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1 rent oxidizing agents (hydrogen peroxide and paraquat).
2 ic insult (i.e., injections of the herbicide paraquat).
3 iotics such as berberine, rhodamine 123, and paraquat.
4  cold and reactive oxygen species-generating paraquat.
5 )O(2) production by the redox cycling agent, paraquat.
6 e susceptible to oxidative stress induced by paraquat.
7 ced tolerance to oxidative stress induced by paraquat.
8 sed resistance to the free-radical generator paraquat.
9 ion has been reported between a cryptand and paraquat.
10 e and Delta sodA1 cells after treatment with paraquat.
11 etected at lower levels after treatment with paraquat.
12 in brain regions of normal mice treated with paraquat.
13 ction exhibit variation in susceptibility to paraquat.
14 factors, we treated DJ-1-deficient mice with paraquat.
15 eroxide generated by the redox-cycling agent paraquat.
16 ent with the superoxide-generating compound, paraquat.
17 ecrotic lesions, and increased resistance to paraquat.
18 of nickel, copper, alkaline pH, menadione or paraquat.
19 he knockdown of TcSOD2 by exposing larvae to paraquat.
20 in; however, the mutant was less tolerant to paraquat.
21 der aerobic conditions or in the presence of paraquat.
22 roxides, and the superoxide-generating agent paraquat.
23 Y) were protected from damage to cadmium and paraquat.
24 /- and Prdx6+/+ mice and those injected with paraquat.
25 onse to nitrite and 37 genes specifically to paraquat.
26 was studied in mice exposed to the herbicide paraquat.
27 ath following exposure to subtoxic levels of paraquat.
28  but not by tert-butylhydroquinone (tBHQ) or paraquat.
29  enhanced by the superoxide-producing agent, paraquat.
30 of c-FLIP(L) protein induced by menadione or paraquat.
31  HeLa cancer cells treated with menadione or paraquat.
32 ts and mitochondria following treatment with paraquat.
33 the superoxide-generating redox-cycling drug paraquat.
34  one of the most powerful hosts reported for paraquats.
35 tri(1,4,7,10,13-pentaoxatridecyl) (3b), with paraquat (1) have 2:1 stoichiometry.
36           3a forms a strong 1:1 complex with paraquat (1) in acetone solution with a high apparent as
37                                              Paraquat (10-100 microm) was found to cause a 2-4-fold i
38 f a tetracationic molecular square, cyclobis(paraquat-4,4'-biphenylene), as the pi-electron deficient
39 ger, square-shaped diradical host, [cyclobis(paraquat-4,4'-biphenylene)](2(+*)) (MS(2(+*))).
40 ant K(a) = 5.0 x 10(6) M(-1) in acetone with paraquat, 9000 times greater than the crown ether system
41 epletion in the presence of methyl viologen (paraquat), a known agent of oxidative stress and source
42  to dopamine cells, suspicion has focused on paraquat, a common herbicide with chemical structure sim
43 atenin signaling manipulation in vitro using paraquat, a known oxidative stress inducer.
44 S1 gene render sos1 mutants more tolerant to paraquat, a non-selective herbicide causing oxidative st
45                                              Paraquat, a prooxidant widely used in stress tests, had
46                                              Paraquat, a reactive oxygen species generator, alone was
47 a producer of reactive oxygen species (ROS), paraquat, all rescued wild-type worms from hemiasterlin
48  higher risk when exposed to either maneb or paraquat alone (odds ratio = 2.27, 95% CI: 0.91, 5.70) o
49  the most severe consequences of exposure to paraquat, an herbicide that causes rapid alveolar inflam
50                                  Exposure to paraquat, an herbicide with structure similar to the dop
51 ed by low levels of the superoxide-generator paraquat and by a mutation that inhibits respiration.
52 utant are killed to a greater extent only by paraquat and diamide, whereas they are less susceptible
53 etermination of two bipyridylium herbicides, paraquat and diquat, in cowpeas by UPLC-MS/MS in a total
54  dietary supplementation with two compounds, paraquat and ethanol, on food ingestion and preference.
