Ionizing radiation induced mitochondrial morphological change during the cell cycle

Noguchi, Miho; Kanari, Yukiko; Kaminaga, Kiichi; Sakamoto, Yuka; Narita, Ayumi; Fujii, Kentaro; Yokoya, Akinari

Most studies of radiation induced biological effect starts from nuclear DNA damage. However, in the case of low dose irradiation, recent reports suggest that extranuclear targets, such as in cytoplasm, may have a role in mediating some important effects of radiation. Cellular effect of cytoplasmic irradiation remains to be elucidated. Mitochondria spread throughout the entire cytoplasm and contain their own genome, and mediate essential cell functions, such as generation of ATP and regulation of cell death. Mitochondria are main source of oxidative stress to generate ROS as by-product of respiration for ATP production. In addition, dysfunctions of mitochondria are involved in a wide variety of diseases. Mitochondrial functions are indispensable for survival. However, radiation effect of mitochondrial functions is not clear. In order to clarify what effects ionizing radiation leads to mitochondrial functions, we first examined the effects of ionizing radiation on mitochondrial morphology in mammalian cells. Mitochondria are dynamic organelles that continuously fuse and divide in response to environment and cellular differentiation. It is known that mitochondrial morphology dynamically change with cell cycle progression. In this study, after irradiation, we labeled mitochondria by Mitotracker Red and analyzed kinetics of mitochondrial morphology for 4 days by live-cell imaging techniques. Cell cycle stages were identified by nuclei staining. We reports the relation between radiation induced cell cycle arrest and mitochondrial dynamics.