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1 the presence of 2-methyl-1,4-naphthoquinone (menadione).
2 d with the reduction-oxidation cycling agent menadione.
3 y directly sense oxidative stresses, such as menadione.
4 y active PKD prevented death from Ro-31-8425/menadione.
5 de I sensitized this cell line to death from menadione.
6 nus kinase 3 (JAK3) by the vitamin K3 analog menadione.
7 oxidant stress from the superoxide generator menadione.
8 stream substrate for JNK, blocked death from menadione.
9 uring oxidant-induced hepatocyte injury from menadione.
10 methyl group and the adjacent ring carbon in menadione.
11 scued by addition of small concentrations of menadione.
12 This was also the case after exposure to menadione.
13 t sensitive to the oxidizing agents H2O2 and menadione.
14 none, 2,3-dimethoxy-1, 4-naphthoquinone, and menadione.
15 e GSH increase to activation of NF-kappaB by menadione.
16 cytotoxicity produced by preincubation with menadione.
17 NF-kappaB, resulted in increased toxicity by menadione.
18 activated by the superoxide anion generator menadione.
19 iation after exposure to H(2)O(2) but not to menadione.
20 but not to the superoxide radical generator menadione.
21 ied by exposing worms to D-penicillamine and menadione.
22 tabolic activation of toxic quinones such as menadione.
23 exacerbated in the presence of the genotoxin menadione.
24 autophagy (CMA) also mediated resistance to menadione.
25 bility to reduce extracellular plumbagin and menadione.
26 ath from normally nontoxic concentrations of menadione.
27 de was elevated with the redox cycling agent menadione.
28 ificity constants are found with the quinone menadione.
29 trically at 490 nm after addition of XTT and menadione.
30 nder exposure to either hydrogen peroxide or menadione.
31 of mtDNA damage in neurons when treated with menadione.
32 genin, 15-deoxy-Delta12,14-prostaglandin-J2, menadione, 1-Cl-2,4-dinitrobenzene, and biotinylated iod
33 ture (40 degrees C), jasmonic acid (200muM), menadione (120muM) and abscisic acid (3.026mM) treatment
34 enzyme-orotate complex reacted rapidly with menadione (180 s(-1)), demonstrating that the reduced en
35 ge cell line (NR8383) was exposed to H2O2 or menadione (2-methyl-1,4-naphthoquinone (MQ)), a quinone
37 idative stress induced in live HeLa cells by menadione (2-methyl-1,4-napthaquinone) was studied in re
38 to 2-methyl-1, 4-naphthoquinone (vitamin K3, menadione, 2MNQ) in the presence of hydrogen peroxide an
40 epared by coupling vitamin K3, also known as menadione (a quinone redox center), to a boron-dipyrrome
41 lphaE2), 17alpha-ethinylestradiol (alphaEE), menadione, a combination of alphaE2 and alphaEE, or a co
43 +) versus ERalpha(-) cells and 4-OHEN versus menadione, a reactive oxygen species (ROS)-generating, b
45 ative stress induced by hydrogen peroxide or menadione activates the heat shock transcription factor
47 f hamsters treated with alphaE2, alphaEE, or menadione alone did not show any gross evidence of tumor
48 ress induced by 0.5 mM H(2)O(2) or 50 microM menadione also caused a greater than 50% reduction in GP
49 SPRR2D, and SPRR2F) were rapidly induced by menadione, an agent that promotes apoptosis through the
51 e exogenous addition of hydrogen peroxide or menadione, an intracellular generator of superoxide anio
53 ures of GlpD bound with ubiquinone analogues menadione and 2-n-heptyl-4-hydroxyquinoline N-oxide, ide
56 ys of hamsters treated with a combination of menadione and alphaEE showed foci of tumor with congeste
57 ys of hamsters treated with a combination of menadione and alphaEE showed increased 8-iso-PGF(2alpha)
59 ng compounds, e.g., the environmental toxins menadione and beta-lapachone (in vivo IC(50) = 0.45 muM)
60 hypersensitivity to the DNA-damaging agents menadione and bleomycin, consistent with a role for AtKu
61 chemical microscopy by exposing the cells to menadione and detecting the menadione-S-glutathione conj
63 under anaerobic conditions was inhibited by menadione and enhanced by benzaldehyde, acetaldehyde, or
64 progression of the in vitro reaction between menadione and glutathione was monitored electrochemicall
66 ated via mutations in menD or hemB, yielding menadione and hemin auxotrophs, respectively, and studie
67 eterminations of the midpoint potentials for menadione and menadione bisulfite indicated that the lat
68 cell population to the redox-cycling agents, menadione and paraquat; this reduced survival was accomp
69 er, when exposed to naphthoquinones, such as menadione and plumbagin, which cause indirect oxidative
74 gested the rate was limited by the uptake of menadione and that the efflux through the glutathione-co
76 eased susceptibility to oxidative (H2 O2 and menadione) and UV stress as compared to wild-type and co
77 an oxidant (H2O2), to a redox-cycling agent (menadione), and to an osmotic challenge with 2.5 M NaCl.
