Person: AKAKIN, DİLEK
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AKAKIN
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DİLEK
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Publication Metadata only The effects of long-term prenatal exposure to 900, 1800, and 2100 MHz electromagnetic field radiation on myocardial tissue of rats(2022-11-01) AKAKIN, DİLEK; Bozok S., Karaagac E., Sener D., AKAKIN D., TÜMKAYA L.It is well-known that wireless communication technologies facilitate human life. However, the harmful effects of electromagnetic field (EMF) radiation on the human body should not be ignored. In the present study, we evaluated the effects of long-term, prenatal exposure to EMF radiation on the myocardium of rats at varying durations. Overall, 18 pregnant Sprague-Dawley rats were assigned into six groups (n = 3 in each group). In all groups other than the control group, three pregnant rats were exposed to EMF radiation (900, 1800 and 2100 MHz) for 6, 12 and 24 h over 20 days. After delivery, the newborn male pups were identified and six newborn male pups from each group were randomly selected. Then, histopathological and biochemical analysis of myocardial samples were performed. When 24-h/day prenatal exposures to 900, 1800, 2100 MHz EMF radiation were evaluated, myocardial damage was greater in the 2100 MHz EMF-24h group than the other groups. In addition, when malondialdehyde (MDA) and glutathione (GSH) levels associated with reactive oxidative species (ROS) were evaluated, the MDA level was higher in the 2100 MHz EMF-24h group compared with the other groups. The GSH level was also lower in the 2100 MHz EMF-24h group. When the 6, 12 and 24 h/day prenatal exposures to 1800 MHz EMF radiation were evaluated, myocardial damage was greater in 1800 MHz EMF-24h group than the remaining groups (p < 0.0001). Also, MDA level was greater in the 1800 MHz EMF-24h group compared with the other groups while the GSH level was lower in this group. It was shown that myocardial tissue was affected more by long-term exposure to EMF radiation at high frequencies. The data raise concerns that the harmful effects of non-ionizing radiation exposure on cardiac tissue will increase with 5G technology.Publication Metadata only Phoenixin 14 ameloriates pancreatic injury in streptozotocin-induced diabetic rats by alleviating oxidative burden(2022-09-01) ÖZDEMİR KUMRAL, ZARİFE NİGAR; YÜKSEL, MERAL; AKAKIN, DİLEK; ERZİK, CAN; HAKLAR, GONCAGÜL; ÖZDEMİR KUMRAL Z. N. , Sen E., Yapici H. B. , Atakul N., Domruk O. F. , Aldag Y., Sen L. S. , Mustafaoglu F. K. , YÜKSEL M., AKAKIN D., et al.Phoenixin-14 (PNX) is a neuropeptide that has been shown to prevent oxidative damage and stimulates insulin secretion. We investigated the effects of PNX on pancreatic injury induced by streptozotocin (STZ), and nicotinamide (NAD). Male Sprague-Dawley rats, in control (C) and diabetic (STZ) groups, were treated with either saline, or PNX (0.45 nmol/kg, or 45 nmol/kg) daily for 3 days 1 week after STZ injection. Fasting blood glucose (FBG) and gastric emptying rate (GER) were measured. Tissue and blood samples were collected. PNX treatments prevented pancreatic damage and beta cell loss. Increased luminol and lucigenin levels in the pancreas, ileum and liver tissues of STZ groups were alleviated by PNX treatment in pancreatic and ileal tissues. PNX0.45 decreased FBG without any change in insulin blood level and pancreatic mRNA. GER increased in all diabetic rats while PNX0.45 delayed GER only in the C group. PNX diminishes pancreatic damage and lowers FBG by reducing oxidative load.Publication Metadata only Obestatin improves oxidative brain damage and memory dysfunction in rats induced with an epileptic seizure(ELSEVIER SCIENCE INC, 2017) YEGEN, BERRAK; Koyuncuoglu, Turkan; Vizdiklar, Caner; Uren, Dogan; Yilmaz, Hakan; Yildirim, Cagan; Atal, Sefa Semih; Akakin, Dilek; Demirci, Elif Kervancioglu; Yuksel, Meral; Yegen, Berrak C.Obestatin was shown to alleviate renal, gastrointestinal and haemorrhage-induced brain injury in rats. In order to investigate the neuroprotective effects of obestatin on seizure-induced oxidative brain injury, an epileptic seizure was induced with a single intraperitoneal (i.p.) close of pentylenetetrazole (PTZ, 45 mg/kg) in male Wistar rats. Thirty minutes before the PTZ injection, rats were treated with either saline or obestatin (1 mu g/kg, i.p.). Seizure was video-taped and then evaluated by using Racine's scoring (0-5). For the assessment of memory function, passive-avoidance test was performed before seizure induction, which was repeated on the 3rd day of seizure. The rats were decapitated at the 