ライフサイエンスコーパス: methemoglobin

1 d by the NO scavenger hemoglobin, but not by methemoglobin.

2 ake rate, but did not reduce the activity of methemoglobin.

3 iled studies of this reaction of low NO with methemoglobin.

4 roid hormone metabolism and the reduction of methemoglobin.

5 result in conversion of plasma hemoglobin to methemoglobin.

6 generates NO and oxidizes deoxyhemoglobin to methemoglobin.

7 ed by Sartor, Mayer, and Johari for hydrated methemoglobin.

8 ccurs during the reaction of hydroxyurea and methemoglobin.

9 by an assay for conversion of hemoglobin to methemoglobin.

10 radation products (intra- and extra-cellular methemoglobin), 3.lipid-containing lesions (lipoma, derm

11 For instance, methemoglobin A in solution is, as expected, nearly indi

12 on reaction that also oxidizes hemoglobin to methemoglobin, a non-oxygen-binding form of hemoglobin t

13 Using a human methemoglobin alpha beta dimer, it has been shown that a

14 In the detoxication of cyanide with methemoglobin, an intermediate dicyanhemimethemoglobin w

15 methemoglobin and nitrite/nitrate or between methemoglobin and any other clinical variable.

16 circulation, whereas controlled infusions of methemoglobin and cyanomethemoglobin, which do not consu

17 Methemoglobin and denatured hemoglobin binding to the RB

18 emoglobin, the differences between deoxy-Hb, methemoglobin and HbCO are smaller than the correspondin

19 ht help prevent the detrimental formation of methemoglobin and hemichrome in vivo, insofar as this is

20 nown to result in oxidation of hemoglobin to methemoglobin and hemichrome.

21 nce (EPR) spectroscopy, DHA oxidized HbNO to methemoglobin and liberated NO from HbNO as determined b

22 reaction with oxyhemoglobin, which produces methemoglobin and nitrate (NO 3 (-)).

23 Circulating methemoglobin and nitrite/nitrate concentrations are inc

24 Circulating methemoglobin and nitrite/nitrate concentrations were si

25 n study entry and every 6 hrs for 72 hrs for methemoglobin and nitrite/nitrate determinations.

26 re were no significant relationships between methemoglobin and nitrite/nitrate or between methemoglob

27 A strong correlation between methemoglobin and plasma nitrate formation was observed,

28 that hydroxyurea oxidizes deoxyhemoglobin to methemoglobin and reduces methemoglobin to deoxyhemoglob

29 droxy group react with oxyhemoglobin to form methemoglobin and variable amounts of nitrite/nitrate.

30 modynamic, gas exchange, pulmonary function, methemoglobin, and nitrite/nitrate measurements were obt

31 ra indicated that hemoglobin was oxidized to methemoglobin, and the addition of catalase demonstrated

32 estimate blood levels of carboxyhemoglobin, methemoglobin, and total hemoglobin (SpHb), as well as t

33 With donor, only nitrate and methemoglobin are formed, stoichiometric with the amount

34 Methemoglobin assay confirmed these results and demonstr

35 encountered with persistently high levels of methemoglobin associated with a left-shift in the oxygen

36 e pH 7.1 and 5.4 crystal structures of horse methemoglobin at 1.6 and 2.1 A resolution, respectively,

37 cells produced almost complete conversion to methemoglobin, but no detectable lipid extraction.

38 Methemoglobin, but not heme-stabilized cyanomethemoglobi

39 tion, blood pressure, oxygen saturation, and methemoglobin concentration.

40 Four patients had methemoglobin concentrations >5%.

41 Maximum methemoglobin concentrations were greater in patients tr

42 throcytes and hemoxidizing the hemoglobin to methemoglobin, cystalysin was also capable of removing t

43 s to ferrous hemoglobin, thus completing the methemoglobin-dependent sulfide oxidation cycle.

44 Methemoglobin-dependent sulfide oxidation in mammals is

45 ion with the alternate crystal structures of methemoglobin establish that the solution structure of w

46 e soluble protein that reduces cytochrome c, methemoglobin, ferricyanide, and molecular oxygen in vit

47 ve been associated with vascular reactivity, methemoglobin formation and development of antibodies.

48 T1 relaxation time was related to thrombus methemoglobin formation and further processing.

49 cibly; (ii) the speed of the reaction limits methemoglobin formation by autooxidation; (iii) there is

50 e membranes exerted an exaggerated effect on methemoglobin formation in solution, an effect completel

51 Major findings include that methemoglobin formation mediated by the lipophilic t-BuB

52 table contrast enhancement and extracellular methemoglobin formation occurs within 24 hours of the co

53 Significantly, Ap44mSe limited deleterious methemoglobin formation, highlighting its usefulness in

54 globin (oxyHb) (96%), which was converted to methemoglobin (>95%) after treatment with 150 microM NO.

55 es a redox cycle between deoxyhemoglobin and methemoglobin has been forwarded to explain these result

56 Consistent with this formation of methemoglobin, human plasma was found to consume approxi

57 scopy shows that the formation of a low-spin methemoglobin-hydroxyurea complex is critical for iron n

58 ied the pathway involved in the reduction of methemoglobin in the family, thereby describing the firs

59 y have been associated with metmyoglobin and methemoglobin in the lesions.

60 in seven patients because of the presence of methemoglobin in the tumor bed.

