The effects of sulfonylurea glyburide on superoxide dismutase, catalase, and glutathione peroxidase activities in the brain tissue of streptozotocin-induced diabetic rat

Nazaroğlu, N. Kemal; Sepici-Dinçel, Aylin; Altan, Nilgün

doi:10.1016/j.jdiacomp.2007.09.001

Cited by 28 publications

(18 citation statements)

References 36 publications

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“…These observations, except in body weight gain, were in accordance with results of Barbera et al [15]. Brain is one of the organs which consumes the greatest amount of oxygen in the body and has the highest polyunsaturated fatty acid and the lowest level of protective antioxidant (CAT and GPX) [31,32]. Therefore, this organ is more vulnerable to damage in conditions that increase free radical production.…”

Section: Discussionsupporting

confidence: 91%

Sodium Tungstate Attenuate Oxidative Stress in Brain Tissue of Streptozotocin-Induced Diabetic Rats

Nakhaee

Bokaeian

Akbarzadeh

et al. 2009

Biol Trace Elem Res

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High blood glucose concentration in diabetes induces free radical production and, thus, causes oxidative stress. Damage of cellular structures by free radicals play an important role in development of diabetic complications. In this study, we evaluated effects of sodium tungstate on enzymatic and nonenzymatic markers of oxidative stress in brain of streptozotocin (STZ)-induced diabetic rats. Rats were divided into four groups (ten rats in each group): untreated control, sodium tungstate-treated control, untreated diabetic, and sodium tungstate-treated diabetic. Diabetes was induced with an intraperitoneal STZ injection (65 mg/kg body weight), and sodium tungstate with concentration of 2 g/L was added to drinking water of treated animals for 4 weeks. Diabetes caused a significant increase in the brain thiobarbituric acid reactive substances (P < 0.01) and protein carbonyl levels (P < 0.01) and a decrease in ferric reducing antioxidant power (P < 0.01). Moreover, diabetic rats presented a reduction in brain glucose-6-phosphate dehydrogenase (21%), superoxide dismutase (41%), glutathione peroxidase (19%), and glutathione reductase (36%) activities. Sodium tungstate reduced the hyperglycemia and restored the diabetes-induced changes in all mentioned markers of oxidative stress. However, catalase activity was not significantly affected by diabetes (P = 0.4), while sodium tungstate caused a significant increase in enzyme activity of treated animals (P < 0.05). Data of present study indicated that sodium tungstate can ameliorate brain oxidative stress in STZ-induced diabetic rats, probably by reducing of the high glucose-induced oxidative stress and/or increasing of the antioxidant defense mechanisms.

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Section: Discussionsupporting

confidence: 91%

Sodium Tungstate Attenuate Oxidative Stress in Brain Tissue of Streptozotocin-Induced Diabetic Rats

Nakhaee

Bokaeian

Akbarzadeh

et al. 2009

Biol Trace Elem Res

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“…This argues against dramatic destructive effects of the drug on β cell mass. Moreover, it has been shown that under diabetic conditions, sulfonylureas influence the activities of antioxidant enzymes: brain SOD and Cat activities are reduced in rats with STZ-induced diabetes, but the decrease in antioxidant status is reversed by glibenclamide treatment (56). According to the current concept, protection against β cell death is attributed to K ATP channel openers (KCOs) instead of channel blockers.…”

Section: Discussionmentioning

confidence: 99%

Suppression of KATP channel activity protects murine pancreatic β cells against oxidative stress

