agents to reverse rotenone-induced cytotoxicity, we developed and validate

162 ial phenotypes, DJ-1 is still active against rotenone-induced damage in the absence of PINK1.

163 e-brain membrane isolates, NIL prevented the rotenone-induced decrease in cell respiration.

164 Correspondingly, rotenone-induced degeneration of nigral dopaminergic neu

165 AA inhibited oxidative stress resulting from rotenone-induced disruption of the mitochondrial respira

166 species as alternative mechanisms underlying rotenone-induced dopamine neuron death.

167 These data suggest that rotenone-induced dopaminergic cell death requires BAD an

168 Rotenone-induced downstream activation of caspase-3 and

169 e increase in DCF fluorescence and prevented rotenone-induced effects on membrane properties; membran

170 usceptibility to acute mitochondrial damage (rotenone-induced impairment in EDD).

171 tenone-induced CI inhibition is reversed and rotenone-induced increase in lactate:pyruvate ratio in w

172 but did not affect the change in the rate of rotenone-induced loss in neuronal ATP.

173 ting redistribution of ATP production during rotenone-induced mitochondrial dysfunction and troglitaz

174 Rotenone-induced mitochondrial dysfunction resulted in n

175 e ATP13A2 offers cellular protection against rotenone-induced mitochondrial stress, which relies on t

176 MitoROS, whereas exogenous spermine quenched rotenone-induced MitoROS via ATP13A2.

177 fer a novel neuroprotective approach against rotenone-induced parkinsonism.

178 ss in 6-hydroxydopamine (6-OHDA)-induced and rotenone-induced rat models of PD.

179 memantine as a neuroprotective agent against rotenone-induced retinal toxicity.

180 rvation that the presence of Ndi1 diminishes rotenone-induced ROS generation from complex I.

181 thioflavin S and with alpha-synuclein during rotenone-induced stress.

182 ealed that FTY720 also attenuated 6-OHDA- or rotenone-induced toxicity in SH-SY5Y cells.

183 d partial resistance to hydrogen peroxide or rotenone-induced toxicity, consistent with the induction

184 yl succinate (vitamin E analogue), prevented rotenone-induced toxicity.

185 Using a rotenone-inducible cellular model of PD, we observed tha

186 he biochemical basis for the function of the rotenone-insensitive internal NADH-quinone (Q) oxidoredu

187 ave shown previously that the single subunit rotenone-insensitive NADH-quinone oxidoreductase (Ndi1)

188 We have shown that expression of a rotenone-insensitive yeast NADH-quinone oxidoreductase (

189 as independent of mitochondrial respiration (rotenone-insensitive) but was inhibited by the flavoenzy

190 Rotenone is a naturally occurring mitochondrial complex

191 Rotenone killed more dopaminergic MN9D cells than non-do

192 ute exposure of VM cultures to the pesticide rotenone leads to dopaminergic neuronal cell death and t

193 ncoded subunits, complex I assembly factors, rotenone-like complex I toxins, or some combination.

194 environmental agents, including paraquat and rotenone, linked to PD in humans.

195 , ATP, monosodium urate, adjuvant aluminium, rotenone, live Escherichia coli, anthrax lethal toxin, D

196 ion (100 mumol/L) was reversed by mitoTEMPO, rotenone, malonate, DIDS (4,4'-diisothiocyanatostilbene-

197 rent Parkinson's disease (PD)-linked toxins (rotenone, maneb, or paraquat) and documented significant

198 l death in neurons treated with brefeldin A, rotenone, maneb, paraquat, or preformed fibrils of alpha

199 Studies indicate that the neurotoxicity of rotenone may be related to its ability to generate react

200 Direct complex I inhibition with rotenone mimicked the restrictive effects of CDK1 inhibi

201 Another complex I inhibitor, rotenone, mimicked the effect of metformin on pro-IL-1be

202 Rotenone, mitoTEMPO, and 4'-chlorodiazepam also blocked

203 ention strategies to block cell death in the rotenone model of Parkinson's disease.

204 conclude that the cell vulnerability in the rotenone model of partial complex I deficiency under the

205 ynuclein knockdown is neuroprotective in the rotenone model of PD and indicate that endogenous alpha-

206 utoimmune encephalomyelitis-, SOD1(G93A) and rotenone models, mimicking these CNS diseases in humans.

