Vanadyl Sulfate Administration Protects the Streptozotocin-Induced Oxidative Damage to Brain Tissue in Rats

Yanardağ, Refiye; Tunalı, Sevim

doi:10.1007/s11010-005-9107-1

Cited by 28 publications

(29 citation statements)

References 53 publications

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“…Studies in human beings have shown that vanadyl sulfate supplements normalize blood glucose levels and reduced HbA1c levels (Boden et al 1996) in patients with noninsulin-dependent diabetes mellitus (NIDDM). The protective effect of vanadyl sulfate on some tissues (Akgün-Dar et al 2007;Yanardag and Tunali 2006;Bolkent et al 2005) has been demonstrated previously by our collegues. It was also suggested that vanadyl sulfate may stimulate amino acid transport into skeletal muscle (Jandhyala and Hom 1983).…”

Section: Introductionsupporting

confidence: 77%

Influence of vanadium supplementation on oxidative stress factors in the muscle of STZ-diabetic rats

Kurt¹,

Yilmaz-Ozden²,

Özsoy³

et al. 2011

Biometals

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In recent years, the role of free radical damage consequent to oxidative stress is widely discussed in diabetic complications. In this aspect, the protection of cell integrity by trace elements is a topic to be investigated. Vanadium is a trace element believed to be important for normal cell function and development. The aim of the present study was to investigate the effect of vanadyl sulfate supplementation on the antioxidant system in the muscle tissue of diabetic rats. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ, 65 mg/kg body weight) to male Swiss albino rats. The rats were randomly divided into 4 groups: Group I, control; Group II, vanadyl sulfate control; Group III, STZ-diabetic untreated; Group IV, STZ-diabetic treated with vanadyl sulfate. Vanadyl sulfate (100 mg/kg) was given daily by gavage for 60 days. At the last day of the experiment, rats were killed, muscle tissues were taken, homogenized in cold saline to make a 10% (w/v) homogenate. Body weights and blood glucose levels were estimated at 0, 30 and 60th days. Antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), as well as carbonic anhydrase (CA), myeloperoxidase (MPO) activities and protein carbonyl content (PCC) were determined in muscle tissue. Vanadyl sulfate administration improved the loss in body weight due to STZ-induced diabetes and decreased the rise in blood glucose levels. It was shown that vanadium supplementation to diabetic rats significantly decrease serum antioxidant enzyme levels, which were significantly raised by diabetes in muscle tissue showing that this trace element could be used as preventive for diabetic complications.

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Section: Introductionsupporting

confidence: 77%

Influence of vanadium supplementation on oxidative stress factors in the muscle of STZ-diabetic rats

Kurt¹,

Yilmaz-Ozden²,

Özsoy³

et al. 2011

Biometals

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“…Our results are consistent with previous studies that show reduction of total antioxidant capacity in brain of experimental diabetic rats [36,37]. Also, other studies have demonstrated a decrease in reduced glutathione (one of the most important intracellular antioxidant) level of brain in diabetes [31,34,35]. In the present study, decreased FRAP level represents increased utilization of nonenzymatic antioxidants due to oxidative stress.…”

Section: Discussionsupporting

confidence: 94%

“…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%

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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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“…Increased NADH causes NADH oxidase to produce ROS (Chung et al, 2003). Decreased levels of GSH and activities of antioxidant enzymes (SOD, CAT, and GP x ) have been reported in different tissues and plasma of diabetic patients and animals (El Boghdady & Badr, 2012;Gumieniczek et al, 2009;Karthik & Ravikumar, 2011;Ozsoy-Sacan et al, 2006;Yanardag & Tunali, 2006). Similarly, in experimental diabetes, the pulmonary oxidative stress was present because of the reduction of antioxidant enzyme activity (Gumieniczek et al, 2002(Gumieniczek et al, , 2009Ozansoy et al, 2005).…”

Section: Discussionmentioning

confidence: 98%

Chard (Beta vulgarisvar.cicla) extract improved hyperglycemia-induced oxidative stress and surfactant-associated protein alterations in rat lungs

Öztay¹,

Saçan

Kayalar³

et al. 2015

Pharmaceutical Biology

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Context: Chard is used as an antidiabetic agent by the diabetic patients in Turkey. Objective: The effect of chard extract [Beta vulgaris L. var. cicla (Chenopodiaceae)] on the antioxidant system and the expression of surfactant-associated proteins (SP) in the lungs of hyperglycemic rats were examined. Materials and methods: Hyperglycemia was induced by a single dose of streptozotocin (60 mg/kg) provided intraperitoneally. Fourteen days after the rats were rendered hyperglycemic, the chard (2 g/kg/d), insulin (6 U/kg/d), and chard plus insulin (as mentioned above) were administered to rats for 45 d. On day 60, rats' lungs were removed. Oxidative stress parameters and SP expression were assayed. Results: The lungs of hyperglycemic rats were characterized by the induced lipid and protein oxidation, elevated myeloperoxidase and xanthine oxidase activities, decreased glutathione levels, and reduced tissue factor and antioxidant enzymes activities (catalase, superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase). Chard treatment alone and chard treatment combined with insulin were capable of achieving a regression of pulmonary oxidative stress, by inhibiting lipid and protein oxidation, and restoring the antioxidant system of hyperglycemic rats. SP-A expressions were significantly unchanged in all groups, whereas pro-SP-C and SP-D expressions were reduced in hyperglycemic rats. Pro-SP-C and SP-D levels were increased by chard and insulin administrations alone and combined in hyperglycemic rats. Discussion and conclusion: All treatments have a positive effect on the surfactant and antioxidant systems of the lungs of hyperglycemic rats. The best therapeutic effect was provided by treatment with chard extract alone in the compensation of hyperglycemic symptoms.

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Vanadyl Sulfate Administration Protects the Streptozotocin-Induced Oxidative Damage to Brain Tissue in Rats

Cited by 28 publications

References 53 publications

Influence of vanadium supplementation on oxidative stress factors in the muscle of STZ-diabetic rats

Influence of vanadium supplementation on oxidative stress factors in the muscle of STZ-diabetic rats

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

Chard (Beta vulgarisvar.cicla) extract improved hyperglycemia-induced oxidative stress and surfactant-associated protein alterations in rat lungs

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