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    Effects of melatonin on streptozotocin-induced diabetic liver injury in rats
    (Elsevier Gmbh, Urban & Fischer Verlag, 2006) Güven, Aysel; Yavuz, Özlem; Çam, Meryem; Ercan, Feriha; Bukan, Neslihan; Çomunoğlu, Cem; Gökçe, Fatih
    This study investigated the possible protective effects of melatonin as an antioxidant against streptozotocin (STZ)-induced diabetic liver injury in rats. Wistar rats were divided into four groups: untreated control (UC), melatonin-treated control (MC), untreated diabetic (UD), and melatonin-treated diabetic (MD). Experimental diabetes was induced by a single-dose (60 mg/kg, intraperitoneally (ip)) STZ injection, and metatonin was injected (200 wg/kg/day, ip) for 4 weeks. Upon light and electron microscopic examination, we observed that metatonin improved the morphological and histopathological changes of the liver caused by diabetes. Malondialdehyde levels in the liver homogenates of UD rats were higher than those of controls and were markedly reduced after melatonin treatment. Although no significant difference was observed with respect to antioxidant status, the superoxide dismutase activity tended to be higher in the UD rats than in the treated rats. Our findings showed that metatonin administration partially reduced liver injury in STZ-induced diabetic rats.
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    Melatonin protects against epirubicin-induced cardiotoxicity
    (Elsevier Gmbh, 2007) Güven, Aysel; Yavuz, Özlem; Çam, Meryem; Ercan, Feriha; Bukan, Neslihan; Çomunoğlu, Cem
    We investigated the cytoprotective effect of melatonin in epirubicin-induced cardiotoxicity using four experimental groups of mate Wistar rats: untreated control rats, epirubicin-treated rats, epirubicin+melatonin-treated rats, and melatonin-treated rats. We examined the histopathological. and biochemical, effects of melatonin on the epirubicin-induced changes and measured the Levels of the lipid peroxication end-product (malondialdehyde, MDA), an indicator of nitric oxide (NO) synthesis (nitrite/nitrate production), and reduced glutathione (GSH) in the heart. We also studied the extracellular matrix components (fibronectin, laminin) in the heart. Vacuole formation, mitochondrial. deformation and degeneration, and disordered myofibrillary structures were detected ultrastructurally in the epirubicin-treated group. The degeneration was reduced in the heart tissues of the epirubicin+melatonin group. Epirubicin increased the nitrite/nitrate production, but did not change the MDA and GSH levels significantly. Melatonin treatment Lowered the nitrite/nitrate concentrations, while increasing the GSH levels, which exceeded the Levels in epirubicin+melatonin-treated rats. We conclude that the epirubicin increased the nitrozative stress, not the oxidative stress, in heart tissue, and the cardioprotective effect of melatonin was partially attributed to the suppression of epirubicin-induced nitrozative stress. These results suggest that melatonin partially protects against epirubicin-induced cardiotoxicity. (C) 2006 Elsevier GmbH. All rights reserved.
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    Protective effects of chronic melatonin treatment against renal injury in streptozotocin-induced diabetic rats
    (Blackwell Munksgaard, 2003) Çam, Meryem; Yavuz, Özlem; Güven, Aysel; Ercan, Feriha; Bukan, Neslihan; Üstündağ, Nil
    The aim of this study was to investigate the effects of melatonin as an antioxidant, on prevention and treatment of streptozotocin (STZ)induced diabetic renal injury in rats. Male Wistar rats were divided into four groups: ( 1) untreated, ( 2) melatonin-treated, ( 3) untreated diabetic (UD), ( 4) melatonin-treated diabetic ( MD). Experimental diabetes was induced by single dose ( 60 mg/kg, i.p.) STZ injection. For 3 days prior to administration of STZ, melatonin was injected ( 200 mug/kg/day, i.p.); these injections were continued until the end of the study ( 4 weeks). Malondialdehyde (MDA) levels as a marker of lipid peroxidation were significantly increased in the renal homogenates of UD animals and decreased after melatonin administration. The activity of the antioxidative enzyme glutathione peroxidase (GSH-Px) was significantly reduced in UD rats. Melatonin treatment reversed STZ-induced reduction of GSH-Px activity without having an effect on blood glucose. Upon histopathological examination, it was observed that the melatonin treatment prevented the renal morphological damage caused by diabetes. Upon immunohistochemical investigation, glomerular anti-laminin beta1 staining decreased in MD rats. Additionally, no tubular anti-IGF-1 staining was observed in melatonin-treated rats. In conclusion, chronically administered melatonin reduced renal injury in STZ-induced diabetic rats and thus it may provide a useful therapeutic option in humans to reduce oxidative stress and the associated renal injury in patients with diabetes mellitus.