24th or 72nd hour of seizures and brain tissues were obtained for histopathological examination and for measuring levels of malondialdehyde (MDA), glutathione (GSH), reactive oxygen radicals and myeloperoxidase (MPO) activity. Obestatin treatment reduced the average seizure score, decreased the occurrence and duration of generalized tonic-clonic seizures, presenting with a shorter latency to their onset. Increased lipid peroxidation and enhanced generation of oxygen-derived radicals detected at the post-seizure 72nd h were suppressed by the consecutive treatments of obestatin, but no changes were observed by the single obestatin treatment in the 24-h seizure group. Neuronal damage and increased GFAP immunoreactivity, observed in the hippocampal areas and cortex of PTZ-induced rats were alleviated in 3-day obestatin-treated PTZ group. PTZ-induced memory dysfunction was significantly improved in obestatin-treated PTZ group as compared to saline-treated rats. The present data indicate that obestatin ameliorated the severity of PTZ-induced seizures, improved memory dysfunction and reduced neuronal damage by limiting oxidative damage. (C) 2017 Elsevier Inc. All rights reserved.Publication Metadata only Protective effects of melatonin against spinal cord injury induced oxidative damage in rat kidney: A morphological and biochemical study(ELSEVIER GMBH, 2013) YEGEN, BERRAK; Akakin, Dilek; Kiran, Demir; Ozkan, Naziye; Ersahin, Mehmet; Ozdemir-Kumral, Zarife Nigar; Yegen, Berrak; Sener, GokselSpinal cord injury (SCI) induced oxidative stress affects multiple organ systems including the kidney. We studied the possible protective effects of melatonin on SCI-induced oxidative damage in renal tissues of rats. Wistar albino rats (n =24) were exposed to SCI and divided into vehicle- or melatonin-treated SCI groups. Melatonin was administred intraperitoneally at a dose of 10 mg/kg for seven days. Renal tissues were investigated by light and electron microscopy. Furthermore, tissue malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and superoxide dismutase (SOD) activities were also determined. In the vehicle-treated SCI group, the renal histology was disturbed compared to controls, whereas the melatonin-treated SCI group showed significantly reduced degeneration of renal tissue as seen by both light and electron microscopy. MDA levels, MPO and SOD activities were increased and GSH levels were decreased in the vehicle-treated SCI group compared to controls. On the other hand, decreased MDA levels and MPO activities and increased GSH levels were observed in the melatonin-treated SCI group compared to vehicle-treated SCI group. These results showed that experimentally induced SCI caused oxidative stress in the rat kidney, whereas melatonin treatment reduced oxidative stress, suggesting that it may be used as a complementary therapy of renal problems occurring following SCI. (C) 2013 Elsevier GmbH. All rights reserved.Publication Metadata only Obestatin alleviates subarachnoid haemorrhage-induced oxidative injury in rats via its anti-apoptotic and antioxidant effects(TAYLOR & FRANCIS LTD, 2013) ŞENER, AZİZE; Ersahin, Mehmet; Ozsavci, Derya; Sener, Azize; Ozakpinar, Ozlem Bingol; Toklu, Hale Zerrin; Akakin, Dilek; Sener, Goksel; Yegen, Berrak C.Objective: The aim was to investigate the putative anti-inflammatory and anti-apoptotic effect of obestatin in a rat model of subarachnoidal haemorrhage (SAH). Methods: To induce SAH, rats were injected with 0.3 mL blood into their cisterna magna. At 48 hours rats were decapitated after neurological examination. Blood-brain barrier (BBB) permeability, brain water content, oxidative stress markers and histological analysis were done in brain tissue. Results: The results showed that neurological examination scores were increased in the SAH group and, moreover, BBB permeability was impaired and oedema formed. SAH resulted in increased levels of plasma tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6 levels and caspase-3 activity. Lipid peroxidation and protein oxidation levels and myeloperoxidase activity were all increased in the brain tissue, with concomitant decreases in antioxidant enzymes. On the other hand, SAH-induced neurological impairment and oxidative brain injury were ameliorated in the obestatin-treated group. Conclusion: The present study provides the first evidence that peripheral administration of obestatin exerts potent anti-inflammatory and neuroprotective effects in SAH-induced oxidative damage by maintaining a balance in oxidant-antioxidant status through the augmentation of endogenous antioxidants and the inhibition of pro-inflammatory mediators.