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 °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).
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