207 ergic neuron death induced by treatment with rotenone, MPP(+), or paraquat is independent of complex

208 s in these cultures to cell death induced by rotenone, MPP(+), or paraquat treatments, the absence of

209 ome oxidase activity were investigated using rotenone, myxothiazol, antimycin A, oligomycin, ascorbat

210 Rotenone, NMDA and uncoupling agents were added to the b

211 ceptors attenuates the selective toxicity of rotenone on DA neurons by activating the MAP kinase path

212 MB rescued the effects of rotenone on mitochondrial complex I-III inhibition and f

213 upling agents would antagonize the effect of rotenone on NMDA current.

214 ultured in a media with or without 200 nM of rotenone or 250 microM of MPP(+) for 48 h.

215 ort DeltaPsi(m) in tubules de-energized with rotenone or after H/R.

216 well as blocking the respiratory chain with rotenone or antimycin A in combination with oligomycin i

217 This was mimicked by cyanide, but not by rotenone or antimycin A, making the involvement of react

218 uitination was observed after treatment with rotenone or antimycin A, which both inhibit mitochondria

219 rom the respiratory chain in the presence of rotenone or antimycin A.

220 nificantly reduced the selective toxicity of rotenone or colchicine.

221 st microtubule-depolymerizing toxins such as rotenone or colchicine.

222 isk factors for Parkinson's disease, such as rotenone or heavy metal ions, had only mild or even no i

223 complex I activity by a specific inhibitor, rotenone or induction of oxidative stress by paraquat le

224 ffect on primary neurons grown in media with rotenone or MPP(+) than those with or without LED treatm

225 2 increased nematode survival in response to rotenone or paraquat, which are agents that cause mitoch

226 The RGCs were treated for 24 hours with rotenone or staurosporine or for 72 hours of hypoxia.

227 wever, in the presence of the C-I inhibitor, rotenone, or the antioxidant, catalase, these effects of

228 ine-derived neurotrophic factor also reduced rotenone- or colchicine-induced microtubule depolymeriza

229 pendent manner, NGF significantly attenuated rotenone- or colchicine-induced microtubule depolymeriza

230 t with this, L-AP-4 significantly attenuated rotenone- or colchicine-induced microtubule depolymeriza

231 atment with NIR-LED significantly suppressed rotenone- or MPP(+)-induced apoptosis in both striatal a

232 ed to paraquat, methyl methanesulfonate, and rotenone (P<0.05 in each case for contrast of GH-treated

233 eted and targeted metabolic profiling of the rotenone PD model in a chronic sleep restriction (SR) (6

234 t the microtubule depolymerizing activity of rotenone plays a critical role in its selective toxicity

235 t the microtubule-depolymerizing activity of rotenone plays a critical role in its selective toxicity

236 epolymerization induced by PD toxins such as rotenone plays a key role in the selective death of dopa

237 one, a mitochondrial complex I inhibitor, or rotenone plus one of three different doses of NIL.

238 duction, an effect inhibited by metformin or rotenone pretreatment.

239 Rotenone produced no significant changes in glial ATP le

240 Rotenone promoted mitochondrial-generated superoxide (Mi

241 NAC or rotenone reduced E2-induced cyclin D1 expression.

242 Acute exposure (20 h) to 20 nM rotenone reduced the number of tyrosine hydroxylase-posi

243 on of mitochondrial respiratory complex I by rotenone reproduces aspects of Parkinson's disease in ro

244 ies with PC-12 cells treated with 6-OHDA and rotenone, respectively.

245 eplication (ethidium bromide), and function (rotenone, rhodamine 6G) blocked E2-induced G1 to S trans

246 Chronic infusion of rotenone (Rot) to Lewis rats reproduces many features of

247 complex I (CI) generated ROS, in response to rotenone (ROT) treatment, is based on the ability of red

248 n (antimycin A (AntA), myxothiazol (Myx), or rotenone (Rot)).

249 Chronic administration of rotenone (RT) produces Parkinson's-like symptoms in rats

250 rdiolipin levels, citrate synthase activity, rotenone-sensitive NADH oxidase activity, and proximal t

251 ance, altered cristae morphology, diminished rotenone-sensitive respiration, and increased susceptibi

252 rates of both reverse electron transport and rotenone-sensitive superoxide production by complex I.