55 hypersensitivity of SelH shRNA HeLa cells to paraquat and H2O2, but not to hydroxyurea, neocarzinosta
56 tenuated neuronal death mediated by combined paraquat and iron treatment.
57 opathology, were treated with the pesticides paraquat and maneb (either singly or together), and thei
58 ergic neurotoxicity produced by the combined paraquat and maneb model of the Parkinson disease phenot
59                                Environmental paraquat and neonatal iron exposure have both been separ
60 HL knockout animals with the potent oxidizer paraquat and observed a robust induction of cellular sen
61 ity to those environmental agents, including paraquat and rotenone, linked to PD in humans.
62 nsitivity to the superoxide-generating agent paraquat and to organic hydroperoxides.
63 nd 4, possessed diminished binding with both paraquats and diquat relative to the 30-crown-based anal
64  pyocyanin (and the closely related molecule paraquat) and the acyl-homoserine lactone 3-OC12-HSL sig
65 as hypersensitive to the redox-cycling agent paraquat, and a plasmid expressing YggX complemented the
66 ed by their respective inducers: salicylate, paraquat, and decanoate.
67  to killing by hydrogen peroxide, menadione, paraquat, and diamide.
68 stimuli such as staurosporine, thapsigargin, paraquat, and H(2)O(2) showed significantly enhanced sur
69 rodegeneration, including hyperoxia, dietary paraquat, and heat stress.
70 ve stresses induced by hydrogen peroxide and paraquat, and it reduced transformation efficiency about
71 P1 to P28 and was also sensitive to hypoxia, paraquat, and myocardial infarction.
72  Environmental toxins, such as the herbicide paraquat, appear to be risk factors, and it has been pro
73 sponse to oxidative stress (i.e. H(2)O(2) or paraquat application), heat shock, or wounding.
74 , Zat7, or WRKY25 in response to H(2)O(2) or paraquat application.
75 l tested compounds, not even of the cationic paraquat at pH 7, 9, and 11.
76 or that can situate alongside a pi-accepting paraquat-based macrocycle by folding of a flexible linke
77 be an aromatic edge-to-face interaction of a paraquat beta-proton with the hydroquinone moiety; this
78  The complex based on dibenzo-24-crown-8 and paraquat bis(hexafluorophosphate) is not ion paired in s
79 e; the value of the dissociation constant of paraquat bis(hexafluorophosphate) was determined to be 4
80           However, exposure to 38 degrees C, paraquat, cadmium, or deletion of SOD1 enhanced two- to
81                                 We find that paraquat can replicate a broad spectrum of parkinsonian
82                                 Ingestion of paraquat causes multi-organ failure.
83 nds the KPF6 and allows the colored cryptand-paraquat complex to reform.
84 red in the presence of paraquat, there was a paraquat concentration-dependent increase in the formati
85  best estimated through measurement of blood paraquat concentrations but this facility is not availab
86 0 nm was linearly proportional to thiram and paraquat concentrations in the ranges from 0.5 to 1000 m
87      We also find that exposure of adults to paraquat converts cytosolic aconitase to IRP1 but has no
88 2 expression is also induced by glutathione, paraquat, copper, and naphthalene acetic acid (NAA) via
89                             Formation of the paraquat/cryptand-based pseudorotaxanes can be switched
90 ement of ROS from NADPH oxidase in mediating paraquat cytotoxicity in BV-2 microglial cells and this
91     Isotopically labeled internal standards, Paraquat-D6 and Diquat-D4, were used and added to the te
92        We found four independent factors for paraquat death prediction: amylase, PaCO2, leukocyte num
93  new cryptands form pseudorotaxanes with the paraquat derivative N,N'-bis(beta-hydroxyethyl)-4,4'-bip
94 atives and bis(p-phenylene)-34-crown-10 with paraquat derivatives are all ion paired in solution and
95       It was found that these cryptands bind paraquat derivatives very strongly.
96               The first cylindrical host for paraquat derivatives was prepared and characterized by X
97                         Their complexes with paraquat derivatives were studied by proton NMR spectros
98 s a luminescent crown ether based host 1 and paraquat derivatives, 2(PF(6))(2) and 3(PF(6))(2), as gu
99               MOF-1001 is capable of docking paraquat dication (PQT2+) guests within the macrocycles
100 e included as controls (simazine, maneb, and paraquat dichloride).
