The partial protective effect of the hydroxyl radical scavenger dimethyl urea on streptozotocin-induced diabetes in the mouse in vivo and in vitro

Sandler, Stellan; Andersson, Arne

doi:10.1007/bf00253747

Cited by 59 publications

(33 citation statements)

References 29 publications

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“…Their mechanisms of action are unknown, but since their actions are inhibited by superoxide dismutase (SOD) [4,5] or a chemical scavenger, such as 1,1-dimethylurea [6], they have been suggested to be related to the formation of free radicals. In fact, some reports strongly support the participation of free radicals in the action of alloxan [7,8].…”

Section: Introduction 2 Materials and Methodsmentioning

confidence: 99%

Enhancement by streptozotocin of O⁻₂ radical generation by the xanthine oxidase system of pancreatic β‐cells

et al. 1988

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Spin-trapping techniques and electron spin resonance (ESR) spectroscopy were used to study the relationship between the effect of streptozotocin (STZ) on pancreatic B-cells and free radical formation by these cells. Results showed that STZ enhanced generation of the DMPO-OH radical adduct, which is a degradation product of the superoxide anion (0;) in the presence of cellular components, in a hypoxanthine-xanthine oxidase (XOD) system with a homogenate of b-cells. This enhancing effect was also observed in a system without cellular components; STZ increased the signal height due to the 0; radical in a concentration-dependent manner and caused a maximum of 150% enhancement at a concentration of 1.5 mM. Thus, STZ seemed to enhance the generation of the 0; radical in the XOD system, probably by some mechanism of its interaction with XOD. Pancreatic @ells exhibited a high XOD activity and a very low superoxide dismutase activity. Therefore, the present result supports the possibility that the cytotoxic effect of STZ is closely related to free radical generation in pancreatic l%ells.

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Section: Introduction 2 Materials and Methodsmentioning

confidence: 99%

Enhancement by streptozotocin of O⁻₂ radical generation by the xanthine oxidase system of pancreatic β‐cells

et al. 1988

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“…Several sections were mounted on glass slides and stained with hematoxylin and eosin. After coding was done, the degree of insulitis was determined blindly by two independent observers according to the grading system previously published (34).…”

Section: Methodsmentioning

confidence: 99%

Multiple low-dose streptozotocin-induced diabetes in the mouse. Evidence for stimulation of a cytotoxic cellular immune response against an insulin-producing beta cell line.

McEvoy¹,

Andersson²,

Sandler³

et al. 1984

J. Clin. Invest.

111

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AbS tract. Mice were examined for the presence of splenocytes specifically cytotoxic for a rat insulinoma cell line (RIN) during the induction of diabetes by streptozotocin (SZ) in multiple low doses (Multi-Strep). Cytotoxicity was quantitated by the release of 5"Cr from damaged cells. A low but statistically significant level of cytolysis (5%) by splenocytes was first detectable on day 8 after the first dose of SZ. The cytotoxicity reached a maximum of -9% on day 10 and slowly decreased thereafter, becoming undetectable 42 d after SZ was first given. The time course of the in vitro cytotoxic response correlated with the degree of insulitis demonstrable in the pancreata of the Multi-Strep mice. The degree of cytotoxicity after Multi-Strep was related to the number of effector splenocytes to which the target RIN cells were exposed and was comparable to that detectable after immunization by intraperitoneal injection of RIN cells in normal mice. The cytotoxicity was specific for insulin-producing cells; syngeneic, allogeneic, and xenogeneic lymphocytes and lymphoblasts, 3T3 cells, and a human keratinocyte cell line were not specifically lysed by the splenocytes of the Multi-Strep mice. This phenomenon was limited to the Multi-Strep mice. Splenocytes from mice made diabetic by a single, high dose of SZ exhibited a very low level of cytotoxicity against the RIN cells. The cytotoxic response was also quantitated Dr.

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“…These findings suggest that streptozotocin may also act as an oxidant, and this action may be associated with its diabetogenic effect. Recent support for this supposition was the finding of Sandler and Andersson (9), that partial protection against streptozotocin-induced diabetes in the mouse was achieved by prior administration of the hydroxyl radical scavenger dimethyl-urea.…”

Section: Introductionmentioning

confidence: 96%

Modification of chemically induced diabetes in rats by vitamin E. Supplementation minimizes and depletion enhances development of diabetes.

Slonim¹,

Surber²,

Page³

et al. 1983

J. Clin. Invest.

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A B S T R A C T Administration of the antioxidant vitamin E to rats, prior to administration of either streptozotocin or alloxan, provided protection against the diabetogenic effect of both these agents. This was demonstrated by their response to a glucose load, their pancreatic insulin content and light microscopy findings. In addition, rats whose antioxidant state was depleted, by being maintained on a vitamin E and selenium-deficient diet, demonstrated increased diabetogenic susceptibility to normally nondiabetogenic doses of streptozotocin. These findings provide indirect support for the suggestion that the chemical agents streptozotocin and alloxan may exert their diabetogenic effect by acting as oxidants or free radical producers.

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The partial protective effect of the hydroxyl radical scavenger dimethyl urea on streptozotocin-induced diabetes in the mouse in vivo and in vitro

Cited by 59 publications

References 29 publications

Enhancement by streptozotocin of O⁻₂ radical generation by the xanthine oxidase system of pancreatic β‐cells

Enhancement by streptozotocin of O⁻₂ radical generation by the xanthine oxidase system of pancreatic β‐cells

Multiple low-dose streptozotocin-induced diabetes in the mouse. Evidence for stimulation of a cytotoxic cellular immune response against an insulin-producing beta cell line.

Modification of chemically induced diabetes in rats by vitamin E. Supplementation minimizes and depletion enhances development of diabetes.

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The partial protective effect of the hydroxyl radical scavenger dimethyl urea on streptozotocin-induced diabetes in the mouse in vivo and in vitro

Cited by 59 publications

References 29 publications

Enhancement by streptozotocin of O−2 radical generation by the xanthine oxidase system of pancreatic β‐cells

Enhancement by streptozotocin of O−2 radical generation by the xanthine oxidase system of pancreatic β‐cells

Multiple low-dose streptozotocin-induced diabetes in the mouse. Evidence for stimulation of a cytotoxic cellular immune response against an insulin-producing beta cell line.

Modification of chemically induced diabetes in rats by vitamin E. Supplementation minimizes and depletion enhances development of diabetes.

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Enhancement by streptozotocin of O⁻₂ radical generation by the xanthine oxidase system of pancreatic β‐cells

Enhancement by streptozotocin of O⁻₂ radical generation by the xanthine oxidase system of pancreatic β‐cells