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    Age-related changes in the rat brain mitochondrial antioxidative enzyme ratios: Modulation by melatonin
    (PERGAMON-ELSEVIER SCIENCE LTD, 2012) Ozturk, Guler; Akbulut, K. Gonca; Guney, Sevin; Acuna-Castroviejo, Dario
    Oxidative stress is an important factor for aging. The antioxidative enzymes glutathione peroxidase (GPx), glutathione reductase (GRd) and superoxide dismutase (SOD) play a crucial role protecting the organism against the age-dependent oxidative stress. Glutathione (GSH) is present in nearly all living cells. GSH is one of the main antioxidants in the cell and it serves several physiological functions. Our purpose was to evaluate the age-related changes in mitochondrial GPx, GRd and SOD activities, and mitochondrial GSH pool in the brains of young (3 months) and aged rats (24 months). We also investigated whether melatonin administration influences these brain mitochondrial enzyme activities and GSH levels in young and aged rats. The results showed that GPx activity increased with age, whereas melatonin treatment decreased GPx activity in the aged rats at levels similar to those in young and young + melatonin groups. The activities of GRd and SOD, however, did not change with age. But, melatonin treatment increased SOD activity in the aged rats. GSH levels, which also increased with age, were not modified by melatonin treatment. The reduction in the SOD/GPx and GR/GPx ratios with age was prevented by melatonin administration. Together, our results suggest that the age-related oxidative stress in rat brain mitochondria is more apparent when the antioxidant enzyme ratios are analyzed instead of their absolute values. The antioxidative effects of melatonin were also supported by the recovery of the enzyme ratios during aging. (C) 2012 Elsevier Inc. All rights reserved.
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    Comparison of Melatonin Effect on Oxidant Status and Antioxidant Capacity in Liver and Heart of Young and Aged Rats
    (ELSEVIER TAIWAN, 2013) Guney, Sevin; Cumaoglu, Ahmet; Ozturk, Guler; Akbulut, K. Gonca; Karasu, Cimen
    Background: Oxidative stress is involved in several pathologic conditions such as metabolic or cardiovascular disease, and in aging. Oxidative damage of biomolecules increases with age. Melatonin is the main neurohormone of the pineal gland and specific antioxidants may act against age-related oxidative damage. Objective: This study investigated the effects of administration of melatonin on aging-related parameters such as total oxidant status (TOS), hydrogen peroxide (H2O2) and lipid hydroperoxide (LOOH) levels and total antioxidant capacity (TAC) in the heart and liver in a rat model of aging. Methods: Young (3-month-old) and aged (24-month-old) male Wistar rats were divided into control and melatonin-treated groups. Melatonin was given for 21 days (10 mg/kg/day). At the end of the treatment period, TOS, TAC, H2O2, and LOOH levels were measured. Results: H2O2 in the liver, but not in the heart, was found to be increased in aged rats. Melatonin treatment diminished H2O2 in the heart of both group of rats compared with those of untreated control rats. Melatonin treatment also led to a decrease in H2O2 in the liver of aged rats. LOOH were found to be increased in both tissues of aged rats whereas melatonin treatment decreased LOOH levels in heart and liver tissues of aged rats. In the young rats melatonin also inhibited LOOH in liver. TAC in heart and liver was not found to be statistically different between young and aged rats. In young rats, melatonin treatment resulted in an increase in TAC that was associated with increased H2O2. In the liver and heart of the rats, TOS was increased with age and was ameliorated by melatonin treatment. Conclusion: Our results demonstrate that there is no dramatic overall decline in the antioxidant system with age. However, total oxidant status increased with age. Melatonin has a restorative effect on oxidative status. Copyright (C) 2012, Taiwan Society of Geriatric Emergency & Critical Care Medicine. Published by Elsevier Taiwan LLC. All rights reserved.
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    Histochemical observations on protective effects of melatonin against carbon tetrachloride (CCl4) - induced hepatotoxicity
    (WILEY-BLACKWELL, 2015) Ozerkan, Dilsad; Ozsoy, Nesrin; Akbulut, K. Gonca; Guney, Sevin; Ozturk, Guler
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    Melatonin with 1,25-Dihydroxyvitamin D3 Protects against Apoptotic Ischemia-Reperfusion Injury in the Rat Kidney
    (INFORMA HEALTHCARE, 2012) Sinanoglu, Orhun; Sezgin, Gulbuz; Ozturk, Guler; Tuncdemir, Matem; Guney, Sevin; Aksungar, Fehime Benli; Yener, Nese
    This study was designed to evaluate the preventive role of melatonin (Mel) and 1,25-dihydroxyvitamin D3 (VD3) in biochemical and apoptotic events leading to tissue injury and renal dysfunction after ischemia-reperfusion (I/R). Thirty male Wistar rats were divided into five groups: sham-operated, I/R, Mel + I/R, VD3 + I/R, and Mel + VD3 + I/R. The rats were intraperitoneally administered with Mel (10 mg/kg), VD3 (0.5 mu g/kg), or Mel (10 mg/kg) plus VD3 (0.5 mu g/kg) each day at 1 week prior to ischemia. Right nephrectomy was initially performed and left renal I/R injury was induced by 45 min of bilateral renal ischemia followed by 45 min of reperfusion. After reperfusion, kidneys and blood were obtained for histopathologic and biochemical evaluation. Mel and VD3 had an ameliorative effect on biochemical parameters such as serum creatinine, blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, and apoptosis (caspase-3 and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining) in the kidneys against renal I/R injury in rats. Additionally, VD3 combined with Mel significantly reduced apoptotic and histological alterations when compared with Mel or VD3 alone. This preventive effect on renal tubular apoptosis was remarkable when Mel was combined with VD3.
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    Protective Effect of Melatonin and 1,25-Dihydroxyvitamin D3 on Renal Ischemia-Reperfusion Injury in Rats
    (INFORMA HEALTHCARE, 2013) Sezgin, Gulbuz; Ozturk, Guler; Guney, Sevin; Sinanoglu, Orhun; Tuncdemir, Matem
    Ischemia-reperfusion (I/R) injury induces the generation of reactive oxygen species (ROS) which affect many organs. This study was designed to investigate the roles of melatonin and 1,25-dihydroxyvitamin D-3 (VD3) on renal I/R injury. Thirty male Wistar albino rats were divided into five groups: group 1, control; group 2, right nephrectomy (RN) + I/R in the contralateral kidney; group 3, melatonin + RN + I/R; group 4, VD3 + RN + I/R; and group 5, melatonin + VD3 + RN + I/R. Melatonin (10 mg/kg), VD3 (0.5 mu g/kg), and melatonin plus VD3 were injected intraperitoneally for 7 days before renal I/R. After 7 days, right nephrectomy was initially performed and left renal artery was clamped for 45 min. After 45-min reperfusion, the serum and kidney tissue samples were obtained for assays. Melatonin and VD3 had an ameliorative effect on biochemical parameters such as serum creatinine (SCr) and blood urea nitrogen (BUN). Renal tissue malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO) levels, and superoxide dismutase (SOD) activity were determined. Renal I/R decreased the kidney tissue GSH levels and SOD activity and increased the NO levels as compared with control group. However, melatonin and VD3 and melatonin plus VD3 treatment significantly increased the tissue GSH levels and SOD activity and decreased the NO levels compared with those of I/R group. Meanwhile, MDA levels were not different between the control and I/R groups. But, MDA levels decreased in all treated groups compared to I/R and control groups. These data support that melatonin and VD3 have beneficial effects on renal injury.