ライフサイエンスコーパス: buthionine sulfoximine

1 the enhancing effects of GSH depletion with buthionine sulfoximine.

2 e gamma-glutamylcysteine synthesis inhibitor buthionine sulfoximine.

3 and direct inhibition of GSH biosynthesis by buthionine sulfoximine.

4 ort in transgenic plants were abrogated by l-buthionine sulfoximine.

5 ll as by treatment with homocysteic acid and buthionine sulfoximine.

6 nt mice, despite further depletion of GSH by buthionine sulfoximine.

7 e (0 to 0.2 mM) with or without GSH ester or buthionine sulfoximine.

8 p to 60% by subcutaneous administration of L-buthionine sulfoximine.

9 tions of inhibition of GSH synthesis with dl-buthionine sulfoximine.

10 mM), and it is inactivated by cystamine and buthionine sulfoximine.

11 to ethacrynic acid (an inhibitor of GST-Pi), buthionine sulfoximine (a glutathione synthesis inhibito

12 Treating tolerant mice with buthionine sulfoximine, a gamma-GCS inhibitor, eliminate

13 NF-alpha neutralizing antibody (Ab) and by L-buthionine-sulfoximine, a GSH-depleting agent.

14 cid, and the glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to imm

15 ibitor of gamma-glutamylcysteine synthetase, buthionine sulfoximine, also decreased intracellular glu

16 maintenance of NFI activity in vivo, we used buthionine sulfoximine, an agent that inhibits GSH synth

17 mmatory cytokine production was inhibited by buthionine sulfoximine, an inhibitor of GCL.

18 in I(Ca,L), dogs were treated for 48 h with buthionine sulfoximine, an inhibitor of glutathione synt

19 Treatment of MCF-7 lines with buthionine sulfoximine, an inhibitor of glutathione synt

20 Treatment with buthionine sulfoximine, an inhibitor of GSH synthesis, a

21 fluent HLE-B3 cells pretreated with 10 mM DL-buthionine sulfoximine and 0.5 mM acivicin were used in

22 Hepatocytes were cultured with buthionine sulfoximine and 1,3-bis(chloroethyl)-1-nitros

23 tants were increased up to 80% with combined buthionine sulfoximine and arsenic treatments, suggestin

24 Both buthionine sulfoximine and BCNU inhibited the induction

25 As with other GCL, buthionine sulfoximine and cystamine inactivate the Arab

26 Although the glutathione-depleting agents buthionine sulfoximine and diethylmaleate were more pote

27 r treatment with the GSH synthesis inhibitor buthionine sulfoximine, and aminonicotinamide (6-ANAM),

28 hydroxymethylcytosine in cells treated with buthionine sulfoximine, and in mice depleted for the maj

29 Aminotriazole, L-buthionine sulfoximine, and sodium azide partly abrogate

30 ma-glutamylcysteine synthetase (gammaGCS) by buthionine sulfoximine augmented the increase in islet p

31 ated by enhanced toxicity in the presence of buthionine sulfoximine (BSO) and attenuation of toxicity

32 Inhibition of GSH and Trx metabolism with buthionine sulfoximine (BSO) and auranofin (AUR), respec

33 vious studies have identified nifurtimox and buthionine sulfoximine (BSO) as effective agents in chil

34 e events, whereas glutathione depletion with buthionine sulfoximine (BSO) augmented them.

35 CYP2E1-expressing cells by treatment with l-buthionine sulfoximine (BSO) causes decreased cell viabi

36 6 hours with 0.2 mmol/L diamide and 1 mmol/L buthionine sulfoximine (BSO) decreased GSH levels and in

37 the present study, we examined the effect of buthionine sulfoximine (BSO) on mutation frequency and t

38 ith the irreversible inhibitor of gammaGCS L-buthionine sulfoximine (BSO) reduced intracellular GSH l

39 Depletion of GSH by buthionine sulfoximine (BSO) restores the sensitivity of

40 Reduction of glutathione levels by buthionine sulfoximine (BSO) significantly enhanced the

41 through day 7, the cells were treated with L-buthionine sulfoximine (BSO) to deplete glutathione stor

42 was further increased after treatment with L-buthionine sulfoximine (BSO) to lower GSH levels.

43 Cell death caused by depletion of GSH by buthionine sulfoximine (BSO) was increased in mE10 and m

44 with As(2)O(3) alone or in combination with buthionine sulfoximine (BSO) was studied in NB4, U937, N

45 NT and on RGC-5 cells treated with glutamate/buthionine sulfoximine (BSO) were determined by RGC dens

46 hiols by treating uninfected astrocytes with buthionine sulfoximine (BSO), a glutathione synthesis in

47 Treatment of cells with buthionine sulfoximine (BSO), an enzyme-activated inhibi

48 Buthionine sulfoximine (BSO), an inhibitor of glutathion

49 ate (DEM), a glutathione-depleting agent, or buthionine sulfoximine (BSO), an inhibitor of glutathion

50 Buthionine sulfoximine (BSO), an inhibitor of glutathion

51 els in surviving T cells and is abrogated by buthionine sulfoximine (BSO), an inhibitor of GSH synthe

52 inhibited when GSH synthesis was blocked by buthionine sulfoximine (BSO), an inhibitor of the enzyme

53 ats received tap water (vehicle) and 30 mM L-buthionine sulfoximine (BSO), an oxidant, with and witho

54 ms examined to date are rapidly inhibited by buthionine sulfoximine (BSO), most reports indicate that

55 eating cells with diethyl maleate (DEM), D,L-buthionine sulfoximine (BSO), or tert-butylhydroquinone

56 onic depletion by 18 hours pretreatment with buthionine sulfoximine (BSO), which depletes GSH by bloc

57 otected the E47 cells against AA toxicity or buthionine sulfoximine (BSO)-dependent toxicity.

