FOOD AND CHEMICAL TOXICOLOGY

The present study was undertaken to evaluate the cardio-protective potential of apricot-feeding in the ischemia-reperfusion (I/R) model of rats in vivo. Rats were divided into three groups of 12 rats each. Group 1 was fed with a standard rat chow, groups 2 and 3 were fed with a standard rat chow supplemented with 10% or 20% dried apricot during 3 months before the beginning of I/R studies. To produce I/R, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Infarct sizes were found significantly decreased in 10% (55.0 +/- 4.3%) and 20% (57.0 +/- 2.9%) apricot-fed groups compared to control group (68.7 +/- 2.0%). Light and electron microscopic evaluations of hearts also demonstrated similar beneficial effects on I/R injury in apricot-fed both groups. Total phenolic contents, DPPH radical scavenging and ferric-reducing power as in vitro antioxidant capacities of rat chows were significantly increased after supplementation with apricot for each ratio. Cu, Zn Superoxide dismutase (Cu, Zn SOD) and catalase (CAT) activities were increased, and lipid peroxidation was decreased significantly in the hearts of 20% apricot-fed group after I/R. In conclusion, we clearly demonstrated in vivo cardio-protective activity of apricot-feeding related to its antioxidant phenolic contents in rats subjected to myocardial I/R. (C) 2009 Elsevier Ltd. All rights reserved

Dual effects of melatonin on uterine myoelectrical activity of non-pregnant rats

Objective: In this experimental study, we aimed to investigate the role of melatonin on uterine myoelectrical activity of non-pregnant rats. Material and Methods: Forty-six female rats were assigned to six groups: (1) control; (0.2 mL 0.9% NaCl was injected intravenously (IV), n=6); (2) melatonin applied as 0.4 mg/kg/IV (n=8); (3) melatonin applied as 4 mg/kg/IV (n=8); (4) single dose of oxytocin (100 mU/kg) injected IV (n=8); (5) melatonin (0.4 mg/kg) plus oxytocin (100 mU/kg) (n=8); and (6) melatonin (4 mg/kg) plus oxytocin (100 mU/kg) injected IV (n=8). Each rat underwent a laparotomy, and uterine myoelectrical signals were recorded. The mean spectrum, averaged over the spectral content of signals in each group, was compared. Results: Melatonin induced uterine myoelectrical activity in a dose-dependent manner. Treatment of melatonin after oxytocin suppressed the mean power of the signals. Serum melatonin concentrations were significantly higher in melatonin-treated rats. Conclusion: Melatonin itself at two different dose levels was found to be equally effective in stimulating the uterine electrical signals, although oxytocin-induced uterine electrical activity was suppressed by melatonin. These findings merit further investigations on the possible beneficial role of melatonin in the treatment of conditions associated with abnormal uterine activity. © 2014 by the Turkish-German Gynecological Education and Research Foundation

Melatonin treatment against remote organ injury induced by renal ischemia reperfusion injury in diabetes mellitus

Oxidative stress may have a role in liver damage after acute renal injury due to various reasons such as ischemia reperfusion (IR). Diabetes mellitus (DM) is an important disease for kidneys and may cause nephropathy as a long term complication. The aim of this study was to investigate protective effect of melatonin, a potent antioxidant, against distant organ injury on liver induced by renal IR in rats with or without DM. The rats were divided into six groups: control (n=7), DM (n=5), IR (n=7), DM+IR (n=7), melatonin+IR (Mel+IR) (melatonin, 4 mg/ kg during 15 days) (n=7), and Mel+DM+IR groups (n=7). Diabetes developed 3 days after single i.p. dose of 45 mg/kg streptozotocin. After 15 day, the left renal artery was occluded for 30 min followed 24 h of reperfusion in IR performed groups. DM did not alter oxidative parameters alone in liver tissue. The levels of malondialdehyde, protein carbonyl and nitric oxide with activities of xanthine oxidase and myeloperoxidase were increased in liver tissues of diabetic and non-diabetic IR groups. Nitric oxide level in DM was higher than control. The activities of catalase and superoxide dismutase were increased in IR groups in comparison with control and DM. ALT and AST levels were higher in IR and DM+IR groups than control and DM. Melatonin treatment reversed all these oxidant and antioxidant parameters to control values as well as serum liver enzymes. We concluded that renal IR may affect distant organs such as liver and oxidative stress may play role on this injury, but DM has not an effect on kidney induced distant organ injury via oxidant stress. Also, it was concluded that melatonin treatment may prevent liver oxidant stress induced by distant injury of kidney IR. © 2008 The Pharmaceutical Society of Korea

