ライフサイエンスコーパス: chromate

1 lity constraints suggest this is released as chromate.

2 cleotide repeat stability and sensitivity to chromate.

3 micronuclei, and apoptosis in human cells by chromate.

4 g moieties are displayed toward the incoming chromate.

5 endent manner after chronic exposure to lead chromate.

6 CysK, YieF, or KatE) were more sensitive to chromate.

7 r stress signaling and survival responses to chromate.

8 zymes responded most strongly to cadmium and chromate.

9 utene, CO(2), and Cr(aq)(3+), in addition to chromate.

10 cyte MOLT4 cells by treatment with potassium chromate.

11 compared to the sulfur-poor or nondoped lead chromates.

12 Chromate adsorption isotherms recorded at pH 7 are sugge

13 tical frequency calculations to characterize chromate adsorption on 2-line ferrihydrite.

14 [Ni(bpe)(2)(MoO(4))], MOOFOUR-1-Ni, and its chromate analogue, CROFOUR-1-Ni, exhibit high CO(2) affi

15 ture calculations also demonstrate that lead chromate and its coprecipitates are p-type semiconductor

16 Selenate, chromate, and arsenate produce transient APX intermediat

17 erienced by Escherichia coli K-12 exposed to chromate, and mechanisms that may enable cells to withst

18 ins with different abilities to reduce iron, chromate, and uranium.

19 iment and continuously infused with lactate, chromate, and various native electron acceptors diverged

20 nalized fused quartz/water interfaces toward chromate are consistent with nearly 50% slower transport

21 inherently as oxo-anions (e.g., perchlorate, chromate, arsenate, pertechnetate, etc.) or organic anio

22 sition and the crystalline structure of lead chromate-based pigments influence their stability.

23 As bacterial chromate bioremediation is limited by the toxicity of ch

24 ctase that has many applications, such as in chromate bioremediation.

25 s stress will improve their effectiveness in chromate bioremediation.

26 Because chromate causes certain nuclear proteins to form complex

27 cluding a cpxR homolog were perturbed in the chromate-challenged mutant.

28 ient and reflection coefficients of the lead chromates change as a result of the sulfate doping in su

29 Molybdate, selenate, chromate ("chromium VI"), arsenate, tungstate, chlorate,

30 The effects of pH, aqueous chromate concentration, ionic strength, and deuterium ex

31 ajor debris component either wooden pallets, chromated copper arsenate (CCA) treated wood, or alkalin

32 The redox chemistry of chromate (Cr(VI)) and arsenite (As(III)) on the iron oxy

33 Contamination of the environment with Cr as chromate (Cr(VI)) from industrial activities is of signi

34 h the transcript and protein levels to acute chromate [Cr(VI)] challenge.

35 Heavy metal chromate (Cr2O7(2-)) anions consisting of chromium Cr(VI

36 lms to U(VI) (uranyl, UO(2)(2+)) and Cr(VI) (chromate, CrO(4) (2-)) using non-invasive nuclear magnet

37 Higher concentrations of chromate cross-linked many other proteins to DNA.

38 Trend analyses on chromate (decreasing), epoxy resin (increasing) and nick

39 tamination by hexavalent chromium [Cr(VI) or chromate] due to anthropogenic activities has become an

40 ubstantial fraction of all Cr-DNA adducts in chromate-exposed cells are represented by ternary comple

41 Chromate exposure depleted cellular levels of reduced gl

42 Specifically, a 24-hour lead chromate exposure induced no aneugenic effect, whereas a

43 we investigated the effects of chronic lead chromate exposure on centrosomes.

44 Within 3 h of chromate exposure, the latter ceased growth and exhibite

45 ent mutant S. oneidensis under conditions of chromate exposure.

46 endent manner with 0.5 and 1 microg/cm2 lead chromate for 120 hours, inducing aberrant centrosomes in

47 ability of the 6 and 90 nm particles to sorb chromate from solution, despite the greater surface area

48 8 h), nor did the organics interact with the chromate in solution.

