Radiotherapy (RT) is the mainstay of brain cancer treatment due the generation of reactive oxygen species that cause double- and single-stranded DNA breaks. Although tumour cells are more radiosensitive, healthy cells are also subject to radiation damage, and as such therapeutic radiation can induce progressive cognitive decline. We investigated whether radiation-induced cognitive impairments could be prevented with the antioxidant tempol. Male C57BL/6 mice aged 27 weeks were administered either tempol (100mg/kg/day) or 0.9% saline for seven consecutive days via the I.P. route. One day after the first dose, mice were subject to a single dose of 20 Gy delivered to the right hemisphere. Sham mice were anaesthetised by not irradiated. The novel object recognition (NOR) test was performed at baseline, 7- and 50-days post-IR; the 3 Chamber Social Interaction (3-CSI) Test 50 days post-IR. At baseline, all groups exhibited normal long-term spatial memory given that the novel object was explored for significantly longer periods of time than the familiar object (saline+sham p=0.0159, saline+RT p=0.0015, tempol+RT p=0.0008). Exposure to radiation impaired this ability after 7 days (saline+sham p=0.0108, saline+RT p=0.2720, tempol+RT p=0.1078). Although tempol did not illicit significantly higher exploration of the novel object, the discrimination index between the two objects was significantly different to a theoretical mean of 0, indicating a preference for novelty (saline+sham p=0.0428, saline+RT p= 0.0859, tempol+RT p=0.0065. As such, we have early indications that minimising oxidative stress could limit the extent of cognitive impairment. Long-term behaviour testing and post-mortem analysis is ongoing.