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1 the presence of 2-methyl-1,4-naphthoquinone (menadione).
2 ied by exposing worms to D-penicillamine and menadione.
3 of mtDNA damage in neurons when treated with menadione.
4 y active PKD prevented death from Ro-31-8425/menadione.
5 de I sensitized this cell line to death from menadione.
6 oxidant stress from the superoxide generator menadione.
7 stream substrate for JNK, blocked death from menadione.
8 uring oxidant-induced hepatocyte injury from menadione.
9 methyl group and the adjacent ring carbon in menadione.
10 This was also the case after exposure to menadione.
11 y directly sense oxidative stresses, such as menadione.
12 nus kinase 3 (JAK3) by the vitamin K3 analog 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 scued by addition of small concentrations of menadione.
19 activated by the superoxide anion generator menadione.
20 iation after exposure to H(2)O(2) but not to menadione.
21 but not to the superoxide radical generator 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 d with the reduction-oxidation cycling agent menadione.
30 trically at 490 nm after addition of XTT and menadione.
31 nder exposure to either hydrogen peroxide or 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
42 lphaE2), 17alpha-ethinylestradiol (alphaEE), menadione, a combination of alphaE2 and alphaEE, or a co
44 +) versus ERalpha(-) cells and 4-OHEN versus menadione, a reactive oxygen species (ROS)-generating, b
46 ative stress induced by hydrogen peroxide or menadione activates the heat shock transcription factor
48 f hamsters treated with alphaE2, alphaEE, or menadione alone did not show any gross evidence of tumor
49 ress induced by 0.5 mM H(2)O(2) or 50 microM menadione also caused a greater than 50% reduction in GP
50 y relevant quinone analogs, such as DHNA and menadione, amongst other structurally similar quinone de
51 SPRR2D, and SPRR2F) were rapidly induced by menadione, an agent that promotes apoptosis through the
53 e exogenous addition of hydrogen peroxide or menadione, an intracellular generator of superoxide anio
55 ures of GlpD bound with ubiquinone analogues menadione and 2-n-heptyl-4-hydroxyquinoline N-oxide, ide
58 ys of hamsters treated with a combination of menadione and alphaEE showed foci of tumor with congeste
59 ys of hamsters treated with a combination of menadione and alphaEE showed increased 8-iso-PGF(2alpha)
61 ng compounds, e.g., the environmental toxins menadione and beta-lapachone (in vivo IC(50) = 0.45 muM)
62 hypersensitivity to the DNA-damaging agents menadione and bleomycin, consistent with a role for AtKu
63 chemical microscopy by exposing the cells to menadione and detecting the menadione-S-glutathione conj
65 under anaerobic conditions was inhibited by menadione and enhanced by benzaldehyde, acetaldehyde, or
66 progression of the in vitro reaction between menadione and glutathione was monitored electrochemicall
68 ated via mutations in menD or hemB, yielding menadione and hemin auxotrophs, respectively, and studie
69 eterminations of the midpoint potentials for menadione and menadione bisulfite indicated that the lat
70 cell population to the redox-cycling agents, menadione and paraquat; this reduced survival was accomp
71 er, when exposed to naphthoquinones, such as menadione and plumbagin, which cause indirect oxidative
76 gested the rate was limited by the uptake of menadione and that the efflux through the glutathione-co
78 eased susceptibility to oxidative (H2 O2 and menadione) and UV stress as compared to wild-type and co
79 an oxidant (H2O2), to a redox-cycling agent (menadione), and to an osmotic challenge with 2.5 M NaCl.
