The role of selenium in bevacizumab induced cardiotoxicity

Abstract

OBJECTIVE: We investigated the role of selenium in bevacizumab induced cardiotoxicity and involvement of transient receptor potential vanilloid 1 (TRPV1) channels in cardiomyocytes. MATERIALS AND METHODS: All cells (Human cardiomyocyte cell line) were cultured at 37 degrees C. We divided the cells into seven groups as control, bevacizumab, bevacizumab + capsazepin, bevacizumab + selenium, bevacizumab + selenium + capsazepin, selenium and selenium + capsazepin groups. Cells in the groups were stimulated with capsaicin and inhibited with capsazepin in related experiments for activation and inactivation of TRPV1 channels, respectively. RESULTS: Cytosolic calcium, apoptosis and intracellular ROS production levels were lower in bevacizumab + selenium group than in the bevacizumab group of cardiomyocytes (p < 0.001). Also, values were markedly lower in the bevacizumab + selenium + capsazepine group when compared to the bevacizumab + selenium group (p < 0.001). CONCLUSION: We found that cytosolic calcium, apoptosis, intracellular ROS production levels were increased in bevacizumab induced cardiotoxicity and selenium treatment could have beneficial effects on these parameters (Fig. 5, Ref. 51). Text in PDF www.elis.sk.