101                             The same dose of paraquat did not interfere with implantation in WT mice.
102                                 K+ displaces paraquat diol from the cryptands, converting yellow-oran
103  been synthesized and their interaction with paraquat diol has been investigated.
104 4,4'-bipyridinium bis(hexafluorophosphate) ("paraquat diol", 6): Ka=1.0x10(4) and 1.4x10(4) M-1, resp
105 ctures are reported for both cryptands, both paraquat diol-based pseudorotaxanes, both NH4PF6 complex
106 aminergic neuron death, and morbidity during paraquat exposure but confer sensitivity to hydrogen per
107  test the hypothesis that chronic, low-level paraquat exposure causes restrictive lung function with
108 es not readily support the causative role of paraquat exposure in idiopathic Parkinson's disease.
109 ence interval = 0.9-3.0) with the cumulative paraquat exposure index in models adjusted for age, weig
110      In linear regression models, cumulative paraquat exposure was not an independent predictor of VA
111                           The association of paraquat exposure with ventilatory equivalent and oxygen
112 gnificantly higher with increased cumulative paraquat exposure.
113       They generated estimates for maneb and paraquat exposures incurred between 1974 and 1999.
114  on mitochondrial aconitase, indicating that paraquat generates superoxide in the cytosol but not in
115 ding to the beta-pyridinium hydrogens of the paraquat guests.
116                            Most (66.6%) were paraquat handlers; 24.8% of handlers and 27.3% of nonhan
117                             Its complex with paraquat has 1:2 stoichiometry.
118            Exposure of mice to the herbicide paraquat has been demonstrated to result in the selectiv
119  exposure to the oxidant-producing herbicide paraquat has been implicated as a risk factor in Parkins
120 such as neurotoxicity induced by rotenone or paraquat--have emphasised that environmental agents may
121 fection, or treatment with salicylate or the paraquat herbicide that generates activated oxygen speci
122 ohistochemistry, and compared the effects of paraquat, hydrogen peroxide, and t-butyl hydroperoxide o
123 Nrf2 activity, increases their resistance to paraquat, hydrogen peroxide, cadmium, and UV light, rend
124 s study assessed the brain uptake of [(11)C]-paraquat in adult male rhesus macaques using quantitativ
125 poptotic gene BAX, and superoxide-generating paraquat in Arabidopsis or Nicotiana benthamiana.
126     Results showed minimal uptake of [(11)C]-paraquat in the macaque brain.
127 be for the sensitive detection of thiram and paraquat in water and food samples.
128 models of Parkinson's disease (PD), MPTP and paraquat, in young animals, its prolonged elevation resu
129  that exposure to a combination of maneb and paraquat increases PD risk, particularly in younger subj
130   Examples include enhanced methyl viologen (Paraquat)-induced oxidative stress tolerance in Mn-super
131                The protocol was set up using Paraquat-induced carbonylation, a model that induces pro
132 ROS and the underlying signaling pathway for paraquat-induced cytotoxicity to BV-2 microglial cells.
133  (EUK-134 and EUK-189) in protecting against paraquat-induced dopaminergic cell death in both the rat
134 thway inhibitor CEP-11004 effectively blocks paraquat-induced dopaminergic neuronal death in vivo.
135 rray analyses were conducted to evaluate the paraquat-induced global transcriptional response of Baci
136 pherol and N-acetylcysteine (NAC) attenuated paraquat-induced implantation failure in P(4)-treated Fk
137 from this enzyme are likely to contribute to paraquat-induced lung toxicity.
138                                       In the paraquat-induced model of Parkinsonism, this nigro-vagal
139 dings support a role for oxidative stress in paraquat-induced neurotoxicity and suggest novel therape
140  EUK-134 or EUK-189 significantly attenuates paraquat-induced neurotoxicity in vitro in a concentrati
141 amine synthesis, can alter susceptibility to paraquat-induced oxidative damage.
