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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 using L-buthionine sulfoxamine eliminated MSC clonogenicity in t
37     Inhibition of glutathione synthesis by L-buthionine sulfoxamine increases potency of citral.
38                            Ascorbic acid and buthionine sulfoxide (BSO) decreased GSH to a greater ex
39 er stress inducers, including Fas ligand and buthionine sulfoxide, also induced Bcl-2 S-nitrosylation
40 amma-glutamylcysteine synthetase inhibitor l-buthionine sulfoxime (BSO).
41 vels of the glutathione synthase inhibitor l-buthionine sulfoxime.
42 to ethacrynic acid (an inhibitor of GST-Pi), buthionine sulfoximine (a glutathione synthesis inhibito
43 ated by enhanced toxicity in the presence of buthionine sulfoximine (BSO) and attenuation of toxicity
44    Inhibition of GSH and Trx metabolism with buthionine sulfoximine (BSO) and auranofin (AUR), respec
45    MTST was used to investigate effects of l-buthionine sulfoximine (BSO) and pyrrolidine dithiocarba
46 vious studies have identified nifurtimox and buthionine sulfoximine (BSO) as effective agents in chil
47 e events, whereas glutathione depletion with buthionine sulfoximine (BSO) augmented them.
48  CYP2E1-expressing cells by treatment with l-buthionine sulfoximine (BSO) causes decreased cell viabi
49 6 hours with 0.2 mmol/L diamide and 1 mmol/L buthionine sulfoximine (BSO) decreased GSH levels and in
50 alogues with glutathione synthesis inhibitor buthionine sulfoximine (BSO) leads to synergistic cell g
51 the present study, we examined the effect of buthionine sulfoximine (BSO) on mutation frequency and t
52 ith the irreversible inhibitor of gammaGCS L-buthionine sulfoximine (BSO) reduced intracellular GSH l
53                          Depletion of GSH by buthionine sulfoximine (BSO) restores the sensitivity of
54           Reduction of glutathione levels by buthionine sulfoximine (BSO) significantly enhanced the
55 through day 7, the cells were treated with L-buthionine sulfoximine (BSO) to deplete glutathione stor
56 was further increased after treatment with L-buthionine sulfoximine (BSO) to lower GSH levels.
57     Cell death caused by depletion of GSH by buthionine sulfoximine (BSO) was increased in mE10 and m
58  with As(2)O(3) alone or in combination with buthionine sulfoximine (BSO) was studied in NB4, U937, N
59 NT and on RGC-5 cells treated with glutamate/buthionine sulfoximine (BSO) were determined by RGC dens
60 icin-resistant cells and tumor xenografts to buthionine sulfoximine (BSO), a drug that interferes wit
61 hiols by treating uninfected astrocytes with buthionine sulfoximine (BSO), a glutathione synthesis in
62                      Treatment of cells with buthionine sulfoximine (BSO), an enzyme-activated inhibi
63 ate (DEM), a glutathione-depleting agent, or buthionine sulfoximine (BSO), an inhibitor of glutathion
64                                              Buthionine sulfoximine (BSO), an inhibitor of glutathion
65                                              Buthionine sulfoximine (BSO), an inhibitor of glutathion
66 els in surviving T cells and is abrogated by buthionine sulfoximine (BSO), an inhibitor of GSH synthe
67  inhibited when GSH synthesis was blocked by buthionine sulfoximine (BSO), an inhibitor of the enzyme
68 ats received tap water (vehicle) and 30 mM L-buthionine sulfoximine (BSO), an oxidant, with and witho
69 ms examined to date are rapidly inhibited by buthionine sulfoximine (BSO), most reports indicate that
70 eating cells with diethyl maleate (DEM), D,L-buthionine sulfoximine (BSO), or tert-butylhydroquinone
71 onic depletion by 18 hours pretreatment with buthionine sulfoximine (BSO), which depletes GSH by bloc
72 otected the E47 cells against AA toxicity or buthionine sulfoximine (BSO)-dependent toxicity.
73 nd were exposed to either L-glutamic acid or buthionine sulfoximine (BSO).
