An early treatment with 17‐β‐estradiol is neuroprotective against the long‐term effects of neonatal ionizing radiation exposure

J. Neurochem. (2011) 118, 626–635. Ionizing radiations can induce oxidative stress on target tissues, acting mainly through reactive oxygen species (ROS). The aim of this work was to investigate if 17‐β‐estradiol (βE) was able to prevent hippocampal‐related behavioral and biochemical changes induced by neonatal ionizing radiation exposure and to elucidate a potential neuroprotective mechanism. Male Wistar rats were irradiated with 5 Gy of X‐rays between 24 and 48 h after birth. A subset of rats was subcutaneously administered with successive injections of βE or 17‐α‐estradiol (αE), prior and after irradiation. Rats were subjected to different behavioral tasks to evaluate habituation and associative memory as well as anxiety levels. Hippocampal ROS levels and protein kinase C (PKC) activity were also assessed. Results show that although βE was unable to prevent radiation‐induced hippocampal PKC activity changes, most behavioral abnormalities were reversed. Moreover, hippocampal ROS levels in βE‐treated irradiated rats approached control values. In addition, αE administered to irradiated animals was effective in preventing radiation‐induced alterations. In conclusion, βE was able to counteract behavioral and biochemical changes induced in irradiated animals, probably acting through an antioxidant mechanism.