ライフサイエンスコーパス: thiobarbituric acid reactive substance

1 MDA was measured as thiobarbituric acid reactive substance.

2 ia and the high K+-mediated increase in lung thiobarbituric acid reactive substance.

3 by 2-hydroxyethidine, and lipid peroxides by thiobarbituric acid reactive substances.

4 ed with decreased urinary levels of H2O2 and thiobarbituric acid reactive substances.

5 ipid peroxidation was determined by assaying thiobarbituric acid-reactive substances.

6 s of headspace aldehydes, malonaldehyde, and thiobarbituric acid-reactive substances.

7 cells were treated with ox-LDL (50 microg/mL thiobarbituric acid reactive substances 12 to 16 nmol/mg

8 xposure to IL-1alpha, TNF-alpha, and ox-LDL (thiobarbituric acid-reactive substances, 13.4 nmol/mg LD

9 es of oxidative stress, urinary excretion of thiobarbituric acid reactive substances, 8-hydroxy--deox

10 Thiobarbituric acid-reactive substances, a less specific

11 lactate dehydrogenase, laccase) and damage (thiobarbituric acid reactive substances, acetylcholinest

12 Thiobarbituric acid reactive substances activity indicat

13 was assessed by histology and measurement of thiobarbituric acid reactive substances and NOX-related

14 Peroxide value, concentration of thiobarbituric acid reactive substances and oxygen uptak

15 Thiobarbituric acid-reactive substance and oxidized and

16 s compared with H441 showed less increase in thiobarbituric acid-reactive substance and phosphatidylc

17 olvents exhibited the lowest peroxide value, thiobarbituric acid-reactive substances and beany odour

18 Both proteins block accumulation of thiobarbituric acid-reactive substances and conjugated d

19 n of 8-epi-PGF2 alpha coincided with that of thiobarbituric acid-reactive substances and lipid hydrop

20 O-deethylase activity), or oxidative stress (thiobarbituric acid-reactive substances and ratios of re

21 incubated with 10 microgram/ml oxLDL (10-15 thiobarbituric acid-reactive substances) and blocking an

22 37, suppressed formation of 8-epi-PGF2alpha, thiobarbituric acid-reactive substances, and lipid hydro

23 eptibility to lipid peroxidation by both the thiobarbituric acid reactive substances assay and the fl

24 oxidants in preventing lipoperoxidation in a thiobarbituric acid reactive substances assay.

25 y measuring malondialdehyde levels using the thiobarbituric acid reactive substances assay.

26 tile base nitrogen, trimethylamine nitrogen, thiobarbituric acid reactive substances, ATP catabolism

27 Quantitative measurements of thiobarbituric acid reactive substances, conjugated dien

28 develop normally, and their plasma levels of thiobarbituric acid-reactive substances do not differ fr

29 of skeletal muscle carbonylated proteins and thiobarbituric acid reactive substances during hyperammo

30 , evidenced by an 80% reduction (P<0.001) in thiobarbituric acid reactive substances, effective inhib

31 f several markers of oxidative status (i.e., thiobarbituric acid-reactive substances, erythrocyte glu

32 stress, as exemplified by the generation of thiobarbituric acid-reactive substances, expression of h

33 throcytes glutathione peroxidase (FB400) and thiobarbituric acid-reactive substances (FB100, FA400, F

34 and alterations in the heat shock response, thiobarbituric acid reactive substances, heat shock prot

35 volume in 1 second (FEV1) with 1) levels of thiobarbituric acid-reactive substances in plasma (p-TBA

36 d deletions in kidney mitochondrial DNA, and thiobarbituric acid-reactive substances in plasma, toget

37 d prevented the diabetes-induced increase in thiobarbituric acid-reactive substances in serum and sig

38 Lipid peroxidation (thiobarbituric acid-reactive substances) increased after

39 ed bacterial cells show an enhanced level of thiobarbituric acid reactive substances, indicating the

40 Heat caused increased thiobarbituric acid reactive substance levels (an indica

41 the diabetes-associated increases in plasma thiobarbituric acid-reactive substances, mitochondrial D

42 low density lipoprotein (measured as either thiobarbituric acid-reactive substances or the oxidant s

43 cellular adhesion molecule-1 (p = 0.001) and thiobarbituric acid reactive substances (p = 0.001) as w

44 We measured diaphragmatic concentrations of thiobarbituric acid reactive substances (TBAR), a marker

45 ioxidant activity, as assessed indirectly by thiobarbituric acid reactive substance (TBARS) formation

46 Spectrofluorometry was used to analyze thiobarbituric acid reactive substance (TBARS); ferric-r

47 creased the hexanal content (0.21mug/ml) and thiobarbituric acid reactive substances (TBARS) (2.56mug

48 ent and composition, free fatty acids (FFA), thiobarbituric acid reactive substances (TBARS) and fluo

49 from W-MR-Al had lower peroxide value (PV), thiobarbituric acid reactive substances (TBARS) and non-

50 tent, total volatile basic nitrogen (TVB-N), thiobarbituric acid reactive substances (TBARS) and pero

51 Results from thiobarbituric acid reactive substances (TBARS) and sens

52 The thiobarbituric acid reactive substances (TBARS) assay is

53 of fish oil oxidation was studied using the thiobarbituric acid reactive substances (TBARS) assay.

