Murine thymic lymphoma cells and 3SBH5 cells are quite sensitive to X-rays and undergo apoptosis shortly after X-irradiation. Phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC), blocked the radiation-induced apoptosis in the 3SBH5 cells. On the other hand, chelerythrine, a PKC inhibitor, enhanced the radiation-induced apoptosis. These results suggest that PKC plays a key role in the regulation of radiation-induced apoptosis in 3SBH5 cells. Irradiation alone had no effect on the distribution of PKC subtypes (α, βI, βII and δ) in the 3SBH5 cells. The amounts of PKC βI in the cytosol of the 3SBH5 cells decreased in the cells pretreated with PMA. Irradiation did not change the decrease of PKC βI. In contrast, treatment with PMA had no effect on the distribution of the other PKC subtypes. PMA appears to influence processes of radiation-induced apoptosis through the change in the distribution of PKC βI. In addition, it was demonstrated that immunoprecipitates by anti-PKC α antibody included Raf-1, one of stress response proteins, in 3SBH5 cells after irradiation. These results suggest that PKC α might participate as a regulator in radiation-induced apoptosis, but PKC βI might influence the apoptosis indirectly through the PMA-induced change of the distribution.

Roles of protein kinase C in radiation-induced apoptosis signaling pathways in murine thymic lymphoma cells (3SBH5 cells)

Abstract Induction of an adaptive response by priming X rays in combination with challenge irradiations from high-LET accelerated heavy ions was attempted in young adult female C57BL/6J Jms mice using 30-day survival after the challenge irradiations as an index. Three kinds of accelerated heavy ions from monoenergetic beams of carbon, silicon and iron ions with LETs of about 15, 55 and 200 keV/μm, respectively, were examined. A priming low dose of 0.50 Gy X rays in combination with a challenging dose of 7.50 Gy was used in the animals serving as a positive control group to confirm the successful induction of an adaptive response. The priming low dose of 0.50 Gy X rays was also used in combination with accelerated heavy ions. The priming low dose of X rays significantly reduced the mortality from the high challenge doses of carbon or silicon particles but not from iron particles. These results indicate that an adaptive response could be induced by priming low-LET X rays in combination with subsequent challenge high-LET irradiations from certain kinds of accelerated heavy ions, and successful induction of an adaptive response would possibly be an event related to the LET and/or the type of heavy ions. This is the first time that the existence of an adaptive response induced by low-LET X rays against high-LET whole-body irradiation in mice has been demonstrated. These findings would provide new insight into the radiation-induced adaptive response in vivo.

SHORT COMMUNICATION X-Ray-Induced Radioresistance against High-LET Radiations from Accelerated Heavy Ions in Mice

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Roles of protein kinase C in radiation-induced apoptosis signaling pathways in murine thymic lymphoma cells (3SBH5 cells)

SHORT COMMUNICATION X-Ray-Induced Radioresistance against High-LET Radiations from Accelerated Heavy Ions in Mice