Untersuchungen �ber das Verhalten der Meerschweinchen gegen�ber verschiedenen diabetogenen Noxen. Alloxan und Dithizon

Maske, Helmut; Weinges, K. F.

doi:10.1007/bf00245832

Cited by 16 publications

(3 citation statements)

References 5 publications

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“…This interpretation is further supported by the observation that islets removed from guinea pigs, which are more resistant than rats to the diabetogenic action of alloxan (28), are 1/5 as sensitive as rat islets to tert-BuOOH (29).…”

Section: Discussionmentioning

confidence: 77%

Determinants of the selective toxicity of alloxan to the pancreatic B cell.

Malaisse¹,

Malaisse‐Lagae²,

Sener³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

248

140

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The diabetogenic agent alloxan exerts a preferential cytotoxic effect on the pancreatic B cell. The determinants of such a tissue specificity were investigated. Alloxan accumulated rapidly in liver and pancreatic islets but much more slowly in muscle. The activity of glutathione peroxidase and the resistance to exogenous peroxide were -20 times higher in liver and kidney than in islets, intermediate values being found in exocrine pancreas and muscle. These findings suggest that the selective cytotoxicity of alloxan to the pancreatic B cell is attributable to the conjunction oftwo features: a rapid cellular uptake ofthe drug and an exquisite sensitivity of the B cell to peroxide.

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Section: Discussionmentioning

confidence: 77%

Determinants of the selective toxicity of alloxan to the pancreatic B cell.

Malaisse¹,

Malaisse‐Lagae²,

Sener³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

248

140

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“…Alloxan rapidly and selectively depolarized the cells from mouse islets of Langerhans. In contrast, guinea-pig islet cells, which are known to be resistant to the diabetogenic properties of alloxan (Maske and Weinges, 1957), are not depolarized by Mloxan (Dean and Matthews, 1968). The rate of onset of depolarization by alloxan, an effect occurring within l0 min, correlates well with the time course of cytological changes which are: a diminution in nuclear and cytoplasmic granules, vacuolation and shrinkage of cytoplasm (Lazarus, Barden and Bradshaw, 1962), with metabolized by hexokinase, it was thought that alloxan might act by inhibiting hexokinase.…”

Section: Discussionmentioning

confidence: 97%

The bioelectrical properties of pancreatic islet cells: Effect of diabetogenic agents

Dean

Matthews

1972

Diabetologia

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Alloxan 5 mM depolarised the islet but not the aeinar cells of mouse pancreatic segments in vitro. This effect was prevented by D-glucose but not by glutathione, 3, 0, methyl-e-D-glucose, D-glucosamine, D-mannoheptulose, or L-leucine. Pretreatment of islet /?-cells with streptozotocin 20 mM caused no depolarization but inhibited the generation of action potentials by D-glucose, L-leueine, D-mannose and D-glyceraldehyde, whereas tolbutamide-induced action potentials were not blocked ; the alkylating moiety of streptozotocin, N-nitroso N-methyl urea produced similar effects. Prior exposure of the islet cells to nicotinamide 4.1 mM conferred protection against streptozotoein action. These observations are discussed in relation to the diabetogenic action of alloxan and streptozotocin. Propridt~s biodlectriques des cellules des ~lots pancrdatiques: Effets des agents diabdtog~nes Rgsumd. L'alloxane (5 raM) a d6polarisd les cellules des ilots, mais non les cellules de l'acinus des segments pancrdatiques chez la souris in vitro. Cet effet 6tait ani-hil6 par le D-glucose, mais non par le glutathion, le 3, 0, mdthyl-~-D-glueose, la D-glucosamine, le D-mannoheptulose ou la L-leucine. Le pr6-traitement des eellules fl des ilots ~ la streptozotoeine (20 mM) n'a pas provoqu6 de d6polarisation, mais a inhibd la gdngration de potentiels d'action par le D-glucose, la L'leueine, le D-mannose et la D-glyc6ralddhyde, tandis que les potentiels d'action pro-voqu~s par la tolbutamide n'dtaient pus bloquds; la partie alkylante de la strep~ozotoeine, la N-nitroso-Nmgthyl ur6e produisaient les mgmes effets. L'exposition prdalable des cellules des ilots ~ l'amide nicotinique (4.1 mM) fournissait une protection contre l'aetion de la streptozotoeine. Ces observations sont diseut~es en relation avee Faction diabdtoggne de l'Mloxane et de la streptozotocine. Die bioelektrischen Eigenschaften yon Inselzellen des Pankreas: Wirkungen diabetogener Substanzen Zusammenfassung. 5 mM Alloxan depolaiisiert die Inseln abet nicht die Azinuszelleu yon Segmenten des M/~usepankre~s in vitro. Diese Wirkung konnte dutch D-Glucose abet nicht durch Glutathion, 3, 0, methyl-e-D-Glucose, D-Glucosamin, D-Mannoheptulose, oder L-Leuein verhindert werden. Die Vorbehandlung yon fl-Zellen der Inseln mit 20ram Streptozotocin verursachte keine Depolarisierung abet verhinderte die Erzeugung von AktionspotentiMen durch D-Glucose, L-Leuein, D-Mannose und D-Glyceraldehyden, w/ihrend durch Tolbutamid induzierte AktionspotentiMe nieht bloekiert wurden. Der alkylierende Tell yon Streptozotocin, der N-nitroso-N-methyl-Harnstoff zeigte /ihnliche Wirkunten. Ein vorheriger Kontakt der Inselzellen mit Nieotinamid 4,1 mM erzeugte einen Schutz gegeniiber der Streptozotocinwirkung. Diese Beobachtungen werden in Verbindung mit der diabetogenen Wirkung von Alloxan und Streptozotocin diskutiert.

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“…Alloxan administration cause hyperglycemia and glucosuria has been described in several species, such as in dogs [ 38 ], in rabbits [ 39 ], in rats [ 40 ] and in other species [ 41 ]. Alloxan resistance has been found in Guinea pig [ 42 ]. Dosage and treatment regimen have been elaborated for the most frequently used species.…”

Section: Experimental Modelsmentioning

confidence: 99%

Acute and chronic animal models for the evaluation of anti-diabetic agents

Kumar

Singh

Vasudeva

et al. 2012

Cardiovasc Diabetol

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Diabetes mellitus is a potentially morbid condition with high prevalence worldwide thus being a major medical concern. Experimental induction of diabetes mellitus in animal models is essential for the advancement of our knowledge and understanding of the various aspects of its pathogenesis and ultimately finding new therapies and cure. Experimental diabetes mellitus is generally induced in laboratory animals by several methods that include: chemical, surgical and genetic (immunological) manipulations. Most of the experiments in diabetes are carried out in rodents, although some studies are still performed in larger animals. The present review highlights the various methods of inducing diabetes in experimental animals in order to test the newer drugs for their anti-diabetic potential.

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Untersuchungen �ber das Verhalten der Meerschweinchen gegen�ber verschiedenen diabetogenen Noxen. Alloxan und Dithizon

Cited by 16 publications

References 5 publications

Determinants of the selective toxicity of alloxan to the pancreatic B cell.

Determinants of the selective toxicity of alloxan to the pancreatic B cell.

The bioelectrical properties of pancreatic islet cells: Effect of diabetogenic agents

Acute and chronic animal models for the evaluation of anti-diabetic agents

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