54 on via oxidative stress was also detected by thiobarbituric acid reactive substances (TBARS) assay.

55 glycated albumin content, by measurement of thiobarbituric acid reactive substances (TBARs) for lipi

56 oxy-9,11-octadecadienoic acid (13-HODE), and thiobarbituric acid reactive substances (TBARS) in 252 w

57 Serum MDA levels were measured as thiobarbituric acid reactive substances (TBARS) in 634 p

58 However, thiobarbituric acid reactive substances (TBARS) increase

59 Oxidative stability was evaluated by thiobarbituric acid reactive substances (TBARS) on day (

60 xidation was monitored in parallel using the thiobarbituric acid reactive substances (TBARS) test.

61 Lipid hydroperoxides and thiobarbituric acid reactive substances (TBARS) were ana

62 ity (ORAC) and lipid peroxidation assayed as thiobarbituric acid reactive substances (TBARS) were mea

63 9-hydroxyoctadecadieneoic acid (9-HODE), and thiobarbituric acid reactive substances (TBARS) were mea

64 Thiobarbituric acid reactive substances (TBARS) were red

65 Serum ALT value, and hepatic thiobarbituric acid reactive substances (TBARS), and hep

66 profiles, formation of hydroperoxides (PV), thiobarbituric acid reactive substances (TBARS), fluores

67 Hydroperoxide, thiobarbituric acid reactive substances (TBARS), malondi

68 The increases in thiobarbituric acid reactive substances (TBARS), p-anisi

69 nally analyzed by two Raman spectroscopy and thiobarbituric acid reactive substances (TBARS).

70 (PFP, 1.18-1.32 mmol peroxides/kg mince) and thiobarbituric acid reactive substances (TBARS, 0.30-0.3

71 ues, was subject to analysis by conventional thiobarbituric acid-reactive substance (TBARS) and ferro

72 e, anserine, homocarnosine, pentosidine, and thiobarbituric acid-reactive substance (TBARS) contents.

73 The peroxide value (PV) and thiobarbituric acid-reactive substance (TBARS) value of

74 lement increased the plasma concentration of thiobarbituric acid-reactive substances (TBARS) (P: = 0.

75 esulted in a fivefold increased formation of thiobarbituric acid-reactive substances (TBARS) and acti

76 Lipid peroxidation was measured as thiobarbituric acid-reactive substances (TBARS) and alph

77 after the heat treatment, there were higher thiobarbituric acid-reactive substances (TBARs) and chol

78 de value (PV) was found and large amount of, thiobarbituric acid-reactive substances (TBARS) and hexa

79 The increases in thiobarbituric acid-reactive substances (TBARS) and p-an

80 significantly reduced (p<0.05) the levels of thiobarbituric acid-reactive substances (TBARS) and prot

81 d symptoms, exercise, ejection fraction, and thiobarbituric acid-reactive substances (TBARS) as an in

82 n a lipid system was determined by using the thiobarbituric acid-reactive substances (TBARS) assay.

83 Glucose, insulin, and thiobarbituric acid-reactive substances (TBARS), a marke

84 Furthermore, the content of thiobarbituric acid-reactive substances (TBARS), and cat

85 e authors analyzed the association of plasma thiobarbituric acid-reactive substances (TBARS), glutath

86 els of lipid peroxidation products including thiobarbituric acid-reactive substances (TBARS), glutath

87 dation, breath ethane (an in vivo assay) and thiobarbituric acid-reactive substances (TBARS, an in vi

88 The commonly used thiobarbituric-acid-reactive-substances (TBARS) assay to

89 ed by measuring lipid peroxides (measured as thiobarbituric acid reactive substances [TBARS]) in reti

90 as determined by conjugated dienes (CDs) and thiobarbituric acid reactive substances (TBARSs) product

91 a lipid antioxidant, suppressed increases in thiobarbituric acid-reactive substances (TBARSs; a measu

92 TBARS (thiobarbituric acid reactive substances) test was used t

93 edium and high oxidative groups according to thiobarbituric acid reactive substances values after 9da

94 Thiobarbituric acid reactive substances values and lipox

95 otype in which oxidative damage (measured as thiobarbituric acid-reactive substances) was significant

96 Lipid oxidation, assessed as thiobarbituric acid reactive substances, was significant

97 The increased trypan blue uptake and thiobarbituric acid reactive substances were inhibited b

98 hydroxy--deoxyguanosine, and H2O2 and plasma thiobarbituric acid reactive substances were significant

99 Thiobarbituric acid-reactive substances were higher prec

100 se, hair copper, urinary copper, and urinary thiobarbituric acid-reactive substances were measured du

101 one-binding globulin, F(2)-isoprostanes, and thiobarbituric acid-reactive substances were measured up

102 ion, hair copper concentrations, and urinary thiobarbituric acid-reactive substances were significant

103 of lipid peroxidation (conjugated dienes and thiobarbituric acid-reactive substances) were also great

104 of low density lipoprotein was measured by a thiobarbituric acid-reactive substance, which was confir