142 uced uterine PRDX6 levels are susceptible to paraquat-induced oxidative stress (OS), leading to impla
143 2-treated UOK262 renal carcinoma cells and a paraquat-induced oxidative stress cell model, demonstrat
144 FOXO transcription factor and protected from paraquat-induced oxidative stress.
145 a53Thr mutant form of the protein, displayed paraquat-induced protein aggregates but were completely
146                                              Paraquat-induced ROS production (including superoxide an
147 d kinases (ERK1/2) could partially attenuate paraquat-induced ROS production and cell death.
148                                              Paraquat-induced ROS production was inhibited by NADPH o
149 f superoxide dismutase (SOD) enzymes against paraquat-induced toxicity, as well as the therapeutic po
150     Apocynin and DPI also rescued cells from paraquat-induced toxicity.
151 selective PKCdelta inhibitor, also inhibited paraquat-induced translocation of p67phox.
152                           Our data show that paraquat induces the sequential phosphorylation of c-Jun
153                     Although intraperitoneal paraquat injections in mice cause a selective loss of do
154 s is sufficient to confer protection against paraquat insult.
155 gly, protection against the neurotoxicity of paraquat is conferred by mutations that elevate dopamine
156  in vivo effects have been ambiguous because paraquat is di-cationic in plasma, which raises question
157         This acute exposure study found that paraquat is excluded from the brain by the blood brain b
158 duced by treatment with rotenone, MPP(+), or paraquat is independent of complex I inhibition.
159                                              Paraquat is known to induce toxicity in cells by stimula
160                                              Paraquat is thus frequently used in the fruit fly Drosop
161 -1)) and very high association constants for paraquats (Ka > 10(5) M(-1)) in acetone at 22 degrees C.
162 rotenone or induction of oxidative stress by paraquat led to an increase in the phosphorylation of v-
163   Non-transgenic mice chronically exposed to paraquat + maneb exhibited significant reductions in loc
164                   Even a single injection of paraquat + maneb in the non-transgenic treated group mod
165   To begin to determine critical pathways of paraquat + maneb neurotoxicity, the functions of cell de
166 d to saline, paraquat, or the combination of paraquat + maneb twice a week for 9 weeks.
167 assertion that protective mechanisms against paraquat + maneb-induced neurodegeneration could involve
168 droperoxides in the midbrain and striatum of paraquat + maneb-treated non-transgenic mice was not det
169 l toxins, including environmental pesticides paraquat, maneb, and rotenone.
170 sociated with the disorder and that iron and paraquat may act via common oxidative stress-mediated me
171 valent and oxygen desaturation suggests that paraquat may be associated with subclinical gas exchange
172 gnaling cascade is a direct activator of the paraquat-mediated nigral dopaminergic neuronal apoptotic
173 antimycin A prevented mitochondrial- but not paraquat-mediated oxygen flux into cells.
174 systemic administration of EUK-189 decreases paraquat-mediated SNpc dopaminergic neuronal cell death
175 the CL mutants do not display sensitivity to paraquat, menadione or hydrogen peroxide (H2O2).
176 hibit excessive elevations of ROS induced by paraquat, menadione, and light stress and prevent cell d
177 ance was observed for fibroblasts exposed to paraquat, methyl methanesulfonate, and rotenone (P<0.05
178               Although in vitro evidence for paraquat neurotoxicity to dopamine cells is well establi
179                                              Paraquat neurotoxicity was compared in control animals v
180 ing microsensors, we measured the effects of paraquat on oxygen flux into murine lung epithelial cell
181 and wild-type (Prdx6+/+) macrophages, and of paraquat on Prdx6-/- and Prdx6+/+ mice.
182                Rats were given injections of paraquat once weekly for 3 weeks to induce features of P
183 osure to reactive oxygen species generators (paraquat or cadmium), or lack of superoxide dismutases.
184 stance of MCF7 breast cancer cells to either paraquat or doxorubicin.
185 ative stress induced by agents such as H2O2, paraquat or oxygen.