et al. 2009

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The enhanced oxidative stress associated with type 2 diabetes mellitus contributes to disease pathogenesis. We previously identified plasma membrane-associated ATP-sensitive K + (K ATP ) channels of pancreatic β cells as targets for oxidants. Here, we examined the effects of genetic and pharmacologic ablation of K ATP channels on loss of mouse β cell function and viability following oxidative stress. Using mice lacking the sulfonylurea receptor type 1 (Sur1) subunit of K ATP channels, we found that, compared with insulin secretion by WT islets, insulin secretion by Sur1 -/-islets was less susceptible to oxidative stress induced by the oxidant H 2 O 2 . This was likely, at least in part, a result of the reduced ability of H 2 O 2 to hyperpolarize plasma membrane potential and reduce cytosolic free Ca 2+ concentration ([Ca 2+ ] c ) in the Sur1 -/-β cells. Remarkably, Sur1 -/-β cells were less prone to apoptosis induced by H 2 O 2 or an NO donor than WT β cells, despite an enhanced basal rate of apoptosis. This protective effect was attributed to upregulation of the antioxidant enzymes SOD, glutathione peroxidase, and catalase. Upregulation of antioxidant enzymes and reduced sensitivity of Sur1 -/-cells to H 2 O 2 -induced apoptosis were mimicked by treatment with the sulfonylureas tolbutamide and gliclazide. Enzyme upregulation and protection against oxidant-induced apoptosis were abrogated by agents lowering [Ca 2+ ] c . Sur1 -/-mice were less susceptible than WT mice to streptozotocin-induced β cell destruction and subsequent hyperglycemia and death, which suggests that loss of K ATP channel activity may protect against streptozotocin-induced diabetes in vivo.

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“…Modulation of antioxidant status during therapy with sulfonylureas has been described for pancreatic tissue and for heart, liver, and brain of STZ-diabetic rats where diabetes-induced alterations in enzyme activity were normalised after 4-5 weeks of glibenclamide treatment [186][187][188]. In addition, serum antioxidant capacity and SOD activity significantly increased in type 2 diabetic patients treated with the K ATP channel inhibitor repaglinide [189].…”

Section: Strategies Targeting Ros or Rns Formation In Beta-cells Cumentioning

confidence: 97%

Oxidative stress and beta-cell dysfunction

Drews

Koehler

Düfer

2010

Pflugers Arch - Eur J Physiol

264

214

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Diabetes mellitus type 1 and 2 (T1DM and T2DM) are complex multifactorial diseases. Loss of beta-cell function caused by reduced secretory capacity and enhanced apoptosis is a key event in the pathogenesis of both diabetes types. Oxidative stress induced by reactive oxygen and nitrogen species is critically involved in the impairment of beta-cell function during the development of diabetes. Because of their low antioxidant capacity, beta-cells are extremely sensitive towards oxidative stress. In beta-cells, important targets for an oxidant insult are cell metabolism and K(ATP) channels. The oxidant-evoked alterations of K(ATP) channel activity seem to be critical for oxidant-induced dysfunction because genetic ablation of K(ATP) channels attenuates the effects of oxidative stress on beta-cell function. Besides the effects on metabolism, interference of oxidants with mitochondria induces key events in apoptosis. Consequently, increasing antioxidant defence is a promising strategy to delay beta cell failure in (pre)-diabetic patients or during islet transplantation. Knock-out of K(ATP) channels has beneficial effects on oxidant-induced inhibition of insulin secretion and cell death. Interestingly, these effects can be mimicked by sulfonylureas that have been used in the treatment of T2DM for many years. Loss of functional K(ATP) channels leads to up-regulation of antioxidant enzymes, a process that depends on cytosolic Ca(2+). These observations are of great importance for clinical intervention because they show a possibility to protect beta-cells at an early stage before dramatic changes of the secretory capacity and loss of cell mass become manifest and lead to glucose intolerance or even overt diabetes.

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The effects of sulfonylurea glyburide on superoxide dismutase, catalase, and glutathione peroxidase activities in the brain tissue of streptozotocin-induced diabetic rat

Cited by 28 publications

References 36 publications

Sodium Tungstate Attenuate Oxidative Stress in Brain Tissue of Streptozotocin-Induced Diabetic Rats

Sodium Tungstate Attenuate Oxidative Stress in Brain Tissue of Streptozotocin-Induced Diabetic Rats

Suppression of KATP channel activity protects murine pancreatic β cells against oxidative stress

Oxidative stress and beta-cell dysfunction

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