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

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

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

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

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

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

15 Alloxan and its auto-oxidation product hydrogen peroxide

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

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

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

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

20 Alloxan diabetic rats and nondiabetic rats that were fed

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

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

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

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

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

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

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

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

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

30 Alloxan-induced diabetes is associated with significant

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

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

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

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

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

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

37 Alloxan-induced diabetic male Yucatan swine underwent 60

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

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

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

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

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

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

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

45 +/- 0.3 to 21.5 +/- 2.2 mmol/l 1 week after alloxan injection.

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

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

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

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

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

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

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

53 8%, and 69% +/- 21% for 0, 45, and 60 mg/kg alloxan, respectively).

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

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

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

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

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

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

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

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

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

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

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