186 und its axis and lies with its smaller side (paraquat or phenyl ring) parallel to the surface to acco
187 eir tolerance to oxidative stress imposed by paraquat or t-butyl hydroperoxide, or were subjected to
188 of fast-exchange host-guest systems based on paraquats or viologens (G(2+)2X(-)) and crown ethers (H)
189  = 2.2 (95% CI: 1.5, 3.3), and the herbicide paraquat (OR(adj) = 1.8 (95% CI: 1.1, 2.8) was significa
190 y (i.e. treatment of mice with the herbicide paraquat) or transgenic protein overexpression, the intr
191 ound that exposure of RPE cells to H(2)O(2), paraquat, or A2E-mediated photooxidation resulted in inc
192 ls with the superoxide generators menadione, paraquat, or buthionine sulfoximine down-regulates c-FLI
193  non-transgenic mice were exposed to saline, paraquat, or the combination of paraquat + maneb twice a
194 RGC5 cells against TNFalpha cytotoxicity and paraquat oxidative stress.
195 lasmic diphenyleneiodonium-sensitive NAD(P)H:paraquat oxidoreductase.
196 ution of the well-known cyclophane, cyclobis(paraquat-p-phenylene) (BB(4+) ), and two cucurbit[7]uril
197 ability of the diradical dicationic cyclobis(paraquat-p-phenylene) (CBPQT(2(*+))) ring to form inclus
198  rings of the bipyridinium units in cyclobis(paraquat-p-phenylene) (CBPQT(4+) or "blue box") and desc
199 otion of the ring-shaped component, cyclobis(paraquat-p-phenylene) (CBPQT(4+)) (denoted as the ring),
200 g interactions taking place between cyclobis(paraquat-p-phenylene) (CBPQT(4+)) and five different mon
201 )) generated by the complexation of cyclobis(paraquat-p-phenylene) (CBPQT(4+)) and the guest molecule
202 dox-active rotaxanes, which drove a cyclobis(paraquat-p-phenylene) (CBPQT(4+)) mobile ring between a
203 pyridinium (P-BIPY(2+)) unit and a cyclobis (paraquat-p-phenylene) (CBPQT(4+)) ring component.
204 istable [2]rotaxane consisting of a cyclobis(paraquat-p-phenylene) (CBPQT(4+)) ring encircling a dumb
205 s mechanically interlocked with the cyclobis(paraquat-p-phenylene) (CBPQT(4+)) ring has also been pre
206             The location of the two cyclobis(paraquat-p-phenylene) (CBPQT(4+)) rings can be controlle
207 nes formed between these stalks and cyclobis(paraquat-p-phenylene) (CBPQT(4+)) rings, and (c) bistabl
208 us series of [2]rotaxanes, in which cyclobis(paraquat-p-phenylene) (CBPQT(4+)) serves as the ring com
209 aphthalene (DNP) units encircled by cyclobis(paraquat-p-phenylene) (CBPQT(4+)), a pi electron-accepti
210 on a tetracationic cyclophane host, cyclobis(paraquat-p-phenylene) (CBPQT(4+)), and a 1,5-dioxynaphth
211 otion of the ring-shaped component, cyclobis(paraquat-p-phenylene) (CBPQT(4+)), between a monopyrrolo
212 ous hosts-cucurbit[7]uril (CB7) and cyclobis(paraquat-p-phenylene) (CBPQT(4+)), respectively-using th
213  with the tetracationic cyclophane, cyclobis(paraquat-p-phenylene) (CBPQT(4+)), was synthesized by do
214 y with the tetracationic cyclophane cyclobis(paraquat-p-phenylene) (CBPQT(4+)), were obtained by dono
215 We find that the orientation of the cyclobis(paraquat-p-phenylene) (CBPQT) ring depends dramatically
216 ur donor-acceptor [2]catenanes with cyclobis(paraquat-p-phenylene) (CBPQT4+) as the pi-electron-accep
217  station, and (iii) a tetracationic cyclobis(paraquat-p-phenylene) (CBPQT4+) pi-electron-acceptor cyc
218 cled by a tetracationic cyclophane, cyclobis(paraquat-p-phenylene) (CBPQT4+), contrary to what is obs
219 e unit, interlocked mechanically by cyclobis(paraquat-p-phenylene) as its tetrachloride, exists as a