74 ere given the glutathione synthase inhibitor buthionine sulfoximine (buthionine sulfoximine [BSO], 30
75  the glutathione (GSH)-depleting compound, L-buthionine sulfoximine (L-BSO), exhibited enhanced sensi
76 e synthase inhibitor buthionine sulfoximine (buthionine sulfoximine [BSO], 30 mmol/L) in drinking wat
77 cid, and the glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to imm
78 fluent HLE-B3 cells pretreated with 10 mM DL-buthionine sulfoximine and 0.5 mM acivicin were used in
79               Hepatocytes were cultured with buthionine sulfoximine and 1,3-bis(chloroethyl)-1-nitros
80 tants were increased up to 80% with combined buthionine sulfoximine and arsenic treatments, suggestin
81                                         Both buthionine sulfoximine and BCNU inhibited the induction
82                           As with other GCL, buthionine sulfoximine and cystamine inactivate the Arab
83    Although the glutathione-depleting agents buthionine sulfoximine and diethylmaleate were more pote
84 ma-glutamylcysteine synthetase (gammaGCS) by buthionine sulfoximine augmented the increase in islet p
85          Conversely, the GSH-depleting agent buthionine sulfoximine completely abolished the protecti
86 uperoxide generators menadione, paraquat, or buthionine sulfoximine down-regulates c-FLIP long (c-FLI
87              Pretreatment of HeLa cells with buthionine sulfoximine greatly potentiated the inactivat
88         Moreover, glutathione depletion with buthionine sulfoximine had no effect on MX transport or
89 ro-injections of the GSH synthesis inhibitor buthionine sulfoximine in the nucleus accumbens impaired
90             We show that nontoxic doses of l-buthionine sulfoximine increase the selectivity of organ
91 l ester decreased, whereas the Gcl inhibitor buthionine sulfoximine increased DomA toxicity.
92                          Pretreatment with L-buthionine sulfoximine increased SFN-induced ARE express
93  glutathione by treatment of Hepa cells with buthionine sulfoximine increased the inducer potencies o
94        Depletion of intracellular GSH by D,L-buthionine sulfoximine increased the intracellular accum
95  H9c2 cardiomyocytes, Rac1 activation with l-buthionine sulfoximine increased; Rac1 inhibition with N
96 n of TrxR activity by ATG and glutathione by buthionine sulfoximine led to overoxidation of Trx1 and
97                 Depleting the GSH pool using buthionine sulfoximine limits fly survival, thus confirm
98                           MK571, PSC833, and buthionine sulfoximine markedly increased cellular arsen
99 ly, intracellular glutathione depletion with buthionine sulfoximine or energy depletion using 2-deoxy
100     Inhibition of glutathione synthesis with buthionine sulfoximine or inhibition of glutathione redu
101          Treatment of HeLa cells with 2 mm l-buthionine sulfoximine promoted the formation of ox-HSF1
102 epletion of glutathione by pretreatment with buthionine sulfoximine rendered cells more susceptible t
103 rols by the glutathione synthetase inhibitor buthionine sulfoximine resulted in more rapid injury by
104 intracellular antioxidant, glutathione, with buthionine sulfoximine significantly increased B[a]P-med
105 ving continuous GSH infusion, treatment with buthionine sulfoximine starting day - 2 decreased sinuso
106        Accordingly, glutathione depletion by buthionine sulfoximine together with restoration of p53
107 tBHQ protected cells from both glutamate and buthionine sulfoximine toxicity.
108                                              Buthionine sulfoximine treatment resulted in a 24% reduc
109 was markedly enhanced after GSH depletion by buthionine sulfoximine treatment.
110 tressed by depleting the glutathione pool by buthionine sulfoximine treatment.
111                  Treating tolerant mice with buthionine sulfoximine, a gamma-GCS inhibitor, eliminate
112 as a requirement for cellular sensitivity to buthionine sulfoximine, a glutathione synthesis inhibito
113 ibitor of gamma-glutamylcysteine synthetase, buthionine sulfoximine, also decreased intracellular glu
114 maintenance of NFI activity in vivo, we used buthionine sulfoximine, an agent that inhibits GSH synth
115 mmatory cytokine production was inhibited by buthionine sulfoximine, an inhibitor of GCL.
