Glioblastoma (GBM) is the most aggressive and common primary brain tumors.This results in resistance to current treatment by low linear energy transfer (LET radiation such as X ray. In addition, many side effect of cisplatin are major drawbacks in radiation therapy of GBM patients. Hence, the aim of the study was to investigate the toxicity of combined high linear energy transfer (LET) carbon ions with cisplatin in bystander normal cells. Briefly, confluent GBM (T98G) cells were treated with cisplatin, followed by carbon ions. Within 20 min following exposure, carbon-irradiated T98G cells were trypsinzied and seeded on the top of insert with bystander normal NB1RGB cells in the presence and absence of gap-junction inhibitor (AGA) at the bottom of it and assayed for further analysis. Our results show that gap junction intercellular communication (GJIC) enhances cisplatin toxicity from carbon-irradiated T98G cells to bystander normal NB1RGB cells. However, the cytotoxicity in the bystander normal cells can be partially suppressed by inhibiting of GJIC. Consequently, the protective mechanism of AGA against the toxic effect of radiochemotherapy was assessed based on the restoration of the antioxidant defenses via activation of Nrf2. This study demonstrates that GJIC inhibitor is a new candidate that the radioprotective effect in bystander normal cells and its combination with high LET carbon ions, is promising method in GBM patients.