220 onor-acceptor [2]catenanes based on cyclobis(paraquat-p-phenylene) as the pi-acceptor ring have been
221 ely strong inclusion complexes with cyclobis(paraquat-p-phenylene) in its diradical dicationic redox
222                     The 'blue box' (cyclobis(paraquat-p-phenylene) or CBPQT(4+)), developed by Stodda
223 tristable [2]rotaxane composed of a cyclobis(paraquat-p-phenylene) ring and a dumbbell with tetrathia
224 d bistable [2]rotaxane containing a cyclobis(paraquat-p-phenylene) ring and tetrathiafulvalene/1,5-di
225 rown ether occupies the cavity of a cyclobis(paraquat-p-phenylene) ring and the other in which a 1,5-
226                                 The cyclobis(paraquat-p-phenylene) ring in the [2]rotaxane can be swi
227       Altering the redox state of a cyclobis(paraquat-p-phenylene) ring simultaneously (i) inverts th
228 sed of two mechanically interlocked cyclobis(paraquat-p-phenylene) rings has been obtained from the o
229 eptor [3]catenane incorporating two cyclobis(paraquat-p-phenylene) rings linked together by a dinapht
230 sed of two mechanically interlocked cyclobis(paraquat-p-phenylene) rings-with "zero", one, and two mo
231 ane composed of two rigid and fixed cyclobis(paraquat-p-phenylene) rings.
232 is [2]rotaxane, which consists of a cyclobis(paraquat-p-phenylene) shuttle (CBPQT(4+))(PF(6)(-))(4) (
233 on of the tetracationic cyclophane, cyclobis(paraquat-p-phenylene), and the radical cation generated
234 xtensively studied macrocyclic host cyclobis(paraquat-p-phenylene)--the so-called "blue-box"--it is s
235 ' (BB(4+)) tetracationic cyclophane cyclobis(paraquat-p-phenylene).
236 with the discovery that MV(+*) and [cyclobis(paraquat-p-phenylene)](2(+*)) (CBPQT(2(+*))) form a stro
237                          Patients with acute paraquat poisoning were recruited.
238 seful prognostic marker of death after acute paraquat poisoning.
239                                              Paraquat (PQ(2+)) is a prototypic toxin known to exert i
240                                              Paraquat (PQ) causes selective degeneration of dopaminer
241                                The herbicide paraquat (PQ) has increasingly been reported in epidemio
242 ttent (biweekly) exposure to intraperitoneal Paraquat (PQ) plus Maneb (MB).
243  function sigma(M) protein, was sensitive to paraquat (PQ), a superoxide-generating reagent, but not
244 ree different isolates of P. aeruginosa with paraquat (PQ), a superoxide-producing agent.
245 ntal oxidative stressors, like the herbicide paraquat (PQ), has been linked to the development of Par
246                                  Exposure to paraquat (PQ), hydrogen peroxide, or organic peroxides s
247                                  Here, using paraquat (PQ)-based in vitro and in vivo PD models, we s
248 as a model organism, we report the effect of paraquat (PQ)-induced OS on wild type worms on the funct
249 H2O2 induced intramitochondrial O2-, whereas paraquat produced O2- outside of the mitochondria, and t
250  or NADPH, and readily generates the reduced paraquat radical.
251 in reductase or recombinant enzyme possessed paraquat reductase activity.
252                                     Purified paraquat reductase from the cells contained thioredoxin
253 ated overexpression of Sod2 neither enhances paraquat resistance in Sod1+ flies nor compensates for l
254 complemented the SNO-dependent phenotypes of paraquat resistant 2-1 (par2-1) plants but not the NO-re
255 od LOQ was 10 and 20mugkg(-1) for diquat and paraquat, respectively.
