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International Journal of Pharmacology

Year: 2021 | Volume: 17 | Issue: 3 | Page No.: 122-129
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Authors

M.S. Cosgun

M.S. Cosgun

R. Coskun

R. Coskun

A.I. Celik

Keywords

Research Article

Effects of Adenosine Triphosphate on Vandetanib-Induced Heart Damage in Rats

M.S. Cosgun M.S. Cosgun's LiveDNA, R. Coskun R. Coskun's LiveDNA and A.I. Celik
Background and Objective: Vandetanib is a drug with anticancer activity that belongs to the tyrosine kinase inhibitor group. Cardiotoxicity is one of the serious side effects induced by vandetanib. Vascular endothelial growth factor (VEGF) inhibition is the main responsible mechanism for this side effect. VEGF increases intracellular adenosine triphosphate (ATP) levels and reduces the production of Reactive Oxygen Species (ROS), protecting the cell from oxidative stress. The study aims to investigate the protective effect of exogenous ATP against possible vandetanib-induced heart damage in rats. Materials and Methods: The animals were divided into three groups; vandetanib (VDB), vandetanib+ATP (VAT) and Healthy Groups (HG). Total Oxidant Status (TOS) and Total Antioxidant Status (TAS) levels and Oxidative Stress Index (OSI) were analyzed from the heart tissue. Troponin I (TP I), creatine kinase-MB (CK-MB) levels were analyzed from the blood sample. The cardiac histopathological examination was also performed. Results: Results shows that the OSI and TOS levels of VDB group animals increased significantly, TAS levels were found to be significantly lower compared to VAT and HG. Both TP I and CK-MB levels were significantly higher in the VDB group. However, the ATP administration to VAT group animals brought these values closer to HG. In histopathological examination, substantial myocardial damage was observed due to vandetanib exposure. However, ATP administration ameliorated structural damage signs induced by vandetanib. Conclusion: Vandetanib exposure substantially induced oxidative stress-related damage in rat heart tissue. Exogenous ATP replacement was able to ameliorate the toxic consequences of vandetanib, biochemically and histopathologically probably due to reduction of the ROS products.
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