58 nd were exposed to either L-glutamic acid or buthionine sulfoximine (BSO).

59 restored GSH synthesis in a Glu (10 mM) plus buthionine-sulfoximine (BSO) (0.2 mM)-treated group, ind

60 athways regulating redox homeostasis using l-buthionine-sulfoximine (BSO, glutathione synthesis inhib

61 e synthase inhibitor buthionine sulfoximine (buthionine sulfoximine [BSO], 30 mmol/L) in drinking wat

62 ere given the glutathione synthase inhibitor buthionine sulfoximine (buthionine sulfoximine [BSO], 30

63 Conversely, the GSH-depleting agent buthionine sulfoximine completely abolished the protecti

64 ng-term process elaboration was blocked by L-buthionine sulfoximine, consistent with mediation by an

65 uperoxide generators menadione, paraquat, or buthionine sulfoximine down-regulates c-FLIP long (c-FLI

66 ess by inhibiting glutathione synthesis with buthionine-sulfoximine dramatically increased red blood

67 ,4,3',4'-tetrachlorobiphenyl, dexamethasone, buthionine sulfoximine, ethacrynic acid, or N-acetylcyst

68 Pretreatment of HeLa cells with buthionine sulfoximine greatly potentiated the inactivat

69 SH synthesis was inhibited by treatment with buthionine sulfoximine, GSH levels rapidly declined in E

70 Moreover, glutathione depletion with buthionine sulfoximine had no effect on MX transport or

71 We show that nontoxic doses of l-buthionine sulfoximine increase the selectivity of organ

72 l ester decreased, whereas the Gcl inhibitor buthionine sulfoximine increased DomA toxicity.

73 Pretreatment with L-buthionine sulfoximine increased SFN-induced ARE express

74 glutathione by treatment of Hepa cells with buthionine sulfoximine increased the inducer potencies o

75 Depletion of intracellular GSH by D,L-buthionine sulfoximine increased the intracellular accum

76 H9c2 cardiomyocytes, Rac1 activation with l-buthionine sulfoximine increased; Rac1 inhibition with N

77 of glutathione using N-acetylcysteine and L-buthionine-sulfoximine indicate that changes in glutathi

78 esistant to glutamate-, homocysteine-, and l-buthionine sulfoximine-induced toxicity.

79 the glutathione (GSH)-depleting compound, L-buthionine sulfoximine (L-BSO), exhibited enhanced sensi

80 n of TrxR activity by ATG and glutathione by buthionine sulfoximine led to overoxidation of Trx1 and

81 Depleting the GSH pool using buthionine sulfoximine limits fly survival, thus confirm

82 MK571, PSC833, and buthionine sulfoximine markedly increased cellular arsen

83 ly, intracellular glutathione depletion with buthionine sulfoximine or energy depletion using 2-deoxy

84 Inhibition of glutathione synthesis with buthionine sulfoximine or inhibition of glutathione redu

85 e), an inhibitor of glutathione synthesis (L-buthionine-sulfoximine) or glutathione reductase (1,3-bi

86 y by the inhibitor of glutathione synthesis, buthionine sulfoximine, or by the precursor of cysteine,

87 Treatment of HeLa cells with 2 mm l-buthionine sulfoximine promoted the formation of ox-HSF1

88 epletion of glutathione by pretreatment with buthionine sulfoximine rendered cells more susceptible t

89 verted or aggravated by N-acetylcysteine and buthionine sulfoximine, respectively.

90 rols by the glutathione synthetase inhibitor buthionine sulfoximine resulted in more rapid injury by

91 intracellular antioxidant, glutathione, with buthionine sulfoximine significantly increased B[a]P-med

92 ving continuous GSH infusion, treatment with buthionine sulfoximine starting day - 2 decreased sinuso

93 enous GSH and intracellular GSH depletion by buthionine sulfoximine, suggesting that GSH transport is

94 Accordingly, glutathione depletion by buthionine sulfoximine together with restoration of p53

95 tBHQ protected cells from both glutamate and buthionine sulfoximine toxicity.

96 uptake kinetics were studied in acivicin and buthionine sulfoximine-treated HLE-B3 cells in NaCl medi

97 blood cell sickling in the sickle kidney: in buthionine-sulfoximine-treated sickle mice, red blood ce

98 Buthionine sulfoximine treatment resulted in a 24% reduc

99 tressed by depleting the glutathione pool by buthionine sulfoximine treatment.

100 was markedly enhanced after GSH depletion by buthionine sulfoximine treatment.

101 two experimental drugs, i.e., auranofin and buthionine sulfoximine, was able to reduce the viral res

102 moter transactivation; whereas TNFalpha or l-buthionine sulfoximine, which depletes GSH, further enha

103 thione (to less than 15% of basal levels) by buthionine sulfoximine, which does not directly modify K