ライフサイエンスコーパス: Tiron

1 igastric artery (21 +/- 2 mmHg; P < 0.01 vs. tiron).

2 d 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron).

3 ed in aqueous solution containing Fe(II) and tiron.

4 antioxidants, such as N-acetyl-l-cysteine or Tiron.

5 chelator competition reaction using EDTA and Tiron.

6 cid)-porphyrin-chloride (200 micromol/L) and Tiron.

7 inoguanidine, L-N(G)-monomethyl arginine, or Tiron.

8 formation of the ternary complexes Fe-hTF/2N-Tiron.

9 We found that suffusion with tiron (1 mM) did not alter basal permeability of the blo

10 es with sodium dihydroxybenzene disulfonate (Tiron, 10(-)(3) mol/L), a cell-permeable superoxide scav

11 re all inhibited by the superoxide scavenger Tiron (4,5-dihydroxy-1,3-benzene disulfonic acid).

12 idants N-acetylcysteine (NAC, 10 mmol/L) and Tiron (5 mmol/L) and the flavin-inhibitor diphenylene io

13 Tiron (a scavenger of O2.-) did not alter the actions of

14 orm-nonselective NO synthase inhibitor), and Tiron (a superoxide radical anion scavenger) on the deve

15 nted by sodium dihydroxybenzene disulfonate (Tiron), a cell-permeable superoxide scavenger.

16 ygen species (ROS) and attenuation of ROS by tiron, a ROS scavenger, reduced the sub-G(1) population

17 Infusion of tiron, a superoxide scavenger, attenuated the exaggerate

18 Tiron added to muscle homogenates reduced ROS production

19 The inhibitory effect of Tiron against bortezomib was selective, since it was not

20 r 4,5-dihydroxy-1,3-benzenedisulphonic acid (Tiron) also reduced the increase in fluorescence observe

21 Tiron, an antioxidant agent, blocked the bortezomib-indu

22 dase activity were inhibited by antioxidants tiron and N-acetylcysteine and the inhibitor of flavopro

23 The ROS scavenger Tiron and the superoxide dismutase mimetic MnTBPA abolis

24 and by ROS scavenger superoxide dismutase or tiron and was not observed in mice lacking the gp91phox

25 an 4,5-dihydroxy-1,3-benzenedisulfonic acid (Tiron) and 4-hydroxy-2,2,6,6-tetramethylpiperydine-1-oxy

26 Antioxidants (N-acetyl-L-cysteine and Tiron) and inhibitors of mitochondrial permeability tran

27 epolarization was attenuated by Z-VDVAD-FMK, tiron, and an inhibitor of the mitochondrial permeabilit

28 which was dose-dependently inhibited by NAC, Tiron, and DPI.

29 s due to fiber treatment with the scavenger, tiron, and the inducer, antimycin A, were easily monitor

30 ts on absorption and fluorescence spectra of Tiron arylboronate esters are characterized.

31 estigate molecules with similar structure to tiron as potent and clinically relevant antioxidants.

32 ria-targeted antioxidants, such as MitoQ and tiron, as potentially effective antioxidant therapies ag

33 n nNOS-/- was restored by preincubation with Tiron, ascorbic acid, Tempol, oxypurinol, or SB203850, a

34 moval kinetics by the high-affinity chelator tiron at pH 7.4.

35 rginine or a superoxide scavenger, tempol or tiron, attenuated sympathetic vasoconstriction in contra

36 at was blocked by the free radical scavenger tiron but not by a caspase-2 inhibitor (benzyloxycarbony

37 e augmented by superoxide dismutase (SOD) or Tiron (but not L-arginine or the TXA(2) receptor antagon

38 by antioxidants such as N-acetylcysteine and Tiron, but not by calcium chelation.

39 ally, we show that the polyhydroxyl compound Tiron can function as a competitive inhibitor of bortezo

40 onsistent with previous work, the 1:2 Fe(II)-tiron complex, FeL2(6-), is the dominant reactive specie

41 The K(obs) for Tiron determined by (11)B NMR titrations are approximate

42 In addition, tiron did not alter baseline diameter of cerebral arteri

43 (3+)FbpA-NTA react differently with EDTA and Tiron during the Fe(3+)-exchange process.

44 th the use of a long quantitative PCR assay, tiron (EC50 10 mM) was found to confer complete (100%) p

45 itors (i.e. MG132) revealed a specificity of Tiron for bortezomib.

46 etyl-L-cysteine, or the superoxide scavenger Tiron, further indicating that inhibition occurs through

47 ers of 4,5-dihydroxy-1,3-benzenedisulfonate (Tiron) generally agree with those expected on the basis

48 se complexes suggest a different ligation of Tiron in the mutants from that in wild-type hTF/2N.

49 T(1) blocker losartan and the O(2) scavenger TIRON: In conclusion, IGF-1 interferes with the developm

50 g, whereas the peak EPR in these rats during tiron infusion averaged 13 +/- 2 mmHg (n = 12; P < 0.001

51 Tiron infusion had no effect on the EPR in rats with pat

52 Conversely, we found no effect of tiron infusion on the pressor reflex in rats with patent

53 MitoQ and Tiron inhibited TGF-beta-induced ASM cell proliferation

54 the EPR, we infused a superoxide scavenger, tiron, into the superficial epigastric artery of decereb

55 tion facilitated N-oxide reduction by Fe(II)-tiron involves a free radical mechanism, and the subsequ

56 /or peroxynitrite with superoxide dismutase, tiron, Mn(III)tetrakis(4-benzoic acid)porphyrin, and ura

57 with ROS scavengers (e.g. MnTBAP, Mn-cpx 3, TIRON) nearly eliminated Ca(2+) sparks.

58 = 12; P < 0.001); the attenuating effect of tiron on the EPR was partly reversed when saline was rei

59 Tiron, on the other hand, does not act as a synergistic

60 normalized to WT levels by the O2- scavenger tiron or by Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin

61 glycine or the superoxide dismutase mimetic, Tiron, or by treating homogenates with dithiothreitol.

62 eiodonium chloride, the superoxide scavenger tiron, or tricarbonyldichlororuthenium(II)-dimer (carbon

63 nitro-L-arginine (an NO synthase inhibitor), Tiron, or urate.

64 other antioxidants such as N-acetylcysteine, Tiron, or vitamin E.

65 The chelator, Tiron, removes iron from hTF/2N with a simple saturation

66 geted and -localized antioxidants (MitoQ and tiron, respectively) with cellular antioxidants against

67 owever, the reaction of the D63 mutants with Tiron results in the formation of the ternary complexes

68 Scavenging of O(2)(*-) with Tiron reversed the NAC-induced G(1) arrest.

69 f2 small interfering RNA both indicated that tiron's mode of action was Nrf2 independent.

70 The comet assay showed that tiron's protective effect against H2O2-induced nuclear D

71 all cell lung cancer were also responsive to Tiron, suggesting a broad impact of this agent as a bort

72 and completely restored by coincubation with tiron, tempol or apocynin.

73 o-administration of the superoxide scavenger Tiron, the peroxynitrite scavenger Urate, or the eNOS in

74 We exploited this novel feature of Tiron to define the "point of no return" of proteasome i

75 nhibitors, including N-acetyl-L-cysteine and Tiron, to block this killing effect.

76 Tiron treatment also protected against the bortezomib-in

77 This particular protective effect of tiron was greater than a range of cellular antioxidants

78 This effect of Tiron was surprising, since it is a classical radical sp