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Öğe Cardioprotective Effect of Selenium Against Cyclophosphamide-Induced Cardiotoxicity in Rats(Humana Press Inc, 2017) Gunes, Sibel; Sahinturk, Varol; Karasati, Pinar; Sahin, Ilknur Kulcanay; Ayhanci, AdnanThe objective of this study is to evaluate the possible protective effects of selenium (Se) against cyclophosphamide (CP)-induced acute cardiotoxicity in rats. A total of 42 male Spraque-Dawley rats were divided into six groups (n = 7). Rats in the first group were served as control. Rats in the second group received CP (150 mg/kg) at the sixth day of experiment. Animals in the third and fourth groups were treated with only 0.5 and 1 mg/kg Se respectively for six consecutive days. Rats in the fifth and sixth groups received respective Se doses (0.5 or 1 mg/kg) for 6 days and then a single dose of CP administered on the sixth day. On day 7, the animals were sacrificed; blood samples were collected to measure malondialdehyde (MDA), glutathione (GSH), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and ischemia-modified albumin (IMA) levels. Heart tissues were processed routinely and tissue sections were stained with H + E for light microscopic examination. In the CP-treated rats MDA, LDH, CK-MB, and IMA serum levels increased, while GSH levels decreased. Microscopic evaluation showed that tissue damage was conspicuously lower in CP plus Se groups. Moreover, 1 mg/kg Se was more protective than 0.5 mg/kg Se as indicated by histopathological and biochemical values. In conclusion, Se is suggested to be a potential candidate to ameliorate CP-induced cardiotoxicity which may be related to its antioxidant activity.Öğe Hepato-preventive and anti-apoptotic role of boric acid against liver injury induced by cyclophosphamide(Elsevier Gmbh, 2019) Cengiz, Mustafa; Yildiz, Songul Cetik; Demir, Cemil; Sahin, Ilknur Kulcanay; Teksoy, Ozgun; Ayhanci, AdnanThis study aims to examine cyclophosphamide (CP) exsposure associated toxicity on rat livers and the likely defensive effects of boric acid (BA). The rats used in this study were divided into four groups: control group, CP group, BA group, and BA + CP group. The present study was carried out using routine histological H&E stain, immunohistochemical stain caspase-3 as apoptotic marker, serum biochemical analysis for liver function markers (alanine transaminase (ALT), aspartate transaminase (AST) and alkalen phosphatase (ALP)), oxidative stress markers (total oxidant status (TOS), oxidative stress index (OSI) and total antioxidant capacity marker (TAC)). In the CP group, the levels of ALT, AST, ALP, TOS, OSI and caspase-3 increased whereas TAC levels decreased compared with the control group. In the BA + CP group, the levels of ALT, AST, ALP, TOS, OSI and caspase-3 decreased whereas TAC levels increased compared with the CP group. The histopathological evaluation of light microscope images and immunohistochemical caspase-3 activity in the BA + CP group were found to be decrease compared with those in the CP group. In conclusion, BA was successful in defending the liver against apoptosis and histopathological changes that are attributable to CP.Öğe Myelosuppression and Oxidative Stress Induced by Cyclophosphamide in Rats: The Protective Role of Selenium(Adiyaman University, 2019) Ayhanci, Adnan; Heybeli, Nilhan; Kulcanay Şahin, İlknur; Cengiz, MustafaAim of this study is to detect the protective role of selenium (Se) against bone marrow and blood toxicity in CP-induced hematoxicity model. We categorized the rats into 6 groups of 7 animals in each group (control; 150 mg/kg CP; 0.5 mg/kg Se; 1 mg/kg Se; 150+0.5 mg/kg CP+Se; 150+1 mg/kg CP+Se). Se injections started 5 days before the CP injections and carried on until the end of the experiment (6th day) for the groups to which CP was injected together with Se. CP was applied as a single dose before anesthesia. For that reason, on the 7th day, blood was taken with cardiac puncture and bone marrow was taken by flushing the femur. Peripheral blood cells and bone marrow nucleated cells were counted on a cell counter. Intraperitoneal CP injection was found to reduce the number of leukocytes by 317%, thrombocyte by 36% and bone marrow nucleated cells by 481% compared to the control group. In the groups where CP was given after 0.5 and 1 mg/kg Se, numbers of leukocyte, thrombocyte and bone marrow nucleated cells were considerably improved compared to the group to which CP was given only (p<0.001). Results show that 1 mg/kg Se has a better protection than 0.5 mg/kg against CP associated hematoxicity and myelosuppression. Our results also imply that the doses of Se could be adjusted according to enhance in CP dose so as to gain a stronger protective effect. We believe there is a need of further studies in which different doses of Se will be used against CP induced hematoxicity. Se can provide protection against CP-induced myelosupression and lipid peroxidation. © 2019, Adiyaman University. All rights reserved.Öğe Selenium Ameliorates Cyclophosphamide - Induced Hepatotoxicity(Wiley-Blackwell, 2015) Ayhanci, Adnan; Acar, Ozge; Sahinturk, Varol; Gunes, Sibel; Sahin, Ilknur Kulcanay; Musmul, Ahmet; Uslu, Sema…Öğe The role of Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways in mediating the protective effect of boric acid on acrylamide-induced acute liver injury in rats(Pergamon-Elsevier Science Ltd, 2022) Cengiz, Mustafa; Ayhanci, Adnan; Akkemik, Ebru; Sahin, Ilknur Kulcanay; Gur, Fatma; Bayrakdar, Alpaslan; Cengiz, Betul PekerIntroduction: This study aims to investigate whether boric acid (BA) can protect rats from acrylamide (AA)induced acute liver injury. Materials and methods: AA was used to induce acute liver injury. Thirty rats were divided into five group including Group 1 (saline), Group 2 (AA), Group 3 (20 mg/kg BA), Group 4 (10 mg/kg BA+AA) and Group 5 (20 mg/kg BA+AA). Their blood and liver were harvested to be kept for analysis. Liver function enzyme activities were performed by spectrophotometric method. Catalase (CAT), superoxide dismutase (SOD) activity, and malondialdehyde levels were determined by colorimetric method. The in-silico studies were performed using the blind docking method. Results: Administration AA to rats, biochemical parameters, liver histology, and expression levels of apoptotic markers were negatively affected. However, after the administration of BA, the altered biochemical parameters, liver histology, and expression levels of apoptotic markers were reversed. Moreover, the mechanisms of AA-induced deterioration in the levels of SOD, CAT, and Nrf2-Keap-1 and the mechanisms of the protective effect of BA against these deteriorations were explained by in silico studies. Conclusion: Thus, the present study could explain the interactions between AA and thiol-containing amino acid residues of Keap-1, the effect of BA on these interactions, and the biochemical toxicity caused by the AA. In this sense, this work is the first of its kind in the literature. Based on the biochemical, histopathological, and in silico results, it can be suggested that BA has the potential to be used as a protective agent against AA-induced liver injury.