116  in I(Ca,L), dogs were treated for 48 h with buthionine sulfoximine, an inhibitor of glutathione synt
117                Treatment of MCF-7 lines with buthionine sulfoximine, an inhibitor of glutathione synt
118                               Treatment with buthionine sulfoximine, an inhibitor of GSH synthesis, a
119 r treatment with the GSH synthesis inhibitor buthionine sulfoximine, and aminonicotinamide (6-ANAM),
120  hydroxymethylcytosine in cells treated with buthionine sulfoximine, and in mice depleted for the maj
121                             Aminotriazole, L-buthionine sulfoximine, and sodium azide partly abrogate
122 ng-term process elaboration was blocked by L-buthionine sulfoximine, consistent with mediation by an
123 ,4,3',4'-tetrachlorobiphenyl, dexamethasone, buthionine sulfoximine, ethacrynic acid, or N-acetylcyst
124 SH synthesis was inhibited by treatment with buthionine sulfoximine, GSH levels rapidly declined in E
125 y by the inhibitor of glutathione synthesis, buthionine sulfoximine, or by the precursor of cysteine,
126 verted or aggravated by N-acetylcysteine and buthionine sulfoximine, respectively.
127 enous GSH and intracellular GSH depletion by buthionine sulfoximine, suggesting that GSH transport is
128  two experimental drugs, i.e., auranofin and buthionine sulfoximine, was able to reduce the viral res
129 moter transactivation; whereas TNFalpha or l-buthionine sulfoximine, which depletes GSH, further enha
130 thione (to less than 15% of basal levels) by buthionine sulfoximine, which does not directly modify K
131 ellular hydrogen peroxide concentrations and buthionine sulfoximine- and auranofin-induced inhibition
132 esistant to glutamate-, homocysteine-, and l-buthionine sulfoximine-induced toxicity.
133 uptake kinetics were studied in acivicin and buthionine sulfoximine-treated HLE-B3 cells in NaCl medi
134 nt mice, despite further depletion of GSH by buthionine sulfoximine.
135 e (0 to 0.2 mM) with or without GSH ester or buthionine sulfoximine.
136 p to 60% by subcutaneous administration of L-buthionine sulfoximine.
137 tions of inhibition of GSH synthesis with dl-buthionine sulfoximine.
138  mM), and it is inactivated by cystamine and buthionine sulfoximine.
139  the enhancing effects of GSH depletion with buthionine sulfoximine.
140 e gamma-glutamylcysteine synthesis inhibitor buthionine sulfoximine.
141 ort in transgenic plants were abrogated by l-buthionine sulfoximine.
142 and direct inhibition of GSH biosynthesis by buthionine sulfoximine.
143 ll as by treatment with homocysteic acid and buthionine sulfoximine.
144 restored GSH synthesis in a Glu (10 mM) plus buthionine-sulfoximine (BSO) (0.2 mM)-treated group, ind
145 athways regulating redox homeostasis using l-buthionine-sulfoximine (BSO, glutathione synthesis inhib
146 ess by inhibiting glutathione synthesis with buthionine-sulfoximine dramatically increased red blood
147  of glutathione using N-acetylcysteine and L-buthionine-sulfoximine indicate that changes in glutathi
148 e), an inhibitor of glutathione synthesis (L-buthionine-sulfoximine) or glutathione reductase (1,3-bi
149 NF-alpha neutralizing antibody (Ab) and by L-buthionine-sulfoximine, a GSH-depleting agent.
150 blood cell sickling in the sickle kidney: in buthionine-sulfoximine-treated sickle mice, red blood ce
151 such as the glutathione synthesis inhibitor, buthionine sulphoximine (BSO), and paclitaxel.
152 her GSH depleters, diethyl maleate (DEM) and buthionine sulphoximine (BSO), only 1 of which (DEM) can
153                      Male CD-1 mice received buthionine sulphoximine (BSO; 7.2 mmol/kg), diethyl male
154 vation of p53 pathway; and synergized with L-buthionine sulphoximine in all samples.
155 hibited myeloma growth and synergized with L-buthionine sulphoximine in vivo.
156 ated by GSH synthetase silencing or by and L-buthionine sulphoximine, an irreversible inhibitor of ga
157  effect was attenuated by GSH depletion with buthionine sulphoximine, even in GSH-containing media.
158 ocyanin-producing grapevine root cultures to buthionine sulphoximine, which reduced GSH levels, a dec

 
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