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1 lical vein endothelial cells is abrogated by t-butyl hydroperoxide.
2 nt functions or to induce p53 in response to t-butyl hydroperoxide.
3 fetal side by inducing oxidative stress with t-butyl hydroperoxide.
4 f HNE when oxidative stress was induced with t-butyl hydroperoxide.
5 in the presence of the organic hydroperoxide t-butyl hydroperoxide.
8 reased sensitivity to high concentrations of t-butyl-hydroperoxide, an oxidizing compound that damage
11 s IL-4, potentiated the cytotoxic effects of t-butyl hydroperoxide and hydrogen peroxide on mouse DA
15 Fs, increased sensitivity to the toxicity of t-butyl hydroperoxide, as measured by colony-forming eff
18 y either exposure to oxidizing agents (H2O2, t-butyl hydroperoxide, cumene hydroperoxide, or diamide)
19 4 in severe asthma (r = -0.55; P = 0.03) and t-butyl-hydroperoxide decreased LXA4 and 15-epi-LXA4 bio
20 r-bound nucleosides underwent oxidation with t-butyl hydroperoxide, deprotection of cyanoethoxy group
21 bmtA mutant was sensitive to treatment with t-butyl hydroperoxide, implying that BmtA, and thus Mn,
22 bosR resulted in differential sensitivity to t-butyl hydroperoxide, indicating that these alleles are
24 ma(-/-) mouse liver were resistant to Ca(2+)/t-butyl hydroperoxide-induced mPTP opening in comparison
25 exin VI from the membrane during exposure to t-butyl hydroperoxide matched elevation of [Ca2+]i as a
26 effects of paraquat, hydrogen peroxide, and t-butyl hydroperoxide on Prdx6-/- and wild-type (Prdx6+/
27 A1 resistance), and cells treated with 10 mM t-butyl hydroperoxide or 10 mM H(2)O(2) show no increase
28 calcium in the presence or absence of either t-butyl hydroperoxide or phenylarsine oxide in compariso
32 e to oxidative stress imposed by paraquat or t-butyl hydroperoxide, or were subjected to osmotic, sal
34 556N mutant is sensitive to 5 mM H(2)O(2) or t-butyl hydroperoxide, similar to a gene knock-out ssk1
35 xposure further potentiated HNE formation in t-butyl hydroperoxide-stimulated fetal liver mitochondri
36 izes MT and releases zinc in the presence of t-butyl hydroperoxide, suggesting that this type of redo
39 on in vitro, APRE-19 cells were treated with t-butyl hydroperoxide (tBH) or hydrogen peroxide (H2O2)
41 oxidized to methionine sulfoxide in vitro by t-butyl hydroperoxide (tBHP) or hydrogen peroxide (H2O2)
43 or oxidation of ferric cyt P450s in films by t-butyl hydroperoxide to active ferryloxy cyt P450s from
44 oxidants (hydrogen peroxide, menadione, and t-butyl hydroperoxide) were investigated in three replic
45 orferi isolate exhibited hypersensitivity to t-butyl hydroperoxide when compared with infectious B. b
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