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1 preventable with a peroxynitrite scavenger, ebselen.
2 n be completely prevented by the antioxidant ebselen.
3 al cells in 22-week-old ZDF was prevented by ebselen.
4 nd provided an additive inhibitory effect to ebselen.
5 diselenides 8 were 3-6-fold more active than ebselen.
6 locked by the glutathione peroxidase mimetic ebselen.
7 d LRRK2/PRDX3 flies with a peroxidase mimic, Ebselen.
8 of catalase as well as by co-treatment with Ebselen.
9 a previously unrecognized in vivo target of ebselen.
10 talase, and the glutathione peroxidase mimic ebselen.
11 eveloping OLs was prevented by the GPx mimic ebselen.
12 restored by the ONOO(-) scavengers urate and ebselen.
18 -benzisoselenazol-3(2H)-ones, represented by ebselen (1a), are being studied intensively for a range
19 lene iodonium, 1.4+/-0.3-fold migration; and ebselen, 2.0+/-0.5-fold migration), as did overexpressio
21 re enrolled and randomly assigned to receive ebselen 200 mg (n=22), 400 mg (n=20), or 600 mg (n=21),
22 of Florida (Gainsville, FL, USA) to receive ebselen 200 mg, 400 mg, or 600 mg, or placebo orally twi
23 S-dependent as assessed by pretreatment with ebselen (3.6 +/- 0.2 versus 1.1 +/- 0.2), diphenylene io
27 ential therapeutics for suicidality, such as ebselen (a lithium mimetic), piracetam (a nootropic), ch
28 ormation was greatly diminished when GSH and ebselen (a selenoperoxidase mimetic) were present, consi
29 Consistent with this idea, it was found that ebselen, a compound with GSHPx-like activity, was able t
30 cysteine (NAC), a non-specific antioxidant, ebselen, a glutathione mimetic, or combined SOD plus cat
32 constants for amino acid hydroperoxides with ebselen, a glutathione peroxidase mimic, were also deter
33 nergic neuronal cells and determined whether ebselen, a glutathione peroxidase-mimetic, protected aga
37 antioxidants pyrrolidine dithiocarbamate and ebselen abolish transcriptional activation of these gene
41 atment with the glutathione peroxidase mimic ebselen also reversed behavioral deficits in this animal
42 and resonance Raman spectroscopy showed that ebselen altered the active site heme of rIDO by inducing
46 n (ZL) rats and after chronic treatment with ebselen, an antioxidant and peroxinitrite scavenger.
47 ent of Zucker diabetic fatty (ZDF) rats with ebselen, an oral GPx mimetic, will prevent beta-cell det
53 structures of Ag85C covalently modified with ebselen and other thiol-reactive compounds, p-chloromerc
54 tential and is inhibited by the antioxidants ebselen and TEMPOL, consistent with the concept that it
55 antioxidants pyrrolidinedithiocarbamate and ebselen and the Cu,Zn superoxide dismutase inhibitor die
56 computed value of 7.1 kcal/mol for the drug ebselen and the experimentally measured barrier of 8.8 k
57 inhibitable by the peroxynitrite scavengers ebselen and uric acid, was markedly increased in apoE(-/
58 re, antiapoptotic antioxidants (e.g. FeTBAP, ebselen, and alpha-phenyl-tert-butyl nitrone) inhibited
61 e (III) tetrakis (4-benzoic acid) porphyrin, ebselen, and N-acetylcysteine failed to prevent cell dea
62 Concomitant with the reversal of senescence, ebselen, and NOHA each restored NO production to levels
63 which is improved by peroxinitrite scavenger ebselen, and thus considered its cause and not consequen
64 est that the anti-inflammatory properties of ebselen are achieved through an inhibition of lung ICAM-
65 tion for further analysis and development of ebselen as a potential treatment for multidrug-resistant
66 H. pylori enzymes, respectively, indicating ebselen as one of the most potent low-molecular-weight i
68 s ROS production in both populations; and 3) ebselen at 5-20 micro M inhibits DC-induced proliferatio
69 nin) or enhancement of peroxide consumption (ebselen) but not inhibition of xanthine oxidase (allopur
74 uction of pre-existing lipid peroxides using ebselen delayed HbLDL kinetics and inhibited HO-1 induct
76 nd, 2-phenyl-1,2-benzisoselenazol-3(2H)-one (ebselen), displayed Ki values equal to 2.11 and 226 nM a
77 re tone audiometry; a reduction of 50% in an ebselen dose group compared with the placebo group was j
81 treatments with the peroxynitrite scavenger, ebselen, eNOS intermediate N(omega)-hydroxy-L-arginine (
84 at 4 kHz was 1.32 dB (SE 0.91) in the 400 mg ebselen group compared with 4.07 dB (0.90) in the placeb
90 n peroxide three times more efficiently than Ebselen in the presence of glutathione as a stoichiometr
91 h from menadione was blocked by catalase and ebselen, indicating that death was secondary to oxidant
104 ompound ebsulfur (EbS), a sulfur analogue of ebselen, is a potent inhibitor of T. brucei growth with
105 d a selenium-containing antioxidant compound ebselen known to modulate both thioredoxin and glutaredo
106 nt response element (ARE) and postulate that ebselen may act both by the transcriptional upregulation
111 Studies using the H(+)-ATPase inhibitor ebselen or a yeast genetic strain with reduced H(+)-ATPa
113 d either the antioxidants, alpha tocopherol, ebselen, or idebenone (a coenzyme Q analogue); or the MP
117 An antioxidant/peroxynitrite scavenger, ebselen, prevented stress-induced SIRT1 depletion and su
118 of oxidative stress is the mechanism whereby ebselen prevents apoptosis and preserves intranuclear Pd
119 labeling and mass spectrometry revealed that ebselen reacted with multiple cysteine residues of IDO.
121 trial with healthy participants, acute oral ebselen reduced brain myo-inositol in the anterior cingu
123 hondria-targeted hydrogen peroxide scavenger ebselen, reduced Sirt3 S-glutathionylation, diminished S
126 s well as reducing lipid hydroperoxides with ebselen, resulted in inhibition of macrophage activation
127 onium, or the glutathione peroxidase mimetic ebselen significantly attenuated migration (PDGF alone,
128 nium or the antioxidants N-acetylcysteine or ebselen significantly inhibited Ang II-induced cAbl phos
129 tion states upon Ag-specific interaction; 2) ebselen significantly inhibits ROS production in both po
130 late, alpha-phenyl-N-tert-butyl nitrone, and ebselen significantly suppressed iNOS transgene inductio
133 as well as a high affinity substrate of TR1, ebselen, to demonstrate that Tat-dependent transcription
134 CuDIPs and the glutathione reductase mimetic ebselen, TPA-stimulated TNFalpha shedding from PKCepsilo
137 ticles, was almost completely prevented when ebselen was administered from 8 to 22 weeks and partiall
142 the corresponding des-bromo compound 3a and ebselen when evaluated in the coupled reductase assay.
143 ith either 5 mM GSH, 2 mM GSH-MEE, or 0.1 mM ebselen, when instilled into the mucosal fluid, resulted
146 postulated that the seleno-organic compound ebselen would attenuate neutrophil recruitment and activ
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