ライフサイエンスコーパス: buthionine

1 sion was examined by treating the cells with buthionine S,R-sulfoximine (BSO); 1-chloro, 2,4-dinitrob

2 ryls (mainly glutathione) in A(L) cells with buthionine S-R-sulfoximine increases the mutagenic poten

3 In contrast, depletion of GSH by L-buthionine (S, R)-sulfoximine up-regulated the above des

4 cy/+ Han:SPRD rats were treated with: (1) L-buthionine(S,R)-sulfoximine (BSO), a specific inhibitor

5 R cells with a nontoxic concentration of D,L-buthionine-S,R-sulfoximine (BSO) caused about 80-88% red

6 ne (GSH) by treatment of AREc32 cells with l-buthionine-S,R-sulfoximine (BSO) did not influence basal

7 l-Buthionine-S,R-sulfoximine (BSO), an inhibitor of GSH sy

8 L-buthionine-S,R-sulfoximine (BSO), an inhibitor of GSH sy

9 ncubation with the GSH synthesis inhibitor L-buthionine-S,R-sulfoximine (L-BSO).

10 carboxylic acid, N-acetyl-l-cysteine, or d,l-buthionine-S,R-sulfoximine.

11 l-Buthionine-S-sulfoximine (BSO) is a mechanism-based inhi

12 Combined BaP/DL-buthionine-(S, R)-sulfoximine challenge was cytotoxic to

13 depleted of glutathione by treatment with L-buthionine-(S,R) sulfoximine and diethyl maleate, reveal

14 evels have been pursued including the use of buthionine-(S,R)-sulfoxime (BSO), a potent and specific

15 G(0) synchronized cultures of vSMCs with DL-buthionine-(S,R)-sulfoximine (0.1 mM), a depletor of cel

16 urs (20 ng/mL) and then were treated with DL-buthionine-(S,R)-sulfoximine (BSO) for an additional 24

17 lar glutathione either by the addition of DL-buthionine-(S,R)-sulfoximine or by removal of L-cystine

18 Treatment with l-buthionine-(S,R)-sulfoximine reduced glutathione content

19 Glutathione depletion by dl-buthionine-(S,R)-sulfoximine rendered hepatocytes suscep

20 After treatment of cells with L-buthionine-(S,R)-sulfoximine to deplete glutathione, sel

21 Moreover, in contrast to AA, l-buthionine-(S,R)-sulfoximine toxicity is not prevented b

22 YP2E1-dependent toxicity can be blocked by l-buthionine-(S,R)-sulfoximine, a specific inhibitor of gl

23 rowing the atgstu17 in solution containing l-buthionine-(S,R)-sulfoximine, a specific inhibitor of GS

24 ound to be more resistant to the toxicity of buthionine-(S,R)-sulfoximine, an inhibitor of glutathion

25 ls by the glutathione synthetase inhibitor L-buthionine-(S,R)-sulfoximine.

26 ished ovariectomy-induced bone loss, while l-buthionine-(S,R)-sulphoximine (BSO), a specific inhibito

27 dl-buthionine-[S, R]-sulfoximine (BSO) decreased intracellu

28 ty during 2-deoxy-D-glucose exposure using l-buthionine-[S,R]-sulfoximine (BSO) significantly enhance

29 We investigated cytoenhancement, using L-buthionine-[S,R]-sulfoximine (BSO) to reduce cellular gl

30 SH) on noise-induced hearing loss by using l-buthionine-[S,R]-sulfoximine (BSO), an inhibitor of GSH

31 An inhibitor of glutathione synthesis, l-buthionine-[S,R]-sulfoximine (BSO), sensitized FaDu cell

32 rther confirmed by exposing BPAE cells to dl-buthionine-[S,R]-sulfoximine (BSO).

33 l line MCF-7, we have shown that 10 microM L-buthionine-[S,R]-sulfoximine (L-BSO), an inhibitor of ga

34 ated with the glutathione-depleting agent, L-buthionine-[S,R]-sulfoximine, and attenuated in cells pr

35 -4 cells with the GSH synthesis inhibitor, L-buthionine-(SR)-sulfoximine, resulted in a time-dependen

36 Inhibition of glutathione synthesis by L-buthionine sulfoxamine increases potency of citral.

37 Ascorbic acid and buthionine sulfoxide (BSO) decreased GSH to a greater ex

38 er stress inducers, including Fas ligand and buthionine sulfoxide, also induced Bcl-2 S-nitrosylation

39 amma-glutamylcysteine synthetase inhibitor l-buthionine sulfoxime (BSO).

40 vels of the glutathione synthase inhibitor l-buthionine sulfoxime.

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

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

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

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

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

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

47 6 hours with 0.2 mmol/L diamide and 1 mmol/L buthionine sulfoximine (BSO) decreased GSH levels and in

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

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

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

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

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

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

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

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

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

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

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

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

60 Buthionine sulfoximine (BSO), an inhibitor of glutathion

61 Buthionine sulfoximine (BSO), an inhibitor of glutathion

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Both buthionine sulfoximine and BCNU inhibited the induction

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 Buthionine sulfoximine treatment resulted in a 24% reduc

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

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

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

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

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

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

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

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

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

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

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

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

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

117 ,4,3',4'-tetrachlorobiphenyl, dexamethasone, buthionine sulfoximine, ethacrynic acid, or N-acetylcyst

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

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

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

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

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

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

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

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

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

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

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

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

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

131 the enhancing effects of GSH depletion with buthionine sulfoximine.

132 e gamma-glutamylcysteine synthesis inhibitor buthionine sulfoximine.

133 and direct inhibition of GSH biosynthesis by buthionine sulfoximine.

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

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

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

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

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

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

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

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

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

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

144 her GSH depleters, diethyl maleate (DEM) and buthionine sulphoximine (BSO), only 1 of which (DEM) can

145 Male CD-1 mice received buthionine sulphoximine (BSO; 7.2 mmol/kg), diethyl male

146 vation of p53 pathway; and synergized with L-buthionine sulphoximine in all samples.

147 hibited myeloma growth and synergized with L-buthionine sulphoximine in vivo.

148 ated by GSH synthetase silencing or by and L-buthionine sulphoximine, an irreversible inhibitor of ga

149 effect was attenuated by GSH depletion with buthionine sulphoximine, even in GSH-containing media.

150 ocyanin-producing grapevine root cultures to buthionine sulphoximine, which reduced GSH levels, a dec