ライフサイエンスコーパス: BHA

1 BHA administration also inhibited estradiol- or estrone-

2 BHA inhibits de novo interferon regulator factor (IRF)-1

3 BHA showed the highest OS, with p-anisidine, PV and inhi

4 BHA shows extraordinary reactivity toward the triester d

5 BHA treatment significantly attenuated RSV-induced lung

6 e decreased by 30-60% in animals fed a 0.75% BHA diet for 18 days prior to the injection of estrogen.

7 In conclusion, feeding a 0.75% BHA-supplemented diet to female CD-1 mice for 2-3 weeks

8 Feeding a 0.75% BHA-supplemented diet to ovariectomized CD-1 mice for 18

9 al, environment and the benzhydroxamic acid (BHA) substrate binding pocket.

10 complexes with INH and benzohydroxamic acid (BHA) are reported.

11 hols catalyzed by Hf(IV)-bishydroxamic acid (BHA) complexes is described.

12 lase inhibitor, aminotriazole, also affected BHA- and tBHQ-stimulated ERK2 activity but not JNK1, ind

13 ave been designed as alternatives to BHT and BHA antioxidants.

14 The presence of lycopene and BHA increases the total phenolic compounds in the enrich

15 c compounds in the enriched egg powders, and BHA exhibits the most antioxidant activity, as quantifie

16 widely used, the butylated hydroxyl anisole (BHA).

17 se kinases was abrogated by the antioxidants BHA and vitamin C.

18 justifying the Briggs-Haldane approximation (BHA).

19 EXT was not as effective as BHA or DHM in soybean oil.

20 tion from digestion was extremely stable, as BHA-inhibitor complexes could be incubated for 24 h in l

21 mple molecular backbone of benzohydroxamate (BHA) and on the more complex structure of the widely use

22 d to 7 synthetic antioxidants including BHT, BHA, TBHQ and PG with regard to their ability to protect

23 2, is responsible for the ERK2 activation by BHA and tBHQ, whereas the JNK1 activation may require a

24 E attenuated ERK2 but not JNK1 activation by BHA and tBHQ.

25 Activation of ERK2 by BHA was rapid and transient, whereas the JNK1 activation

26 ng a kinetics different from that induced by BHA.

27 ss and body weight loss were also reduced by BHA treatment, which inhibited neutrophil recruitment to

28 tment of c-Jun to this proximal AP-1 site by BHA was confirmed by chromatin immunoprecipitation analy

29 rmally when BHA was supplemented in trans by BHA-expressing cells.

30 In contrast, BHA administration had little or no effect on the liver

31 liver or Hepa1c1c7 cells treated with either BHA or acrolein.

32 Furthermore, BHA and tBHQ activation of ERK2 was strongly inhibited b

33 Furthermore, BHA-induced apoptosis appeared to be independent of form

34 nts decreased in the order ETX>TR>PG>AA>TBHQ>BHA.

35 , purified HA trimers (bromelain-cleaved HA [BHA]) are used to examine the properties and binding cha

36 Influenza B virus hemagglutinin (BHA) contains a predicted cytoplasmic tail of 10 amino a

37 ith the antioxidant butylated hydroxyanisol (BHA), as well a panel of chemically unrelated antioxidan

38 n of 0.75% 2(3)-tert-butyl-4-hydroxyanisole (BHA) in AIN-76A diet to female CD-1 mice for 3 weeks inc

39 similar to that of butylated hydroxyanisole (BHA) and higher than that of other synthetic antioxidant

40 O-induced ROS with butylated hydroxyanisole (BHA) does not affect Nrf2 activation or cell death.

41 enolic antioxidant butylated hydroxyanisole (BHA) is a commonly used food preservative with broad bio

42 Butylated hydroxyanisole (BHA), a commonly used food preservative, is reported to

43 rally administered butylated hydroxyanisole (BHA), an antioxidant.

44 ed the antioxidant butylated hydroxyanisole (BHA), and others were given daily intraperitoneal inject

45 olic antioxidants, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT) and tert-butyl hydr

46 Butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), and tert-butylhydr

47 rbamate (PDTC) and butylated hydroxyanisole (BHA), indicating that the generation of free oxygen radi

48 hin, lycopene, and butylated hydroxyanisole (BHA)] for conjugated dienes (during a 90-day period) and

49 acrolein p.o.) or butylated hydroxylanisole (BHA) (0.45% in the diet) and of cytosolic NAD(+)-depende

50 aken together, our results indicate that (i) BHA and its metabolite tBHQ differentially regulate MAPK

51 for 24 h in low pH with almost no change in BHA structure.