49 0-hour exposure to 0.5 and 1 microg/cm2 lead chromate induced 55% and 60% aneuploid metaphases, respe

50 suggest that one possible mechanism for lead chromate-induced carcinogenesis is through centrosome dy

51 Fe homeostasis and the cellular response to chromate-induced stress in S. oneidensis.

52 t exposure of mouse hepatoma Hepa-1 cells to chromate inhibits the induction of the Cyp1a1 and Nqo1 g

53 The color of the pigment, in which the chromate ion acts as a chromophore, is related to its ch

54 calculations on permanganate ion as well as chromate ion and iron tetraoxide.

55 The reduction site of the chromate ion in D. acetoxidans is occupied by a sulfate

56 atisfactory results for permanganate ion and chromate ion.

57 ellow pigments, caused by a reduction of the chromate ions to Cr(III) compounds, is known to affect t

58 ir maximum adsorption potential for lead and chromate ions.

59 Chromate is retained on the anion-exchange resin from wa

60 bioremediation is limited by the toxicity of chromate, minimizing oxidative stress during bacterial c

61 Chromate mobility, reactivity, and bioavailability in so

62 istant to effects of sulphate-mimetics (like chromate or molybdate) on sulphate transport.

63 Elevated chromate or sulfate anion concentrations can interfere w

64 ulates may provide more chronic exposures to chromate over time.

65 other anionic pollutants from water such as chromate, pertechnetate, or arsenate may be possible by

66 hanges in each of these amino acids enhanced chromate reductase activity of the enzyme, showing that

67 enzyme that has also been characterized as a chromate reductase; yet we propose that it is the quinon

68 minimizing oxidative stress during bacterial chromate reduction and bolstering the capacity of these

69 g that this network is centrally involved in chromate reduction.

70 t this is the oligomeric form that catalyzes chromate reduction.

71 able production of H(2)O(2) that accompanies chromate reduction.

72 ier to be overcome was the separation of the chromates reduction carried out by ethylene from the sub

73 Thus, enhancing the activity of ChrR in a chromate-remediating bacterial strain may not only incre

74 The path leading to chromate resembles the CH(3)C(O)OO(*) reaction.

75 ical environments can significantly increase chromate residence times.

76 have important implications for the fate of chromate, selenate, and sulfate in subsurface environmen

77 e characterized the adsorption mechanisms of chromate, selenate, and sulfate on Al-substituted ferrih

78 affinity (approximately 5 microM), sulfate, chromate, selenate, phosphate, and chlorate did not bind

79 by an in-frame deletion resulted in enhanced chromate sensitivity and a reduced capacity to remove ex

80 Magnetite-chromate sorption experiments were conducted with approx

81 g/L) of organics had no noticeable impact on chromate sorption, whereas concentrations of 50 mg/L or

82 g/L or more resulted in decreased amounts of chromate sorption.

83 impact the redox chemistry of the magnetite-chromate system over the duration of the experiments (8

84 rove the higher tendency of sulfur-rich lead chromates to darken.

85 Thus, oxidative stress plays a major role in chromate toxicity in vivo, and cellular defense against

86 ial strain may not only increase the rate of chromate transformation, it may also augment the capacit

87 se were also found to cross-link with DNA by chromate treatment.

88 imarily complexed to DNA following 25 microM chromate treatment.

89 Chromate was used as a chemical probe to investigate the

90 apted by overnight growth in the presence of chromate were less stressed than nonadapted controls.

91 In the absence of scavengers, nitrite and chromate were produced.

92 istic effects dominating the interactions of chromate with surface-bound amido acids indicates that c

93 rrant mitosis after chronic exposure to lead chromate with the emergence of disorganized anaphase and

94 ound to be mechanism-specific in the case of chromate, with bidentate complexes disproportionately su

95 ancers with microsatellite instability among chromate workers.

96 The darkening of lead chromate yellow pigments, caused by a reduction of the c