80 ssive elevations of ROS induced by paraquat, menadione, and light stress and prevent cell death induc
81 dative stress (e.g. H(2)O(2), peroxynitrite, menadione, and paraquat) through transient alterations i
82 highly sensitive to the redox cycling agent menadione, and showed fragmentation of the large vacuole
83 treatment with oxidants (hydrogen peroxide, menadione, and t-butyl hydroperoxide) were investigated
85 ate prevented the activation of NF-kappaB by menadione, and under these conditions, salicylate potent
86 the sensitivity to added prooxidants such as menadione, antimycin A, H(2)O(2), and 4-hydroxynonenal w
87 eractivation of JNK and c-Jun in response to menadione as determined by in vitro kinase assay and imm
89 ain neurons leads to enhanced sensitivity to menadione, as indicated by increased levels of DNA stran
90 the XTT method (100 microg/ml XTT, 25 microM menadione) at 6, 8, or 12 h after inoculation and the CL
91 1 (Deltapsi -100 mV; a respiration-deficient menadione auxotroph of 6850) were used to assess the inf
95 of the midpoint potentials for menadione and menadione bisulfite indicated that the latter compound w
96 the structure of reduced PutA complexed with menadione bisulfite reveals the elusive quinone-binding
97 When another cell line was assayed utilizing menadione bisulfite, an apparent activity of about three
100 n enhances sensitivity to UV, gamma rays and menadione, but ectopic expression of RAD9 or NEIL1 resto
101 creased sensitivity to benomyl, diamide, and menadione, but not 4-NQO, cycloheximide, or fluconazole.
104 SR and HPLC-EC analysis of the metabolism of menadione by either HepG2 cells or isolated rat hepatocy
110 l characterizations of the QsrR-DNA and QsrR-menadione complexes further reveal that the covalent ass
113 epatocytes to death from previously nontoxic menadione concentrations in association with sustained J
114 and 35 microM upon exposure of the cells to menadione concentrations of 500, 250, and 125 microM, re
116 pe tip current of yeast cells suspended in a menadione-containing solution, the export of the conjuga
119 (astrocytes), and enzyme histochemistry for menadione-dependent a-glycerophosphate dehydrogenase (M-
120 ecombinant HemG was shown to be capable of a menadione-dependent conversion of protoporphyrinogen IX
123 ther reveal that the covalent association of menadione directly leads to the release of QsrR from ope
124 cells with the hOGG1 fusion protein prior to menadione exposure resulted in an increase in the rate o
131 including osmotic stress, hydrogen peroxide, menadione, heat shock, and the protein synthesis inhibit
132 tance to death from the superoxide generator menadione in the hepatocyte cell line RALA255-10G is dep
133 menaquinone-4 or whether it is converted to menadione in the intestine followed by delivery of menad
134 2 cells with low, nontoxic concentrations of menadione increased the viability of the cells against t
135 -lapachone and related naphthoquinones, like menadione, induce protein-linked DNA breaks in the prese
136 uction of O2*- by the redox cycling compound menadione induced MEK-1-independent cellular growth and
139 cts on cellular survival, protecting against menadione-induced apoptosis, but sensitizing to necrotic
140 uced DNA damage in ERalpha(+) cells, whereas menadione-induced damage was not dependent on cellular E
142 species per se but significantly potentiated menadione-induced effects, probably via enhancement of o
143 orylation constitutes a major feature of the menadione-induced oxidative injury in these neuronal cel
145 e hepatocyte injury response, the effects of menadione-induced oxidative stress were examined in the
149 licylate, plumbagin, 2, 4-dinitrophenol, and menadione-inducers of the marRAB operon in whole cells-a
150 the strategy can be extended to observe how menadione induces superoxide generation in mitochondria.
