Elimination of Reactive Oxygen Species Formed by Chemotherapeutic Agent in Imatinib Resistant K562r Cell Line by Sweetgum Oil

Objective: The antibacterial, antioxidant, antiseptic, and anti-inflammatory properties of Sweetgum oil (SO), a resinous exudate obtained from the injured trunk of the Liquidambar orientalis tree and named locally as “SO”, have been reported in many studies. Methods: In this study, cytotoxic doses of imatinib and ponatinib combined with SO were applied to determine differences in reactive oxygen species (ROS) formation in resistant K562R and susceptible K562S cell lines and to observe the effects of ROS on autophagy. Cytotoxicity, ROS formation, DNA damage due to ROS, autophagy, and the expression of Atg4A, Atg5, LC3α/β proteins in cell lines were investigated. In the cytotoxicity studies, the IC50 values of SO in K562R and K562S cells were determined as 250 μg/mL and 150 μg/mL. Results: 21.9% more ROS was observed in K562R cells. It was observed that the amount of ROS formed in the cells to which SO was applied was 28.8% less in K562R cells and 23.8% in K562S cells. In combined applications, ROS was decreased by 67.56% in K562R cells and by 60.9% in K562S cells. The effects of SO on autophagic activation were observed by fluorescence microscopy. Conclusion: SO increased autophagic activation compared with ponatinib in K562R cells and decreased autophagic activation compared with imatinib in K562S cells. Expression levels of Atg4A, LC3α/β and Atg5 indicate that autophagy is induced and ROS formation is reduced in combined applications.