256                        The administration of paraquat resulted in significantly higher 24-h mortality
257 rythroid progenitor cells by the pro-oxidant Paraquat reversed the effect of UCP2 deficiency on cell
258  confers tolerance against stress induced by Paraquat, Rose Bengal, heavy metal, and the synthetic au
259  with the oxidative stress-producing reagent paraquat showed a breakdown of sleep:wake cycles similar
260                           On the other hand, paraquat showed average recoveries between 68 and 103% w
261             DJ-1-deficient mice treated with paraquat showed decreased proteasome activities and incr
262 elta sodA1) had transcriptional responses to paraquat similar to, but notably larger than, those of t
263 anipulations did not increase sensitivity to paraquat, sodium azide, divalent metal ions (Fe(II) or C
264 onionic pollutants were highly linear, while paraquat sorption was strongly concentration dependent.
265  Binding of two different 4,4'-bipyridinium (paraquat) species (3) and 2,2'-bipyridinium (diquat) 4 b
266 al of dopaminergic neurons and resistance to paraquat stress, but showed acute sensitivity to hydroge
267 he ROS-generating herbicide methyl viologen (paraquat), suggesting a common protective role for proli
268 reated cultures, but not in those exposed to paraquat, suggesting that this response involves a speci
269 ss adaptation and produces the male-specific paraquat (superoxide) stress adaptation.
270 ress, whereas males but not females adapt to paraquat (superoxide) stress.
271 's disease in males, male Drosophila exhibit paraquat symptoms earlier than females.
272 nding constant (Ka = 2.4 x 10(5) M(-1)) with paraquats than the analogous dibenzo-30-crown-10-based c
273 owth traits under heat stress, arsenite, and paraquat, the majority of which were best explained by a
274                            Under exposure to paraquat, the yggX deletion strain showed a deficiency i
275 ase protein were cultured in the presence of paraquat, there was a paraquat concentration-dependent i
276 n to the redox-cycling agents, menadione and paraquat; this reduced survival was accompanied by an ac
277 e.g. H(2)O(2), peroxynitrite, menadione, and paraquat) through transient alterations in gene expressi
278 ne, and 2-naphthol), and of the organocation paraquat to unreduced and electrochemically reduced Leon
279 subsequent pro-apoptotic insults and reduces paraquat toxicity in Drosophila.
280 ne protein that has been shown to counteract paraquat toxicity in other experimental models and could
281  dopaminergic neurons protects flies against paraquat toxicity in vivo, ameliorating defects in dopam
282 uclein within nigral dopaminergic neurons of paraquat-treated and alpha-synuclein-overexpressing anim
283 ting against the oxidative damage induced by paraquat treatment, our data demonstrated that in Drosop
284 levels was examined by using heat stress and paraquat treatment.
285 yperresponsive to oxidative damage caused by paraquat treatment.
286 are sensitive to oxidative stress induced by paraquat treatment.
287 o cell death induced by rotenone, MPP(+), or paraquat treatments, the absence of complex I activity d
288 in wild-type worms using ethidium bromide or paraquat triggered statin resistance, and similar observ
289 pts a folded conformation, where each of two paraquat units remain sandwiched between the two aromati
290  Detailed (1)H NMR studies revealed that two paraquat units were bound cooperatively by the two crown
291 exposure of M17 cells to the oxidizing agent paraquat was manifested as a shift in pI of endogenous D
292                      Tolerance to Cu, Zn and paraquat was unaffected by MT deficiency but these plant
293                The highest concentrations of paraquat were seen in the pineal gland and the lateral v
294 asts are more sensitive to streptonigrin and paraquat when deleted for Ku80 as compared with Ku70.
295 nematode survival in response to rotenone or paraquat, which are agents that cause mitochondrial dysf
296                           Rearing mutants on paraquat, which generates toxic free radicals in vivo, c
297 nitrogen species (RNS) generator, and 0.5 mM paraquat, which produces reactive oxygen species (ROS),
298 ence links chronic exposure to the pesticide paraquat with the incidence of the disease, most probabl
299 d the heart from oxidative stress induced by paraquat, with increased expression of antioxidants, suc
300 PH oxidase inhibitor, blocked the effects of paraquat without altering mitochondrial respiration.

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