151 n contrast, the oxidizing agents diamide and menadione inhibited the development of hillocks triggere
152 se results provide unequivocal evidence that menadione is a catabolic product of oral phylloquinone a
153 vity, to superoxide anion (O(2)()) formed by menadione is attenuated, whereas induction by heme is no
154 yte resistance to oxidant-induced death from menadione is dependent on ERK, whereas cell death is med
157 s low concentrations of H2O2 (0.1-0.2 mM) or menadione (less than = 10 microM) induced myeloid cell a
159 odies in muscle biopsy sections stained with menadione-NBT followed by clinical, histological, ultras
162 ults suggest that acute generation of ROS by menadione occurs via redox cycling, the net effect of wh
167 Arabidopsis cell culture for 16 h with H2O2, menadione or antimycin A induced an oxidative stress dec
168 ortic endothelial cells after treatment with menadione or antimycin A to induce intracellular reactiv
169 ibited NADPH quinone reductase activity with menadione or benzoquinone and weak activity with cytochr
170 Notably, the superoxide-generating drug menadione or H(2)O(2) was sufficient to trigger differen
180 tathione (GSH)-S-transferase family, NAD(P)H menadione oxidoreductase 1, and the ferritin light chain
183 ayed as either dicumarol-inhibitable NAD(P)H:menadione oxidoreductase or dicumarol-inhibitable NAD(P)
187 r PPC-1 cells with the superoxide generators menadione, paraquat, or buthionine sulfoximine down-regu
188 ogen, benzyl viologen, and diquat but not to menadione, plumbagin, pyrogallol, or nitrofurantoin.
189 he results of the current study suggest that menadione pretreatment protects Hep G2 cells from oxidat
190 An increased level of GSH was observed after menadione pretreatment; this increase was blocked by sal
191 n blot technology, we found that exposure to menadione produced detectable mtDNA damage in HeLa cells
192 reatment, and exposure to sodium arsenite or menadione, proved more toxic to those cells expressing t
194 e three groups were: CYP2D6, CYP2E1, NAD(P)H-menadione reductase, glutathione transferases M1 and T1,
196 recovery of virulence factor expression and menadione resistance, and in restoration of virulence.
197 ing the cells to menadione and detecting the menadione-S-glutathione conjugate (thiodione) that is fo
198 osines from the 2-methyl-1,4-naphthoquinone (menadione)-sensitized 365-nm irradiation of d(CpC).
199 ibition induced by oxidative stress (H2O2 or menadione), significantly ameliorated the H2O2-dependent
206 cytotoxicities of four oxidative stressors (menadione, tert-butyl hydroperoxide, 4-hydroxynonenal, a
209 gen peroxide, the superoxide-generating drug menadione, the sulfhydryl-oxidizing agent diamide, the d
210 MA inhibition sensitized cells to death from menadione through a mechanism different from that of a l
214 one in the intestine followed by delivery of menadione to tissues and subsequent conversion to menaqu
215 rthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNO
216 YP2E1-overexpressing cells were resistant to menadione toxicity through an ERK1/2-dependent mechanism
218 cells within 5 min, whereas in ERalpha(-) or menadione-treated cells, no selectivity was observed.
224 f 25 protein spots increased >3-fold in H2O2/menadione treatments, a subset of these increased in ant
226 ts and measurements of phylloquinone-derived menadione using high resolution MS analysis and a bioass
227 QR2 catalyzes the two-electron reduction of menadione via the oxidation of N-alkylated or N-ribosyla
228 ures of QR2: in its native form and bound to menadione (vitamin K(3)), a physiological substrate.
230 uinone but a strong prenylation activity for menadione (vitamin K3), which has long been postulated a
232 l death caused by H(2)O(2), antimycin A, and menadione was considerably suppressed in both the mC5 an
235 water-soluble bisulfite addition product of menadione was used as the electron acceptor, an artifact
237 OP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected
239 c concentrations of the superoxide generator menadione were established in the RALA255-10G rat hepato
240 nduced by redox cycling agents plumbagin and menadione, whereas an fgd mutant of M. smegmatis used G6
241 d by aminotriazole and to a lesser extent by menadione, whereas ZmMRP2 was expressed at a lower const
242 ts of 37 degrees C "heat shock" or sublethal menadione, which generates superoxide and hydrogen perox
243 tained the binary complex structures with GS-menadione, which in its reduced form, GS-menadiol, is a
244 nhibitors exemplified by the natural product menadione, which is shown in mouse tumor models to have
247 the product generated from the incubation of menadione with recombinant UBIAD1 revealed that the hydr
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