82 orter genes respond to different mycotoxins, menadione, and hydrogen peroxide in a distinguishable ma
83 ssive elevations of ROS induced by paraquat, menadione, and light stress and prevent cell death induc
84 dative stress (e.g. H(2)O(2), peroxynitrite, menadione, and paraquat) through transient alterations i
85 highly sensitive to the redox cycling agent menadione, and showed fragmentation of the large vacuole
86 treatment with oxidants (hydrogen peroxide, menadione, and t-butyl hydroperoxide) were investigated
88 ate prevented the activation of NF-kappaB by menadione, and under these conditions, salicylate potent
89 the sensitivity to added prooxidants such as menadione, antimycin A, H(2)O(2), and 4-hydroxynonenal w
92 eractivation of JNK and c-Jun in response to menadione as determined by in vitro kinase assay and imm
94 ain neurons leads to enhanced sensitivity to menadione, as indicated by increased levels of DNA stran
95 the XTT method (100 microg/ml XTT, 25 microM menadione) at 6, 8, or 12 h after inoculation and the CL
96 1 (Deltapsi -100 mV; a respiration-deficient menadione auxotroph of 6850) were used to assess the inf
100 of the midpoint potentials for menadione and menadione bisulfite indicated that the latter compound w
101 the structure of reduced PutA complexed with menadione bisulfite reveals the elusive quinone-binding
102 When another cell line was assayed utilizing menadione bisulfite, an apparent activity of about three
105 n enhances sensitivity to UV, gamma rays and menadione, but ectopic expression of RAD9 or NEIL1 resto
106 creased sensitivity to benomyl, diamide, and menadione, but not 4-NQO, cycloheximide, or fluconazole.
109 SR and HPLC-EC analysis of the metabolism of menadione by either HepG2 cells or isolated rat hepatocy
116 l characterizations of the QsrR-DNA and QsrR-menadione complexes further reveal that the covalent ass
119 epatocytes to death from previously nontoxic menadione concentrations in association with sustained J
120 and 35 microM upon exposure of the cells to menadione concentrations of 500, 250, and 125 microM, re
122 pe tip current of yeast cells suspended in a menadione-containing solution, the export of the conjuga
123 uperoxide stress triggered by the uncoupler, menadione, Cygb had a prominent role in superoxide metab
126 (astrocytes), and enzyme histochemistry for menadione-dependent a-glycerophosphate dehydrogenase (M-
127 ecombinant HemG was shown to be capable of a menadione-dependent conversion of protoporphyrinogen IX
130 ther reveal that the covalent association of menadione directly leads to the release of QsrR from ope
131 cells with the hOGG1 fusion protein prior to menadione exposure resulted in an increase in the rate o
138 including osmotic stress, hydrogen peroxide, menadione, heat shock, and the protein synthesis inhibit
139 tance to death from the superoxide generator menadione in the hepatocyte cell line RALA255-10G is dep
140 menaquinone-4 or whether it is converted to menadione in the intestine followed by delivery of menad
141 2 cells with low, nontoxic concentrations of menadione increased the viability of the cells against t
142 -lapachone and related naphthoquinones, like menadione, induce protein-linked DNA breaks in the prese
143 uction of O2*- by the redox cycling compound menadione induced MEK-1-independent cellular growth and
146 cts on cellular survival, protecting against menadione-induced apoptosis, but sensitizing to necrotic
147 uced DNA damage in ERalpha(+) cells, whereas menadione-induced damage was not dependent on cellular E
149 species per se but significantly potentiated menadione-induced effects, probably via enhancement of o
150 and suppresses lipid hydroperoxidation in a menadione-induced model of oxidative stress in a glutama
151 orylation constitutes a major feature of the menadione-induced oxidative injury in these neuronal cel
153 e hepatocyte injury response, the effects of menadione-induced oxidative stress were examined in the
157 licylate, plumbagin, 2, 4-dinitrophenol, and menadione-inducers of the marRAB operon in whole cells-a
158 the strategy can be extended to observe how menadione induces superoxide generation in mitochondria.
159 n contrast, the oxidizing agents diamide and menadione inhibited the development of hillocks triggere
160 se results provide unequivocal evidence that menadione is a catabolic product of oral phylloquinone a
161 vity, to superoxide anion (O(2)()) formed by menadione is attenuated, whereas induction by heme is no
162 yte resistance to oxidant-induced death from menadione is dependent on ERK, whereas cell death is med
165 s low concentrations of H2O2 (0.1-0.2 mM) or menadione (less than = 10 microM) induced myeloid cell a
167 imilarly, modeling of rosette formation with menadione (MN), led to phospho-Parkin accumulation in fr
168 odies in muscle biopsy sections stained with menadione-NBT followed by clinical, histological, ultras
171 ults suggest that acute generation of ROS by menadione occurs via redox cycling, the net effect of wh
176 Arabidopsis cell culture for 16 h with H2O2, menadione or antimycin A induced an oxidative stress dec
177 ortic endothelial cells after treatment with menadione or antimycin A to induce intracellular reactiv
178 ibited NADPH quinone reductase activity with menadione or benzoquinone and weak activity with cytochr
179 Notably, the superoxide-generating drug menadione or H(2)O(2) was sufficient to trigger differen
187 ress was induced by prolonged treatment with menadione or rotenone and expression of genetic alterati
189 e other hand, treatment of chondrocytes with menadione (oxidative stress inducer) induced oxidation o
191 tathione (GSH)-S-transferase family, NAD(P)H menadione oxidoreductase 1, and the ferritin light chain
192 an electron acceptor as shown by the formate:menadione oxidoreductase activity of both enzymes, their
195 ayed as either dicumarol-inhibitable NAD(P)H:menadione oxidoreductase or dicumarol-inhibitable NAD(P)
199 r PPC-1 cells with the superoxide generators menadione, paraquat, or buthionine sulfoximine down-regu
200 ogen, benzyl viologen, and diquat but not to menadione, plumbagin, pyrogallol, or nitrofurantoin.
