Inactivated Sendai virus induces reactive oxygen species-mediated mitochondrial apoptosis in human renal carcinoma cells.

Aim: This study was aimed to investigate the proapoptotic effect of ultraviolet-inactivated Sendai virus strain Tianjin (UV-Tianjin) on human renal carcinoma A498 cell line in vitro and the possible molecular mechanisms. Materials & methods: Apoptosis, the levels of mitochondrial membrane potential, and reactive oxygen species (ROS) were assessed by flow cytometry. The expressions of apoptosis-related proteins in A498 cells were evaluated by western blotting. Results: UV-Tianjin induced mitochondria-dependent apoptosis in A498 cells, which was confirmed by the loss of mitochondrial membrane potential and the changes in expression of apoptosis-related proteins. Additionally, increased ROS generation was also proved to be involved in UV-Tianjin-induced apoptosis in A498 cells. Conclusion: UV-Tianjin triggered apoptosis through the ROS-mediated mitochondrial pathway in A498 cells. [ABSTRACT FROM AUTHOR]