ライフサイエンスコーパス: alloxan

1 y 60% reduction in beta-cell mass induced by alloxan.

2 Sp allele, were injected intravenously with alloxan (100 mg/kg), and plasma glucose was measured 3 d

3 iabetes mellitus was induced in male rats by alloxan (140 mg/kg, i.p.).

4 using a pancreatic beta-cell specific toxin, alloxan (150 mg/kg; n=8).

5 to acutely inhibit GK activity, 3) high-dose alloxan (24 microg), or 4) an adenovirus expressing GK s

6 A) to increase VMH GK activity, 2) low-dose alloxan (4 mug) to acutely inhibit GK activity, 3) high-

7 -hydroxyuracil, 5-hydroxy-5-methylhydantoin, alloxan, 5, 6-dihydroxycytosine, 5,6-dihydroxyuracil, 5-

8 Weanling CD1 mice (n=5) were injected with alloxan (50 mg/kg i.v.) to induce IDDM.

9 research aimed to detect potassium bromate, alloxan (a by-product of bleaching agents), and titanium

10 1 mice, with selection for susceptibility to alloxan, a generator of highly reactive oxygen free radi

11 vic counterregulatory responses, we injected alloxan, a GK inhibitor and toxin, into the third ventri

12 Alloxan administration resulted in a significant reducti

13 DM was induced by alloxan, after which periodontitis was induced by ligatu

14 The Alloxan (AL) Resistant (R) Leiter (Lt) mouse strain, clo

15 elected for susceptibility and resistance to alloxan (AL)-induced diabetes.

16 t only 8% of NG neurons and the GK inhibitor alloxan altered [Ca(2+)](i) oscillations in approximatel

17 Alloxan and its auto-oxidation product hydrogen peroxide

18 ation effectively reduced potassium bromide, alloxan, and titanium dioxide concentrations in spiked (

19 insulinoma cells from interleukin-1beta and alloxan cytotoxicity in vitro.

20 unaffected by glucokinase inhibitors such as alloxan, D-glucosamine, and N-acetyl-D-glucosamine, and

21 sing is unaffected by glucokinase inhibitors alloxan, d-glucosamine, and N-acetyl-d-glucosamine; and

22 , vitamin K, ubiquinone, juglone, ninhydrin, alloxan, dehydroascorbate, DTNB, lipoic acid/lipoamide,

23 ulin release or recovery of beta cells after alloxan destruction.

24 Alloxan diabetic rats and nondiabetic rats that were fed

25 xcised isodialuric acid, 5-hydroxyuracil and alloxan from DNA with apparent K(m) values of approximat

26 in trapping techniques, we demonstrated that alloxan generated ROS in the pancreas 15 min after admin

27 lasts (WI-38) and XP-A fibroblasts to repair alloxan-generated oxidative damage to nuclear and mtDNA

28 at the combination of a synthetic flavin and alloxan generates a catalyst system which facilitates bi

29 " the condensed-phase structure of anhydrous alloxan has largely been settled, but literature inconsi

30 UV-visible spectroscopy detected alloxan in 37.5 % of bakeries.

31 The glucokinase inhibitor alloxan increases KATP single-channel currents in glucos

32 he anti-diabetic potential in normoglycemic, alloxan-induced and glucose-loaded diabetic rats.

33 The alloxan-induced approximately 60% deficit in beta-cell m

34 Cells are protected against the alloxan-induced channel opening and consequent cell depo

35 Rats with alloxan-induced diabetes and rats fed a 30% galactose di

36 o glucose both in vitro and in vivo, prevent alloxan-induced diabetes in mice and respond to anti-dia

37 Alloxan-induced diabetes is associated with significant

38 two groups: a control group (n = 18) and an alloxan-induced diabetes mellitus (DM) group (n = 18).

39 r experiments performed in a rabbit model of alloxan-induced diabetes produced comparable results.

40 d-deprived (18 h) control rats and rats with alloxan-induced diabetes were orally administered saline

41 terize this phenomenon in an animal model of alloxan-induced diabetes.