253 using pyruvate + malate (PM) or succinate + rotenone (SR) as substrates.

254 AICAR- and rotenone-stimulated glucose transport was fully inhibite

255 rated that carnosic acid protects cells from rotenone stress by significant induction of HSP70 expres

256 HPV is mimicked by the Complex I inhibitor, rotenone, the molecular identity of the O(2) sensor is u

257 the mitochondrial inhibitors tested, such as rotenone, thenoyltrifluoroacetone, or carbonyl cyanide m

258 nylpyridinium, lipopolysaccharide (LPS), and rotenone, three toxins often used to create PD models, p

259 antly antagonized and delayed the ability of rotenone to potentiate NMDA currents.

260 Administration of rotenone to rats reproduces many features of Parkinson's

261 mice receiving 6-hydroxydopamine (6-OHDA) or rotenone to simulate PD.

262 (Ang II) protects dopamine (DA) neurons from rotenone toxicity in vitro.

263 tional changes observed were aftereffects of rotenone toxicity in vivo.

264 Rotenone toxicity is mimicked by the microtubule-depolym

265 The potentiating effect of EGCG on rotenone toxicity may be attributed to the enhanced prod

266 The exacerbating effect of EGCG on rotenone toxicity may involve an apoptotic mechanism as

267 es, and this action significantly attenuates rotenone toxicity on dopaminergic neurons.

268 gonists (e.g., L-AP-4) significantly reduced rotenone toxicity on midbrain TH+ neurons in culture.

269 ve growth factor (NGF) significantly reduced rotenone toxicity on TH(+) neurons in midbrain neuronal

270 Enhanced rotenone toxicity to dopamine neurons from Ndufs4 knocko

271 The protective effect of NGF against rotenone toxicity was occluded by the microtubule-stabil

272 The protective effect of L-AP-4 against rotenone toxicity was occluded by the microtubule-stabil

273 ed significantly lower dopamine uptake after rotenone toxicity, due to reduced striatal synaptosomal

274 protein response for neuroprotection against rotenone toxicity.

275 of dopamine metabolism significantly reduced rotenone toxicity.

276 AT2 receptor protects dopamine neurons from rotenone toxicity.

277 e energy charge (AEC) levels for control and rotenone treated cells were evaluated.

278 reduction in the AEC values was observed for rotenone treated cells.

279 striatal mitochondrial Complex-I (NDUFS4) in rotenone-treated mutant but not in similarly treated wil

280 nger (NCX) with KB-R7943 partially protected rotenone-treated neurites from degeneration, suggesting

281 spase-2 as an initiator caspase activated in rotenone-treated primary neurons.

282 in dopaminergic substantia nigra neurons of rotenone-treated rats.

283 activity and activation of other caspases in rotenone-treated SH-SY5Y cells.

284 , high levels of ROS in HSP60 knockdowned or rotenone-treated U87 cells contributed to EMT.

285 Rotenone treatment induced a larger loss of dopamine mar

286 nhanced in caspase-2 knock-out neurons after rotenone treatment, and this response was important in p

287 acid that can effectively protect cells from rotenone treatment.

288 in vivo in response to hypoxic exposure and rotenone treatment.

289 The neurotoxic effect of rotenone was also reflected as a decrease in total cell

290 PGC-1alpha induction in response to rotenone was inhibited by silencing the expression of CR

291 le for H2O2, the inhibition of DA release by rotenone was prevented by catalase, a peroxide-scavengin

292 mitochondrial ROS by treatment of cells with rotenone was sufficient to amplify RLR signaling in WT c

293 of mitochondrial superoxide production with rotenone was sufficient to reduce AMPK phosphorylation i

294 orward electron transport in the presence of rotenone was uniquely related to NAD redox state.

295 on of ERK1/2 or PI3-kinase protected against rotenone, whereas inhibition of either pathway attenuate

296 ministered 0, 1, 2, and 6h after addition of rotenone, which generates reactive oxygen species via a

297 tical neurons with oligomycin, antimycin, or rotenone, which inhibit different elements of the electr

298 In naive animals, rotenone, which is a respiration chain complex I inhibit

299 Thus, rotenone, which produces a model of Parkinson's disease

300 rtholog of ATF4, causing hypersensitivity to rotenone, which was reversible with MitoTEMPO.