Protective Effect of Adenosine Triphosphate Against Bevacizumab-Induced Mandibular Bone Damage in Rats

Bevacizumab is the anticancer drug used as an anti-angiogenic inhibitor of vascular endothelial growth factor (VEGF)-A. Bevacizumab causes toxicity by decreasing adenosine triphosphate (ATP) and increasing through reactive oxygen species (ROS) production. Male Albino Wistar rats were divided into 3 groups healthy (HG), bevacizumab administered (BVZ) and ATP+bevacizumab administered (ATP+BVZ). In the ATP+BVZ group, 25mg/kg ATP was injected between the mandibular gingiva and the bone. One hour after the application, 10 mg/kg bevacizumab was administrated intraperitoneally to the ATP+BVZ and BVZ groups. Two doses of bevacizumab were administered on the 1st and 15th days. ATP administration was continued once a day for 30 days. intoATP significantly prevented the increase in malondialdehyde (MDA) and total oxidant status (TOS) levels and the decrease in total glutathione (tGSH) and total antioxidant status (TAS) levels in the mandible bone tissue. ATP alleviated the histopathological damage associated with bevacizumab.