ライフサイエンスコーパス: rotenone

1 e in mitochondrial biogenesis in response to rotenone.

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

3 ation in response to the mitochondrial toxin rotenone.

4 sed to the mitochondrial complex I inhibitor rotenone.

5 dopaminergic neurons were more sensitive to rotenone.

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

7 cells from death as induced by etoposide and rotenone.

8 redox potential high even in the presence of rotenone.

9 50 muM EGCG potentiated the cytotoxicity of rotenone.

10 e, was substantial but markedly inhibited by rotenone.

11 ce of the mitochondrial complex I inhibitor, rotenone.

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

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

14 , including diphenyleneiodonium chloride and rotenone.

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

16 uced by DA or 6-OHDA, but not by H(2)O(2) or rotenone.

17 ed protection from the neurotoxic effects of rotenone.

18 role in response to complex I inhibition by rotenone.

19 when mitochondrial complex I is inhibited by rotenone.

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

21 tress induced by the mitochondrial inhibitor rotenone.

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

23 nvironmental pesticides paraquat, maneb, and rotenone.

24 of substrates and by the complex I inhibitor rotenone.

25 ex I activity from the inhibitory effects of rotenone.

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

27 ochondria exposed to the complex I inhibitor rotenone.

28 in activity, also antagonized this action of rotenone.

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

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

31 the induction of this pathway in response to rotenone.

32 st injury from mitochondrial poisons such as rotenone.

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

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

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

36 a and the striatum of rats after infusion of rotenone (2 mg/kg per day s.c.) for 21 days.

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

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

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

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

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

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

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

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

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

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

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

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

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

50 When infused in rats, rotenone, a mitochondrial complex I inhibitor, induces a

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 CCCP (a protonophore; 1 microm) and rotenone (an electron transport chain complex I inhibito

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

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 of catalase or acute in vitro treatment with rotenone, an inhibitor of mitochondrial complex I, or th

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

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

75 vals following chronic exposure to nanomolar rotenone, an irreversible complex I inhibitor.

76 ed, perfused rabbit hearts were treated with rotenone, an irreversible inhibitor of complex I in the

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

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

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

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

81 Under current clamp conditions rotenone and CN(-) caused a rapid membrane depolarizatio

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

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

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

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

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

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

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

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

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

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

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

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 Inhibition of mitochondrial function with rotenone, antimycin A, KCN, carbonylcyanide-m-chlorophen

101 potential neuroprotective mechanisms against rotenone are not well defined.

102 n a subset of animals, supporting the use of rotenone as a model of Parkinson's disease under careful

103 ked by the mitochondrial complex I inhibitor rotenone as well as the glucose transport inhibitor phlo

104 Rotenone at 20 nM inhibited basal and carbonyl cyanide p

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

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

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

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

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

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

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

112 Rotenone caused severe dopamine depletion in the striatu

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

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

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

116 Rotenone, cyanide, myxothiazol and oligomycin significan

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

118 played a more important role in MN9D cells: rotenone decreased mitochondrial membrane protential and

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

120 Rotenone derivatives have shown promise in myocardial pe

121 hronic subcutaneous infusion of low doses of rotenone does not induce significant striatal neuronal l

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

123 However, the specificity of rotenone effects has been challenged recently.

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

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

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

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

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

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

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

131 Chronic rotenone exposure and commensurate reduction of metaboli

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

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

134 These findings indicate that, during chronic rotenone exposure, MN9D cells die primarily through mito

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

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

137 In the absence of ADP or in the presence of rotenone, H(2)O(2) production rates correlated with the

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

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

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

141 e have re-examined the alterations caused by rotenone in the substantia nigra and the striatum of rat

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

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

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

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

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

147 Rotenone induced a decrease in visual function, as deter

148 Rotenone induced a severe loss of nigral dopaminergic ne

149 Rotenone induced an increase in cell death and oxidative

150 Rotenone induced profound axonal degeneration in DRG neu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 Correspondingly, rotenone-induced degeneration of nigral dopaminergic neu

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

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

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

171 Rotenone-induced downstream activation of caspase-3 and

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

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

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

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

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

177 Rotenone-induced mitochondrial dysfunction resulted in n

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

179 Oxidative stress played an important role in rotenone-induced neurodegeneration of MN9X cells, but no

180 ion appeared to be related to suppression of rotenone-induced oxidative stress as well as mitochondri

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

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

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

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

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

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

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

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

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

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

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

192 Rotenone is a naturally occurring mitochondrial complex

193 Rotenone killed more dopaminergic MN9D cells than non-do

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

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

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

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

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

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

200 tein (hsp) 70, not only protected cells from rotenone-mediated cytotoxicity but also decreased solubl

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

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

208 e have therefore investigated the effects of rotenone, myxothiazol, antimycin A, cyanide (CN(-)) and

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

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

219 nificantly reduced the selective toxicity of rotenone or colchicine.

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

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

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

223 Neither rotenone or myxothiazol prevented D-GLYC-induced increas

224 2 increased nematode survival in response to rotenone or paraquat, which are agents that cause mitoch

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

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

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

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

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

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

231 eneration of MN9X cells, but not MN9D cells: rotenone oxidatively modified proteins more in MN9X cell

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

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

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

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

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

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

238 Rotenone produced no significant changes in glial ATP le

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

259 tone body, D-beta-hydroxybutyrate, decreased rotenone toxicity in MN9D cells, but not in MN9X cells.

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

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

262 Rotenone toxicity is mimicked by the microtubule-depolym

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

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

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

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

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

268 han in MN9D cells and antioxidants decreased rotenone toxicity only in MN9X cells.

269 Enhanced rotenone toxicity to dopamine neurons from Ndufs4 knocko

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

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

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

273 n resulted in an increased susceptibility to rotenone toxicity, whereas transfection with a lentivira

274 of dopamine metabolism significantly reduced rotenone toxicity.

275 AT2 receptor protects dopamine neurons from rotenone toxicity.

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

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

278 ough cytochrome oxidase also was improved in rotenone-treated hearts.

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 Rotenone treatment of isolated subsarcolemmal mitochondr

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

288 acid that can effectively protect cells from rotenone treatment.

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

290 dance in AS complexes under conditions where rotenone was cytotoxic and induced formation of cytoplas

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

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

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

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

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

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

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

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

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

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