52 rial permeability transition pore, inhibited BHA-induced loss of Deltapsi(m), cytochrome c release, c

53 Instead, BHA and tBHQ substantially reduced the amount of intrace

54 ion but acquired additional mutations in its BHA, neuraminidase (NA), and M1 proteins.

55 onstrating the flexible nature of the Hf(IV)-BHA system.

56 duced particles containing dramatically less BHA.

57 erivatives from 2-tert-butyl-4-methylphenol, BHA, creosol, isoeugenol and di-o-propenyl p-cresol, few

58 6-well format after O-benzylhydroxylamine (O-BHA) derivatization under aqueous conditions.

59 is effect is mediated through the ability of BHA to inhibit RSV-induced interferon regulatory factor

60 derlying these diverse biological actions of BHA is thus of great importance.

61 Analysis of BHA after photoaffinity analog binding and UV cross-link

62 ytoplasmic tail abrogated the association of BHA with Triton X-100-insoluble lipid rafts.

63 se results indicate that the cytotoxicity of BHA is due to the induction of apoptosis that is mediate

64 indicate that the cytoplasmic tail domain of BHA is important for efficient incorporation of BHA into

65 is important for efficient incorporation of BHA into virions and tight lipid raft association.

66 Indeed, direct incubation of BHA with isolated mitochondria triggered cytochrome c re

67 e LSV response (anodic peak current, Ipa) of BHA and BHT by 2- and 20-times, respectively.

68 Although the levels of BHA cell surface expression were indistinguishable betwe

69 r the multiplex detection and measurement of BHA, BHT, and TBHQ levels in complex food samples using

70 significance to understand the mechanism of BHA-induced toxicity.

71 A major metabolite of BHA, tert-butylhydroquinone (tBHQ), also activated ERK2

72 estradiol and estrone by liver microsomes of BHA-treated animals as determined by substrate disappear

73 kinetic analysis showed that replication of BHA cytoplasmic tailless viruses could be improved by co

74 However, the use of BHA as a chemopreventive agent against cancer in human h

75 Addition of either INH or BHA to KatG induces only minor changes in the resonance

76 Ps at 121 degrees C exhibited higher AA than BHA.

77 DHM was more potent than BHA in preventing soybean oil oxidation.

78 MRPs showed higher PRS and RP than BHA.

79 Here we demonstrate that BHA is capable of activating distinct mitogen-activated

80 has been challenged by the observation that BHA may exert toxic effect in some tissues of animals.

81 Here, we report that BHA induces apoptosis in freshly isolated rat hepatocyte

82 BHA compared with controls, suggesting that BHA-induced expression is independent of nuclear factor

83 and substrate concentrations where both the BHA and the QEA are invalid and allows us to define prec

84 ectomy, whereas Nemo(Deltahepa) mice fed the BHA diet were protected from carcinogenesis.

85 a recombinant influenza B virus lacking the BHA cytoplasmic tail domain.

86 ly, long-term culture of a virus lacking the BHA cytoplasmic tail in Madin-Darby canine kidney (MDCK)

87 in that overlaps the validity domains of the BHA and the QEA and only slightly extends them.

88 SA) overlaps and extends the validity of the BHA and the QEA, and that it is at least roughly valid f

89 assignment strategy is then extended to the BHA:HRPC-CN complex.

90 nding pocket and suggest a model whereby the BHA is able to undergo a partial, reversible structural

91 of enzyme-to-substrate ratios for which the BHA is invalid, including the extreme of enzyme excess.

92 Cross-linking of the photoaffinity analog to BHA under neutral (native) pH conditions identified a st

93 eneration of H2O2 after exposure of cells to BHA or tBHQ using a H2O2-sensitive fluorescent probe, 2'

94 re shown to be in primary dipolar contact to BHA.

95 The addition of Trolox, BHA, and propyl gallate had no significant effect on fur

96 tinguishable between truncated and wild-type BHA, the BHATail(-) virus produced particles containing

97 at of wild-type virus but grew normally when BHA was supplemented in trans by BHA-expressing cells.

98 icetin (DHM) were analysed and compared with BHA in two model systems, soybean oil and cooked ground

99 Treatment of hepatocytes with BHA also induced loss of mitochondrial transmembrane pot

100 rf2(+)/(+) and Nrf2(-)/(-) mice treated with BHA compared with controls, suggesting that BHA-induced