61 deoxyhemoglobin, and high-spin and low-spin methemoglobins in each spectrum collected as the reactio

62 oxyheme of hemoglobin (producing nitrate and methemoglobin) is extremely rapid, it has been proposed

63 ed normal 2,3-bisphosphoglycerate (2,3-BPG), methemoglobin levels and intracellular pH.

64 Because methemoglobin levels are modified by several mechanisms

65 TAK-242 resulted in mild increases in serum methemoglobin levels but was otherwise well tolerated.

66 ic oxide at doses of < or =20 ppm maintained methemoglobin levels of <3.0% and circuit concentrations

67 Transient, dose-related increases in methemoglobin levels were observed with TAK-242 treatmen

68 tients with HbE beta thalassemia showed that methemoglobin levels were significantly increased and th

69 on, a highly significant correlation between methemoglobin levels, splenectomy, and factors that modi

70 d not cause systemic hypotension or increase methemoglobin levels.

71 no clinically significant increase in blood methemoglobin levels.

72 the reactions of hydroxyurea and deoxy- and methemoglobin likely proceed by inner-sphere mechanisms.

73 Circulating methemoglobin measurements are not superior to plasma ni

74 s was investigated through the evaluation of methemoglobin (MetHb) and malondialdehyde (MDA) levels.

75 t IsdX2 NEAT domains only scavenge heme from methemoglobin (metHb) and that autoxidation of oxyhemogl

76 studies have demonstrated that 3-AP induces methemoglobin (metHb) formation and hypoxia in patients,

77 yanide toxicity can be reduced by the use of methemoglobin (MetHb) formers, and antidotal dosage is b

78 ectrons in the four heme groups of deoxy and methemoglobin (metHb) gives these species paramagnetic p

79 d as nitrosylhemoglobin (HbNO) in an aqueous methemoglobin (MetHb) solution.

80 that of Hb(III)NO formed when NO reacts with methemoglobin (MetHb), but is similar to metHb resulting

81 ransfer between the various couples of human methemoglobin (metHb), IsdA, IsdB, IsdC, and IsdE by spe

82 reversibly bound O2, or paramagnetic ferric methemoglobin (metHb).

83 s well established and generates nitrate and methemoglobin (metHb).

84 Methemoglobin (Mhb) remained low in all subjects breathi

85 resistance index (SVRI), cardiac index (CI), methemoglobin, nitrite/nitrate, or lung pathology scores

86 s ascribed to a faster reaction of NO with a methemoglobin-nitrite complex.

87 conditions the product stoichiometry is 1:1 (methemoglobin:nitrosylhemoglobin), and unexpectedly, the

88 rhage by taking advantage of the short T1 of methemoglobin present in acute thrombus and intraplaque

89 OOPE5 was the most active against methemoglobin production (53.7% reduction), whereas OOPE

90 in-induced vaso-occlusion was blocked by the methemoglobin reducing agent methylene blue, haptoglobin

91 (HbA) tetramers or inhibit the activities of methemoglobin reductase and four selected glycolysis pat

92 een cytochrome b5 reductase 3, also known as methemoglobin reductase, and oxidized sGC.

93 dely distributed hemoglobins, and associated methemoglobin reductases, than dioxygen transport and st

94 hrocytes, soluble cytochrome b5 functions in methemoglobin reduction.

95 olesterol biosynthesis, drug metabolism, and methemoglobin reduction.

96 2 whereas the yield of trapping of NO(-) by methemoglobin remained unaffected.

97 he reactions of hydrogen peroxide with human methemoglobin, sperm whale metmyoglobin, and horse heart

98 protein, hemoglobin, which in the ferric or methemoglobin state binds H2S and oxidizes it to a mixtu

99 After all the oxyHb reacts with NO to form methemoglobin, the disappearance rate of NO slows greatl

100 nitric oxide or nitric dioxide or increased methemoglobin, the risk of complications with inhaled ni

101 s oxidized 85-90% of plasma oxyhemoglobin to methemoglobin, thereby inhibiting endogenous NO scavengi

102 deoxyhemoglobin to methemoglobin and reduces methemoglobin to deoxyhemoglobin.

103 at hydroxyurea reacts with oxy-, deoxy-, and methemoglobin to produce 2-6% of iron nitrosyl hemoglobi

104 d co-workers reported that crystalline horse methemoglobin undergoes a large lattice transition as th

105 ectron-transfer rate from cytochrome b(5) to methemoglobin using a formalism developed by Marcus.

106 form with NO exposure <2 microM, but plasma methemoglobin was detectable by paramagnetic resonance s

107 also associated with severity and fatality, methemoglobin was only modestly increased in patients wi

108 , PaCO2, pH, heart rate, blood pressure, and methemoglobin were recorded at baseline and after inhali

109 tilatory settings, arterial blood gases, and methemoglobin were recorded at each study period.

110 udying a complex between apo-HasAp and human methemoglobin were stymied by the rapid heme capture by

111 if infused hemoglobin was first oxidized to methemoglobin, which does not scavenge NO.

112 /HarA NEAT domains bind a single molecule of methemoglobin, while the distantly related NEAT domain f

113 tectable as a quintet at room temperature in methemoglobin with identical spectral features to those

114 mbus imaging (MRDTI) is capable of detecting methemoglobin within intraplaque hemorrhage.