Chemotherapeutic agents increase mitochondrial oxidative stress and apoptosis in optic nerve

Abstract

Chemotherapeutic agents such as cisplatin and 5fluorouracil are very effective and commonly used chemotherapeutic agents in treatment of several cancers including breast, testicular, ovarian and lung cancers. However, they have adverse effects and apoptosis in normal cells and neurons including optic nerve (Cardellicchio et al. 2014). Oxidative stress occurs during the several physiological functions such as mitochondria and phagocytosis. If the products of oxidative stress such as superoxide radical and hydrogen peroxide will be controlled by antioxidants the cell injury in normal tissue will not be occur. Results of recent reports indicated that optic nerve injury was induced through excessive production of reactive oxygen species (ROS) in rats by chemotherapeutic agents, although ROS were scavenged by antioxidants such as pycnogenol and rutin (Icel et al. 2018; Taşlı et al. 2018). It seems that the chemotherapeutic agentsinduced excessive ROS production results in increased levels of lipid peroxidation as malondialdehyde and inflammation markers such as TNF-α and NF-κB levels, but decrease of glutathione and total antioxidant levels. Apoptosis in the optic nerve was induced in ARPE19 eye cells by activation of intrinsic apoptosis pathway and death receptor signaling (Güçlü et al. 2018). In the presentation, we discussed novel effects of oxidative stress and apoptosis on the optic nerve injury in rodentsand human.  The results of current data suggest that oxidative stress has a main role in chemotherapeutic agentsinduced optic nerve injury in rodents, although the injury was attenuated by the antioxidant treatment.