Low-dose ionizing radiation (LDIR) at a dose reported in the radiation hormesis effect and adaptive response enhances antioxidant abilities and DNA repair abilities. In this study, we investigated the effects of radiation at 0.1–3 Gy on apoptosis induced by serum removal. Irradiation of 1 Gy at the timing of apoptosis induction improved cell viability. The inhibitory effect on apoptosis was strongly observed at 1 Gy of radiation rather than 0.1 Gy, which is the dose reported in the radiation hormesis effect and adaptive response. To study the effect of irradiation on cell cycle and DNA damage repair system, we investigated the activation of cyclin A and the phosphorylation of KAP1, and results showed that the irradiation decreased cyclin A and activated KAP1, suggesting cell cycle arrest and the activation of DNA damage repair system after the irradiation. Next, we investigated the increased phosphorylation of p38 and Jun-N-terminal kinase (JNK), stress response factors, that occurs during the progression of apoptosis by serum removal, and results showed that 1 Gy of irradiation increased p38 but decreased JNK. We investigated the effect of the irradiation on the regulation of DUSP1, which is a substrate specificity for MAPK, and results showed that the irradiation maintained the expression level for the transient induction of DUSP1 expression by serum removal. The results suggest that in LDIR at 1 Gy, apoptosis was suppressed by the activation of DNA damage repair signaling and crosstalk signaling between the p38 and JNK pathways mediated by DUSP1 induction.