Protective role of melatonin in pinealectomized rat brains: in vivo magnetic resonance spectroscopic analysis

The goal of this study was to investigate the effect of melatonin on basic cerebral metabolites in pinealectomized (Px) rat brains. Twenty-one rats were randomly divided into three groups with seven rats per group. The study groups included sham-operated rats, Px rats and Px rats treated with melatonin. Melatonin administration began at 60 days following pinealectomy and continued for 21 days. At the end of the study, in vivo single voxel magnetic resonance spectroscopy was performed on whole brains to determine choline (Cho), creatine and N-acetyl aspartate (NAA) concentrations. Px rats had significantly lower NAA levels (P<0.05), and significantly higher Cho levels (P<0.05) when compared with sham-operated rats. Administration of melatonin had normalized NAA and Cho levels in Px rats. We propose that pinealectomy causes significant changes in cerebral metabolites which are compatible with neural loss. Melatonin administration prevents the disruptive effects of pinealectomy on brain tissue

Cytoprotective effects of molsidomine against methotrexate-induced hepatotoxicity: an experimental rat study

Emine Turkmen Samdanci,1 Mustafa Huz,1 Onural Ozhan,2 Kevser Tanbek,3 Esra Pamukcu,4 Ayse Nur Akatli,1 Hakan Parlakpinar21Department of Pathology, Inonu University School of Medicine, Malatya, Turkey; 2Department of Pharmacology, Inonu University School of Medicine, Malatya, Turkey; 3Department of Physiology, Inonu University School of Medicine, Malatya, Turkey; 4Department of Statistics, Firat University Faculty of Science, Elaziğ, TurkeyIntroduction and aim: Methotrexate (Mtx) is an antineoplastic and immunosuppressive drug that may cause hepatotoxicity, whereas molsidomine (Mol) is a vasodilating and antioxidant agent. This study aimed to investigate the potential protective effects of Mol in Mtx-induced liver toxicity in rats.Materials and methods: Forty Wistar albino rats were equally divided into five groups: control, Mol, Mtx, Mol–Mtx, and Mtx–Mol. Following treatment, the animals were sacrificed, and liver tissue samples were histopathologically evaluated using Roening grading and Bcl-2 antibody staining. Tissue oxidants, antioxidants, and serum transaminases were measured and statistically compared across all groups.Results: No hepatic fibrosis or steatosis was observed in any of the groups. In the Mtx group, grade 2 liver injury and score 2 Bcl-2 antibody staining were observed; however, in the Mol–Mtx group, these were lower (grade 1, score 1). There were no statistically significant differences in serum transaminase levels among groups. Malondialdehyde levels were higher in all rats that received Mtx, but no differences in myeloperoxidase levels were observed among the groups. Levels of tissue antioxidants, including superoxide dismutase, glutathione (GSH) peroxidase (GSH-Px), and reduced GSH, were significantly higher in the Mol-treated and Mol pre-treated groups. Catalase (CAT) levels were elevated in all Mol-treated groups, but only in that group were CAT levels statistically significantly higher than in the control group.Conclusion: Our results suggest that some oxidant levels could increase following Mtx administration in the liver, possibly contributing to liver damage, whereas Mol could mitigate the histopathological and biochemical effects of hepatotoxicity. However, molecular studies are required to understand the exact mechanisms of these alterations.Keywords: methotrexate, molsidomine, hepatotoxicity, hepatic fibrosi