201 he results of the current study suggest that menadione pretreatment protects Hep G2 cells from oxidat
202 An increased level of GSH was observed after menadione pretreatment; this increase was blocked by sal
203 n blot technology, we found that exposure to menadione produced detectable mtDNA damage in HeLa cells
204 tment of S. aureus with respiration-reducing menadione protected Deltaagr cells from killing by H(2)O
205 reatment, and exposure to sodium arsenite or menadione, proved more toxic to those cells expressing t
207 e three groups were: CYP2D6, CYP2E1, NAD(P)H-menadione reductase, glutathione transferases M1 and T1,
209 recovery of virulence factor expression and menadione resistance, and in restoration of virulence.
210 ing the cells to menadione and detecting the menadione-S-glutathione conjugate (thiodione) that is fo
211 osines from the 2-methyl-1,4-naphthoquinone (menadione)-sensitized 365-nm irradiation of d(CpC).
212 ibition induced by oxidative stress (H2O2 or menadione), significantly ameliorated the H2O2-dependent
215 show that a pro-oxidant vitamin K precursor [menadione sodium bisulfite (MSB)] suppresses PC progress
220 cytotoxicities of four oxidative stressors (menadione, tert-butyl hydroperoxide, 4-hydroxynonenal, a
223 gen peroxide, the superoxide-generating drug menadione, the sulfhydryl-oxidizing agent diamide, the d
224 MA inhibition sensitized cells to death from menadione through a mechanism different from that of a l
228 one in the intestine followed by delivery of menadione to tissues and subsequent conversion to menaqu
229 rthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNO
230 YP2E1-overexpressing cells were resistant to menadione toxicity through an ERK1/2-dependent mechanism
232 cells within 5 min, whereas in ERalpha(-) or menadione-treated cells, no selectivity was observed.
238 f 25 protein spots increased >3-fold in H2O2/menadione treatments, a subset of these increased in ant
240 ts and measurements of phylloquinone-derived menadione using high resolution MS analysis and a bioass
241 QR2 catalyzes the two-electron reduction of menadione via the oxidation of N-alkylated or N-ribosyla
242 ures of QR2: in its native form and bound to menadione (vitamin K(3)), a physiological substrate.
244 uinone but a strong prenylation activity for menadione (vitamin K3), which has long been postulated a
246 l death caused by H(2)O(2), antimycin A, and menadione was considerably suppressed in both the mC5 an
247 nt of HEK293T cells, whereas the response to menadione was distinct, suggesting that this collaborati
250 water-soluble bisulfite addition product of menadione was used as the electron acceptor, an artifact
252 OP2 poisons (e.g. amonafide, batracylin, and menadione) was only slightly (less than 3-fold) affected
254 c concentrations of the superoxide generator menadione were established in the RALA255-10G rat hepato
255 nduced by redox cycling agents plumbagin and menadione, whereas an fgd mutant of M. smegmatis used G6
256 d by aminotriazole and to a lesser extent by menadione, whereas ZmMRP2 was expressed at a lower const
257 ts of 37 degrees C "heat shock" or sublethal menadione, which generates superoxide and hydrogen perox
258 tained the binary complex structures with GS-menadione, which in its reduced form, GS-menadiol, is a
259 nhibitors exemplified by the natural product menadione, which is shown in mouse tumor models to have
262 the product generated from the incubation of menadione with recombinant UBIAD1 revealed that the hydr