42 divided into five groups, were induced with alloxan-induced diabetes.

43 bacteremia, and improved sepsis survival in alloxan-induced diabetic and spontaneous NOD mice.

44 to local metabolic coronary vasodilation in alloxan-induced diabetic dogs.

45 Alloxan-induced diabetic male Yucatan swine underwent 60

46 In alloxan-induced diabetic mice, the AFS methanol extract

47 yrcanicum extract on diabetic nephropathy in alloxan-induced diabetic mice.

48 d to a full-thickness cutaneous wound in the alloxan-induced diabetic rabbit ear ulcer model in a dos

49 improves responsiveness to acetylcholine in alloxan-induced diabetic rabbits.

50 racts of P. americana bark, leaf and root to alloxan-induced diabetic rats resulted in significant (P

51 Alloxan-induced diabetic wild- type mice (diabetic) deve

52 (NAC, 500 mg/kg), a GSH precursor, inhibited alloxan-induced NFkappaB activation and reduced hypergly

53 es and were the most responsive positions to alloxan-induced oxidative stress.

54 Two weeks after alloxan injection, 3v tanycyte destruction was reversed

55 Four and 6 days after 3v, but not 4v, alloxan injection, alloxan-treated rats ate only 30% and

56 High-fat diet (HFD), streptozotocin and alloxan injection, and glucose immersion have all been u

57 c nuclear extracts was observed 30 min after alloxan injection, as assessed by an electrophoretic mob

58 +/- 0.3 to 21.5 +/- 2.2 mmol/l 1 week after alloxan injection.

59 Alloxan is an important toxic glucose analogue used to i

60 ubstrates near and around the 3v affected by alloxan may be critically involved in the expression of

61 before and after induction of diabetes with alloxan monohydrate (40-60 mg/kg intravenously).

62 Prompt recrystallization of alloxan monohydrate from boiling water does not alter th

63 acid-d(4)), hydration at the C5 carbonyl of alloxan monohydrate occurs quantitatively to form the C5

64 These findings probe the exact structure of alloxan monohydrate to guide future research efforts in

65 the liquid-phase structure and reactivity of alloxan monohydrate.

66 the C5 gem-diol and planar tetraketo form of alloxan monohydrate.

67 structure of the typically employed reagent alloxan monohydrate.

68 ently use treatment with diabetogens such as alloxan or streptozotocin to render hosts hyperglycemic.

69 NOD/ShiLtJ mice conplastic for the alloxan resistant (ALR)/Lt-derived mt-Nd2(a) allele (NOD

70 n in combination with nuclear genes from the alloxan-resistant (ALR) strain, mt-Nd2(c) increases ROS

71 rce of mitochondria, alloxan-susceptible and alloxan-resistant mice were used.

72 monocyte ROS with diabetes resistance in the alloxan-resistant mouse, and NOD-Ncf1(m1J) mice with a g

73 8%, and 69% +/- 21% for 0, 45, and 60 mg/kg alloxan, respectively).

74 As a source of mitochondria, alloxan-susceptible and alloxan-resistant mice were used

75 at destroyed islets from the related NOD and alloxan-susceptible strains.

76 Addition of 5 mM alloxan to cultured rat cells increased the rate of oxid

77 Rabbits were treated with alloxan to destroy pancreatic islet cells, or mock-treat

78 erglycemia may have similar effects, we gave alloxan to mongrel dogs (group 2) to induce impaired glu

79 ays after 3v, but not 4v, alloxan injection, alloxan-treated rats ate only 30% and their blood glucos

80 the total endocrine mass was increased after alloxan treatment (26% +/- 4%, 43% +/- 8%, and 69% +/- 2

81 ion in adult pancreatic duct cells (low-dose alloxan treatment and pancreatic duct ligation) and line

82 pontaneously between 6 and 8 weeks of age in alloxan-untreated males.

83 o spontaneous type 2 diabetes development in alloxan-untreated males.

84 Alloxan was used to induce diabetes in the rats in group

85 Swine made diabetic with intravenous alloxan were euthanized at times varying from 0 to 90 da